Reduction In Mean Arterial Blood Pressure Research Articles

The effect of transcutaneous electrical acupoint stimulation on postoperative awakening after general anaesthesia: a systematic review and meta-analysis.

The existing body of research concerning the impact of transcutaneous electrical acupoint stimulation (TEAS) on early postoperative recovery is marked by a lack of consensus. This meta-analysis, encompassing a systematic review of randomised controlled trials, seeks to critically assess the efficacy of TEAS in relation to awakening from general anaesthesia in the postoperative period. The inclusion criteria for this study were peer-reviewed randomised controlled trials that evaluated the influence of TEAS on the process of regaining consciousness following general anaesthesia. A comprehensive search was conducted across several reputable databases, including PubMed, Embase, the Cochrane Library, the China National Knowledge Infrastructure, the VIP Database, the SinoMed Database, and the WANFANG Medical Database. The search was not limited by date, extending from the inception of each database up to December 2023. The methodological quality and risk of bias within the included studies were appraised in accordance with the guidelines outlined in the Cochrane Handbook for Systematic Reviews of Interventions, version 5.1, and its associated tool for assessing risk of bias. The analysis encompassed 29 studies involving a total of 2,125 patients. Participants in the TEAS group demonstrated a significantly shorter duration to achieve eye-opening [mean difference (MD), -3.16 min; 95% confidence interval (CI), -3.93 to -2.39], endotracheal extubation (MD, -4.28 min; 95% CI, -4.79 to -3.76), and discharge from the post-anaesthesia care unit (MD, -8.04 min; 95% CI, -9.48 to -6.61) when compared to the control group receiving no or sham stimulation. Additionally, the TEAS group exhibited markedly reduced mean arterial blood pressure (MD, -9.00 mmHg; 95% CI, -10.69 to -7.32), heart rate (MD, -7.62 beats/min; 95% CI, -9.02 to -6.22), and plasma concentrations of epinephrine (standardised MD, -0.81; 95% CI, -1.04 to -0.58), norepinephrine (MD, -47.67 pg/ml; 95% CI, -62.88 to -32.46), and cortisol (MD, -110.92 nmol/L; 95% CI, -131.28 to -90.56) at the time of extubation. Furthermore, the incidence of adverse effects, including agitation and coughing, was considerably lower in the TEAS group relative to the control group (odds ratio, 0.30; 95% CI, 0.22-0.40). The findings of this study indicate that TEAS may hold promise in facilitating the return of consciousness, reducing the interval to awakening post-general anaesthesia, and enhancing the awakening process to be more tranquil and secure with a diminished likelihood of adverse events. However, caution must be exercised in interpreting these results due to the notable publication and geographical biases present among the studies under review. There is an imperative for further high-quality, low-bias research to substantiate these observations. The review protocol was registered with the PROSPERO International Prospective Register of Systematic Reviews (CRD42022382017).

Abstract P175: The Effect of TRF on Hypertension Development in Male Dahl Salt-Sensitive Rats

Time restricted feeding (TRF), or food consumption restricted to <10 hrs/day, has been shown to improve blood pressure in various cardiometabolic diseases, yet there is limited data on the effect in SS hypertension. The goal of this study was to examine the effect of TRF on disease development in the Dahl SS rat. We hypothesized that implementing TRF during a critical timepoint in disease progression would reduce mean arterial blood pressure (MAP). To study this, femoral catheters were surgically implanted in male Dahl SS rats at 9±0.5 weeks of age (n=5-7/group), allowing for urine and arterial blood sample collection from conscious rats during continual blood pressure recording. After 1 week of recovery, rats either continued a low salt (LS;0.4% NaCl) diet or were switched to a high salt diet (HS;4% NaCl) with ad libitum (ad lib) access for 1 week. At the start of week 2, a subset of rats began TRF, in which food was provided for 8 hrs (10PM-6AM) during their active period for an additional week. Rats meeting the following criteria were included in analysis: pulse pressure > 10 mmHg, baseline MAP of 115-130 mmHg, and a 10-20 mmHg increase in MAP after 1 week on HS. Differences in MAP were analyzed by 2-way ANOVA with Tukey multiple comparisons and data are reported as mean ± SEM. By the end of week 2, HS TRF rats trended toward lower average MAP compared to HS ad lib rats (141.51±3.41 vs 149.49±1.65 mmHg; p=0.07). However, we found that the HS TRF rats had reduced MAP during their active period (6PM-6AM), compared to the HS ad lib rats (142.60±2.99 vs 151.65±1.862 mmHg; p<0.05), but no difference during the inactive period (6AM-6PM). At the end of the study, average MAP was calculated every 4 hrs to identify the timing at which TRF reduced MAP. We found that the HS TRF rats had lower MAP from 6PM to 10PM (134.61±2.34 vs 146.75±1.21 mmHg; p<0.05) and 10PM to 2AM (144.58±2.79 vs 154.70±2.18 mmHg; p<0.05) when compared to the HS ad lib rats. The LS TRF group also had lower pressure from 6PM-10PM compared to the LS ad lib group (124.93±1.19 vs 130.56±0.73 mmHg; p<0.05), suggesting that this time-specific reduction in MAP may be due to fasting, as there were no other differences in MAP within the LS groups. This suggests that TRF may slow progression of hypertension development in the Dahl SS rat, primarily by affecting MAP during the active period. Future studies will examine how TRF affects Na + handling to further understand these time-dependent effects.

The role of protein prenylation inhibition through targeting FPPS by zoledronic acid in the prevention of renal fibrosis in rats

Renal fibrosis (RF) represents the most widespread pathological condition in chronic kidney disease (CKD). Recently, protein prenylation has been implicated in the fibrosis’s progression. The research examined the renoprotective effect of zoledronic acid (ZA) (50 µg/kg/week) in a rat model of carbon tetrachloride (CCl4)-induced RF through targeting protein prenylation. Forty Wistar male rats were split up into the control group, vehicle-treated group, model-RF group, and RF-ZA group. Mean arterial blood pressure (MBP), BUN, serum creatinine, and urine albumin–creatinine ratio (uACR), protein levels of farnesyl pyrophosphate (FPP), tumour necrosis factor-alpha (TNF-α), transforming growth factor-β (TGF-β), and malondialdehyde (MDA), and catalase and gene expression of farnesyl pyrophosphate synthase (FPPS) and nuclear factor-kB (NF-κB) were measured. Immunohistochemical staining for renal interleukin-6 (IL-6), α-smooth muscle actin (α-SMA), and caspase-3, as well as histopathological alterations, were assessed. ZA considerably ceased the reduction in MBP, markedly reduced uACR, serum creatinine, BUN, and expression of FPPS, FPP, NF-κB, TGF-β, TNF-α, and MDA, and significantly increased catalase levels compared to the model-RF rats. ZA ameliorated the CCl4-induced histopathological alterations and suppressed the expression of caspase-3, α-SMA, and IL-6. In conclusion, ZA preserved renal function and prevented renal fibrosis in a rat model. These were achieved through targeting protein prenylation mainly by inhibiting FPPS.

Consumption of a Byproduct of Chia Seed Oil Extraction by Cold Pressing Ameliorates Cardiovascular Risks Factors in an Experimental Model of Metabolically Unhealthy Normal Weight.

The byproduct of Salvia hispanica (chia) seed oil extraction by cold pressing, also known as expeller, possesses a high nutritional value. It is rich in proteins, fibers, minerals, and has a residual oil content of 7-11%, which is rich in omega 3 linolenic acid (ALA). However, this byproduct has been historically undervalued. Thus, the aim of current work was to study the effects of consuming of a rich in chia expeller diet on a rabbit model of metabolically unhealthy normal weight to validate their use as a functional food. Rabbits were fed different diets for a period of 6 weeks: a standard diet (CD), a high-fat diet (HFD), a rich in expeller CD (Exp-CD) and a rich in expeller HFD (Exp-HFD). The Exp-HFD attenuated the rise in basal glucose, TyG index, triglycerides, cholesterol and non-HDL cholesterol induced by the HFD. Both rich in expeller diets reduced mean arterial blood pressure (MAP) and increase liver and fat ALA levels compared to their respective controls. Furthermore, the angiotensin converting enzyme (ACE) activity was lower in the lungs of animals fed on rich in expeller diets compared to their respective controls. In vitro studies showed that ALA inhibited ACE activity. The evaluation of vascular reactivity revealed that rich in expeller diets improved angiotensin II affinity and reduced contractile response to noradrenaline. In conclusion, the consumption of rich in expeller diets showed beneficial effects in preventing cardiovascular risk factors such as insulin resistance, dyslipidemia and MAP. Therefore, its use as functional ingredient holds significant promise.

Treatment of Hypotension with Phenylephrine Increases Cerebral Microvascular Perfusion in a Rat Model of Acute Hemodilution

Intraoperative blood loss is associated with reduced mean arterial blood pressure (MAP), which may endanger vital organ perfusion, including the brain. Phenylephrine (PE), an α1-receptor agonist, is clinically utilized to treat intraoperative hypotension through vasoconstriction of resistance arterioles. Clinical studies suggest that raising MAP with PE may decrease perfusion to vital organs such as the brain. Experimental studies suggest that lower α-receptor density in the cerebral resistance arteries may lead to preserved brain perfusion after PE administration. We hypothesize that treatment of hypotension with PE will result in preserved brain perfusion due to different microvascular blood flow and tissue oxygen tension (pO2) responses in the brain and skeletal muscle in an experimental rat model. With Animal Care and Use Committee approval in accordance with ARRIVE-2 guidelines, spontaneously breathing anesthetized rats (1.5% isoflurane) underwent hemodilution by exchanging 40-50% estimated blood volume 1:1 with saline over 10 minutes to achieve a 10-20 mmHg drop in MAP. MAP (tail artery) was measured continuously. Hypotension was treated with PE (10-20 μg/kg/min iv) to increase MAP to a target above baseline MAP. Shed blood was re-infused after stopping the PE infusion. Microvascular blood flow (Oxyflo; Oxford Optronix, Oxford, UK, n=7) or microvascular pO2 (OxyLED, Oxyphor G4, Oxygen Enterprises Ltd., Philadelphia, PA, n=6) were measured continuously in the cerebral cortex (burr hole) and biceps femoris muscle simultaneously in each rat. Results were analyzed via one or two-way ANOVA, with significance achieved at p<0.05. Baseline and post-hemodilution MAP values were comparable in both groups. PE infusion increased MAP to a mean level near 100 mmHg in both groups (p<0.05). Microvascular blood flow and tissue pO2 were greater in the brain as compared to the muscle at all time points (p<0.01 for both). PE infusion resulted in an increase in cerebral microvascular blood flow from baseline (1465±689 vs. 687±453 blood perfusion units (BPU); p<0.001) that was sustained after discontinuing PE and during blood reinfusion. No changes in muscle microvascular flow were observed after PE infusion (294±129 vs. 168±113 BPU). A sustained increase in cerebral microvascular pO2 was measured following PE infusion (50.2±8.6 vs. 40.6±4.6 mmHg; p=0.02), whereas muscle tissue pO2 did not change (22.2±5.6 vs. 25.0±2.5 mmHg). A differential blood flow and microvascular pO2 response was observed following PE infusion in brain and skeletal muscle. Both cerebral microvascular blood flow and tissue pO2 demonstrated sustained increases after PE infusion. By contrast, no changes were observed in muscle microvascular blood flow and pO2. These results suggest that treatment of hypotension with PE administration preferentially increased cerebral vs. muscle perfusion in an experimental model of acute blood loss and fluid resuscitation. Canadian Anesthesiologists’ Society and University of Toronto Merit Award Support. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Heat Stress but Not Capsaicin Application Alleviates the Hypertensive Response to Isometric Exercise

Heat stress and cutaneous capsaicin application act independently to reduce mean arterial blood pressure (MAP) at rest. The present study investigated whether a mixed intervention might alleviate to a greater extent the hypertensive response to isometric exercise. An end-exercise systolic blood pressure (SBP) lower than 215 mmHg or higher than 220 mmHg was set for the inclusion in the group observed with typical (CON, n = 9) or hypertensive (HRE, n = 8) response to dynamic exercise, respectively. The participants performed four trials held in thermoneutral (TN:23 °C) or hot (HT:33 °C) conditions with capsaicin (CA:4.8 mg·patch−1) or placebo (PL) patches (12 × 18 cm2) applied to their two quadriceps, left pectoralis major and left scapula. The trials comprised: a 5 min baseline period preceding patch application, a 30 min rest period and a 5 min isometric handgrip exercise (20% maximal voluntary contraction, 10.1 ± 1.9 kg). Thermoregulatory and cardiovascular data were analyzed using mixed three-way ANOVA. End-resting MAP and pain sensation were higher in PL-TN (p = 0.008) and CA-HT (p = 0.012), respectively. End-exercise SBP tended to be higher in HRE individuals across environments (p = 0.10). Total peripheral resistance and MAP remained lower in HT across groups (p < 0.05). Despite the alleviating effect of the heat stressor, an augmented burning sensation-induced peripheral vasoconstriction might have blunted the pressure-lowering action of capsaicin.

Effects of dexmedetomidine, fentanyl and magnesium sulfate added to ropivacaine on sensory and motor blocks in lower abdominal surgery: a randomized clinical trial.

This study aimed to compare the effects of intrathecal dexmedetomidine, fentanyl and magnesium sulfate added to ropivacaine on the onset and duration of sensory and motor blocks in lower abdominal surgery. This double-blind randomized clinical trial included 90 patients scheduled for lower abdominal surgery at Vali-Asr Hospital in Arak, Iran. The enrolled patients were randomly divided into three equal groups and then underwent spinal anesthesia. The first group received 10 μg of dexmedetomidine, the second group received 50 μg of fentanyl, and the third group received 200 mg of 20% magnesium sulfate intrathecally in addition to 15 mg of 0.5% ropivacaine. In the dexmedetomidine group, the mean arterial blood pressure was lower than the other two groups (P = 0.001). Moreover, the time to onset of sensory block (P = 0.001) and the mean duration of sensory block (P = 0.001) were shorter and longer, respectively, in the dexmedetomidine group than in the other two groups. In the dexmedetomidine group, the mean time to onset of motor block (P = 0.001) and the mean duration of motor block (P = 0.001) were lower and higher than in the other two groups, respectively. There was no significant difference in visual analog scale score, heart rate, administered opioid, and drug side effects among the three groups. Dexmedetomidine caused early sensory and motor blocks while prolonging the duration of sensory and motor blocks compared with the other two groups. In addition, dexmedetomidine reduced mean arterial blood pressure in patients. Based on the findings of this study, it is recommended that dexmedetomidine can be used in order to enhance the quality of sensory and motor block in patients.

PS-B05-7: HYPERTENSION IN A MODEL OF PKD IS NOT DEPENDENT ON THE SHORT-TERM ACTIONS OF TUMOUR NECROSIS FACTOR-A IN THE SFO

Objective: The development of hypertension in the Lewis polycystic kidney (LPK) disease model of kidney disease is caused, in part, by neuronal overactivity in the subfornical organ (SFO). Circulating proinflammatory cytokines, namely TNFα, are suggested to act in the central nervous system to produce an increase in neuronal excitability. As circulating cytokines are increased in kidney disease, we hypothesised that TNFα acts on the SFO to increase neuronal activity, therefore contributing to the development of hypertension in this animal model. Design and Methods: Urethane anaesthetised Lewis control (n = 23 total) and LPK (n = 18 total) animals were instrumented to record blood pressure and perform microinjections of TNFα (1–300pg/50nl), TNFα receptor 1 (TNFRI) neutralising antibody (1ng/50nl) or minocycline (0.5 μg/50nl), an inhibitor of microglial activation. Results: Exogenous TNFα microinjected into the SFO elicited a significant pressor response in the Lewis control but not the LPK animals (9 ± 2 mmHg vs -1 ± 3 mmHg, Lewis vs LPK peak change from baseline, P = 0.04). Acute inhibition of actions of local TNFα via administration of TNFRI neutralising antibody in the SFO did not reduce mean arterial blood pressure in Lewis control or LPK animals (1 ± 1mmHg vs -1 ± 1mmHg, Lewis vs LPK change from baseline, P = 0.59). Acute blockade of the actions of all proinflammatory cytokines on microglia via microinjection of minocycline in the SFO did not reduce blood pressure in Lewis control or LPK animals (-1 ± 1mmHg vs -1 ± 1mmHg, Lewis vs LPK change from baseline, P = 0.11). Prior microinjection of TNFRI neutralising antibody into the SFO abolished the pressor response observed upon microinjection of TNFα in Lewis rats (9 ± 2 mmHg vs 1 ± 1 mmHg, TNFα vs TNFα after TNFRI Ab peak change from baseline, P = 0.01), whereas prior microinjection of minocycline into the SFO only attenuated the pressor response observed upon TNFα microinjection in Lewis rats (9 ± 2 mmHg vs 3 ± 1 mmHg, TNFα vs TNFα after Minocycline peak change from baseline, P = 0.04) Conclusions: Overall, these findings demonstrate that although hypertension observed in the LPK is sustained by an increase in SFO activity, the short-term control of mean arterial blood pressure activity is not dependent on the actions of endogenous TNFα or generalised microglial activation by proinflammatory cytokines in the SFO.

HYPERTENSIVE ENCEPHALOPATHY: TO BE DIAGNOSED AND TREATED IMMEDIATELY

It is important to have a good understanding of the pat­hogenetic diagnosis and treatment features of the severe complication with high mortality – hypertensive encepha­lopathy (HE) because of the amount of people suffering from chronic arterial hypertension is constantly increa­sing. Thus, this article briefly reviews the mechanism of cerebral blood flow autoregulation, HE pathophysiology, and the main aspects of diagnosis and treatment. An HE episode is caused by a sudden and significant increase in arterial blood pressure, when the autoregulatory mecha­nism of cerebral blood flow becomes ineffective. Along with increased blood pressure, the patient gradually deve­lops neurological symptoms ranging from intense heada­che to vision loss, loss of consciousness, and convulsions. The diagnosis of HE is based on the clinical signs – acute arterial hypertension and the subsequent neurological symptoms. Also, the diagnosis of HE can be determined retrospectively when the neurological symptoms rapi­dly disappear with effective antihypertensive treatment. Computed tomography is important in differentiating HE from intracerebral hemorrhage and ischemic stroke. In management of HE it is recommended to return to the limits of cerebral blood flow autoregulation by immedi­ately reducing mean arterial blood pressure by 20-25%. In order to achieve the maximum rapid antihyperten­sive effect, it is suggested to administer the medication only intravenously. Labetalol and sodium nitroprusside are currently recommended first-line drugs for the treat­ment of HE. Patients with HE should be hospitalized in the intensive care unit for continuous control of decre­asement of arterial blood pressure while observing the cautious dynamics of the neurological condition. The outcome of patients depends on the urgency and effici­ency of treatment in returning arterial blood pressure to the limits of cerebral blood flow autoregulation, as well as on comorbidities, the severity of the condition and possible complications.

Malate reduced blood pressure and exerted differential effects on renal hemodynamics; role of the nitric oxide system and renal epithelial sodium channels (ENaC)

Malate regulates blood pressure via nitric oxide production in salt-sensitive rats, a genetic model of hypertension. This study investigated the possible contributions of malate to blood pressure regulation and renal haemodynamics in normotensive rats. Malate (0.1, 0.3 and 1 μg/kg, iv) was injected into rats or L-nitro-arginine methyl ester (L-NAME)-treated rats and mean arterial blood pressure (MABP), cortical blood flow (CBF), and medullary blood flow (MBF), was measured. The clearance study involved infusion of malate at 0.1 μg/kg/h into rats, and MABP, CBF, MBF, glomerular filtration rate (GFR), urine volume (UV) and sodium output (UNaV) were determined. Mechanistic studies to evaluate the role of renal sodium channels involved the treatment with malate (600 mg/kg, po), amiloride (2.5 mg/kg, po) or hydrochlorothiazide (HCTZ) (10 mg/kg, po), and UV and UNaV were determined. Malate elicited significant peak reductions in MABP (124 ± 6.5 vs 105 ± 3.1 mmHg) at 0.1 μg/kg), CBF (231 ± 18.5 vs 205 ± 10.9 PU). L-NAME did not reverse the effect of malate on MABP but tended to blunt the effect on CBF (40%) and MBF (87%) at 0.3 μg/kg. Infusion of malate reduced MABP, CBF, and MBF in a time-dependent manner (p<0.05). Malate exerted a three-fold decrease in GFR in a time-related fashion (p<0.05) as well as increased UV. UNaV increased by 86% in malate-treated-amiloride rats (p<0.05). These data indicate that malate modulates blood pressure and exerts vascular and tubular effects on renal function that may involve epithelial sodium channels (ENaC).

Antihypertensive activity and acute toxicity of turmeric (Curcuma longa L.) in L-NAME-induced hypertension animals

Hypertension is one of the significant risk factors for cardiovascular disease and can lead to complications. Uncontrolled hypertension can lead to vascular endothelial dysfunction and other complications of cardiovascular disease. This study aimed to determine the effect of turmeric rhizome (Curcuma longa L.) in extracts and the fractions on a hypertensive rat’s model induced by L-NAME 40 mg/kg for three weeks and an acute toxicity study of the extract. Antihypertensive research was performed on male Wistar rats utilizing non-invasive procedures. Turmeric extract at doses of 50, 100, and 200 mg/kg and its fraction of n-hexane, acetyl acetate, and ethanol at a dose of 25 mg/kg, respectively, were given daily per oral for three weeks to 2.5 mg/kg captopril. The systolic and diastolic blood pressure were measured at 0, 21, and 42 days after treatment and was calculated as mean arterial blood pressure (MAP). Acute toxicity testing refers to the OECD 420 Fixed-Dose method with several dosage levels, consists of 300, 2000, and 5000 mg/kg. The turmeric extract at doses of 50, 100, and 200 mg/kg and its fraction of n-hexane, acetyl acetate, and ethanol significantly reduced mean arterial blood pressure (p&lt;0.05) compared to the control group. Acute administration of turmeric extracts up to a dose of 5000 mg/kg in test animals did not show any death. Turmeric and its components are considered to possess antihypertensive actions. Antihypertensive activity increased in a dose-dependent manner. Turmeric extract is categorized as being almost entirely non-toxic.

Interleukin-1 blockade attenuates white matter inflammation and oligodendrocyte loss after progressive systemic lipopolysaccharide exposure in near-term fetal sheep

BackgroundIncreased systemic and tissue levels of interleukin (IL)-1β are associated with greater risk of impaired neurodevelopment after birth. In this study, we tested the hypothesis that systemic IL-1 receptor antagonist (Ra) administration would attenuate brain inflammation and injury in near-term fetal sheep exposed to lipopolysaccharide (LPS).MethodsChronically instrumented near-term fetal sheep at 0.85 of gestation were randomly assigned to saline infusion (control, n = 9), repeated LPS infusions (0 h = 300 ng, 24 h = 600 ng, 48 h = 1200 ng, n = 8) or repeated LPS plus IL-1Ra infusions (13 mg/kg infused over 4 h) started 1 h after each LPS infusion (n = 9). Sheep were euthanized 4 days after starting infusions for histology.ResultsLPS infusions increased circulating cytokines and were associated with electroencephalogram (EEG) suppression with transiently reduced mean arterial blood pressure, and increased carotid artery perfusion and fetal heart rate (P < 0.05 vs. control for all). In the periventricular and intragyral white matter, LPS-exposure increased IL-1β immunoreactivity, numbers of caspase 3+ cells and microglia, reduced astrocyte and olig-2+ oligodendrocyte survival but did not change numbers of mature CC1+ oligodendrocytes, myelin expression or numbers of neurons in the cortex and subcortical regions. IL-1Ra infusions reduced circulating cytokines and improved recovery of EEG activity and carotid artery perfusion. Histologically, IL-1Ra reduced microgliosis, IL-1β expression and caspase-3+ cells, and improved olig-2+ oligodendrocyte survival.ConclusionIL-1Ra improved EEG activity and markedly attenuated systemic inflammation, microgliosis and oligodendrocyte loss following LPS exposure in near-term fetal sheep. Further studies examining the long-term effects on brain maturation are now needed.

The Evaluation Point-of-Care Ultrasound in the Post-Anesthesia Unit-A Multicenter Prospective Observational Study.

Introduction: Point-of-care ultrasound (POCUS) is the most rapidly growing imaging modality for acute care. Despite increased use, there is still wide variability and less evidence regarding its clinical utility for the perioperative setting compared to other acute care settings. This study sought to demonstrate the impact of POCUS examinations for acute hypoxia and hypotension occurring in the post-anesthesia care unit (PACU) versus traditional bedside examinations. Methods: This study was designed as a multi-center prospective observational study. Adult patients who experienced a reduced mean arterial blood pressure (MAP < 60mmHG) and/or a reduced oxygen saturation (SpO2 < 88%) in the PACU from 7AM to 4PM were targeted. POCUS was available or not for patient assessment based on PACU team training. All providers who performed POCUS exams received standardized training on cardiac and pulmonary POCUS. All POCUS exam findings were recorded on a standardized form and the number of suspected mechanisms to trigger the acute event were captured before and after the POCUS exam. PACU length of stay (minutes) across groups was the primary outcome. Results: In total, 128 patients were included in the study, with 92 patients receiving a POCUS exam. Comparison of PACU time between the POCUS group (median = 96.5 min) and no-POCUS groups (median = 120.5 min) demonstrated a reduction for the POCUS group, p = 0.019. Hospital length of stay and 30-day hospital readmission did not show a significant difference between groups. Finally, there was a reduction in the number of suspected diagnoses from before to after the POCUS examination for both pulmonary and cardiac exams, p-values < 0.001. Conclusions: Implementation of POCUS for assessment of acute hypotension and hypoxia in the PACU setting is associated with a reduced PACU length of stay and a reduction in suspected number of diagnoses.

Hypertension in an Animal Model of Kidney Disease is not Dependent on the Short‐Term Actions of Endogenous Tumour Necrosis Factor‐α in the SFO

Introduction The development of hypertension in the Lewis polycystic kidney (LPK) disease model of kidney disease is caused, in part, by the overactivation of the subfornical organ (SFO). Circulating proinflammatory cytokines, namely tumour necrosis factor-α (TNFα), are suggested to act in the central nervous system to produce an increase in neuronal excitability. As circulating cytokines are increased in kidney disease, we hypothesised that TNFα acts on the SFO to increase neuronal activity, therefore contributing to the development of hypertension. Methods Urethane anaesthetised Lewis control (n=18 total) and LPK (n=18 total) rats were instrumented to record blood pressure and perform microinjections of TNFRI neutralising antibody (1ng/50nl) or minocycline (0.5µg/50nl), an inhibitor of microglial activation, followed by a GABAa agonist (10mM isoguvacine) into the SFO. Results Exogenous TNFα microinjected into the SFO elicited a significant pressor response in the Lewis control but not the LPK rats (9±2mmHg vs 3±4mmHg peak change from baseline, P=0.0004). Acute inhibition of local TNFα by microinjection of a TNFRI neutralising antibody into the SFO did not reduce mean arterial blood pressure in Lewis control or LPK rats (1±1mmHg vs -1±1mmHg change from baseline, P=0.78). Similarly, acute non-specific blockade of proinflammatory cytokines by microinjection of minocycline in the SFO did not reduce blood pressure in Lewis control or LPK rats (-1±1mmHg vs -1±1mmHg change from baseline, P=0.98). Microinjection of a GABAa agonist into the SFO caused a significant depressor response that was not altered by the pre-treatment with a microinjection of TNFRI neutralising antibody in either strain (P>0.05), demonstrating that pre-treatment did alter the tonic activation of neurons within the SFO. Interestingly, pre-treatment with a microinjection of minocycline increased the tonic activation in the LPK (P=0.04), but not Lewis (P=0.15), as indicated by the increased depressor response to GABAa agonist microinjection. Conclusions Overall, these findings demonstrate that although the hypertension observed in the LPK is sustained by an increase in SFO activity, the short-term control of blood pressure is not dependent on the actions of endogenous TNFα or generalised microglial and neuronal activation by proinflammatory cytokines in the SFO.

Vitexin Anew Antihypertensive Drug (Isolated from prosopis farcta [Iraq endogenus] plants)

Vitexin was isolated and identified from pods of prosopis farcta (Iraqi endogenous). In vitro and in vivo cardiovascular actions of vitexin were studied. Vitexin produced positive inotropic effect which was not related to B1 adrenergic receptor activation. Vitexin has a vasodilator activities and it could reverse thevasoconstrictor response of isolated pulmonary artery to potassium chloride and phenylphrine. Vitexin has produced a significant increase in ejection fraction in volunteers with mild heart failure. Also vitexin has produced a significant increase in urinary flow and urinary sodium and potassium excretions in healthy and mild hypertensive volunteers, it’s significantly reduced mean arterial blood pressure of the mild hypertensive volunteers. The positive inotropic effect of vitexin is most properly related to the inhibition of phosphodiesterase enzyme by vitexin. The vasodilator activities of vitexin could be mostly associated to the increase in cGMP (attributed to phosphodiesterase inhibitory effect of vitexin) and the activation of K+-channels. The diuretic effects of vitexin could be attributed to the inhibition of Na-Cl symporter system in the renal distal tubule. The most likely mechanisms of action of vitexin as a hypotensive compound are through its vasodilator and diuretic effects. So this agent could be a best new antihypertensive drug compared with present antihypertensive drugs which are in the market now. In addition to that vitexin can be used in heart failure as cardiotonic drug

Protective Effects of Thymus schimperi and Moringa stenopetala Leaf Extracts on Arterial Blood Pressure and Urine Protein Level in Pre-eclampsia Rat Models

Background: Pre-eclampsia (PE) is a common hypertensive disorder during pregnancy and one of the leading causes of perinatal mortality and morbidity. There is no curative modern drug to treat PE. Therefore, researches done on traditional medications have paramount importance in discovering therapeutic and /or protective agents from plant materials. In Ethiopia, there are claims that some indigenous medicinal plants such as Thymus and Moringa can have potential protective functions against PE. The aim of this study was to prove the claims.&#x0D; Methods: Experiments were performed to investigate the effects of aqueous leaf extracts of Thymus schimperi (ALETS) and Moringa stenopetala (ALEMS) on PE rat models induced by nitro-L-arginine methyl ester (L-NAME); a nitric oxide synthase inhibitor. A non-invasive tail cuff blood pressure recorder (Model 179 Amplifier, IITC INC, Life Science Instruments, Woodland Hills, California) was used to determine the arterial blood pressure from rat tail. Urine analysis to determine protein levels was performed using a dipstick, semi-qualitative method as per manufacturer’s instructions (CYBO DFI Korea).&#x0D; Results: ALETS treated PE rat models showed significantly reduced mean arterial blood pressure (MAP) in mmHg; 108±3 (P&lt;0.05), 105±1 (P&lt;0.01) and 99±2 (P&lt;0.01); also the same pattern of results were seen in ALEMS treated PE groups with MAP of 106±1 (P&lt;0.05), 103±1 (P&lt;0.05) and 101±1 (P&lt;0.05) at daily doses of 250 mg/kg, 500 mg/kg and 1000 mg/kg, respectively, compared to untreated case group that had 123±3.7 mmHg at gestation day (GD) 19 . Untreated PE rat models showed significant proteinuria (2000±20 mg/L) throughout the gestation period; while PE rat models treated with either ALETS or ALEMS had significantly reduced (p&lt;0.05) proteinuria in dose dependent pattern (150±15 mg/L) at a dose of 1 gm/kg for each plant extract at GD 19.&#x0D; Conclusion: Aqueous leaf extracts of either Thymus schimperi or Moringa stenopetala might reduce and control arterial pressure in PE rat models in a dose dependent manner. The extracts also could reduce level of proteinuria in the same pattern. Further investigation should, however, be carried out to confirm their uses in prevention and/or treatment of pregnancy-induced hypertension among human cases.

Blood pressure lowering effect of the aqueous extract of &lt;i&gt;Satureja&lt;/i&gt;

Satureja punctata Benth. Briq. (Lamiaceae) is a small shrub known by its vernacular name “Lomishet”. It is used in Ethiopian traditional medicine for the treatment of hypertension, diabetes, liver disease, headache and febrile illness. Mean Arterial Blood Pressure (MABP) lowering effect and vasorelaxant activity of the aqueous extract of aerial parts of the plant were studied. Intravenous administration of the aqueous extract at different doses brought a fall in MABP in normotensive guinea pigs and also in renovascular hypertensive guinea pigs. The extract also caused a dose-dependent relaxation of precontracted aorta; with a maximum relaxation of 98.19% achieved at 40 mg/ml. Preparative reversed-phase HPLC analyses of the extract resulted in the isolation of two phenolic compounds, namely, rosmarinic acid and linarin. The structures of these compounds were elucidated using UV, IR, MS, and NMR (1D and 2D) techniques. Furthermore, rosmarinic acid showed significant (p &lt; 0.01) reduction of MABP in normotensive guinea pigs at doses of 0.75, 1.50 and 3.00 mg/kg. The findings of this study suggest that the aerial parts of S. punctata have genuine antihypertensive activity.&#x0D;

Fumarate Reduced Mean Arterial Blood Pressure and Improved Renal Outcomes in DOCA/salt Hypertension

The mitochondria, through the tricarboxylic (TCA) acid cycle, converts organic molecules into energy that drives intricate renal blood‐pressure regulatory functions. The TCA cycle intermediaries regulate the metabolic state of the mitochondria and by extension, the redox status of the cell. Recently, fumarase, a major TCA cycle enzyme that converts fumarate to malate, has been linked to L‐arginine metabolism and implicated in the pathophysiology of Dahl‐salt sensitive hypertension. This study aimed to investigate the role of fumarase and L‐arginine in deoxycorticosterone (DOCA)/salt hypertension, a non‐genetic model of hypertension. Hypertension was induced in uninephrectomised rats with DOCA (25 mg/kg) + 1 % NaCL. Mean arterial blood pressure was measured in conscious rats via carotid cannulation. Biochemical and western blot analyses were carried out on homogenized kidney fractions. Fumarate reduced arterial blood pressure (198±5 vs 167±7 mmHg, P&lt;0.01). There were no changes in urinary output and sodium excretion in fumarate‐treated DOCA rats (P&gt;0.05). Superoxide dismutase and catalase activities were higher in the cortex, but not the medulla of DOCA‐hypertensive rats and were exacerbated by fumarate (P&lt;0.01). There was a selective increase in catalase activity in the medulla of fumarate‐treated DOCA‐hypertensive rats (P&lt;0.01). Fumarate also reduced urinary protein excretion in DOCA‐hypertensive rats (23.6 %, P&lt;0.05). Fumarate evoked a selective increase in nitric oxide in the medulla (34.1±2.9 vs 47.3±2.8 nM/μg, P&lt;0.05) of DOCA‐hypertensive rats. Consistent with this, Fumarate also tended to increase arginase activity in the cortex but not the medulla of DOCA‐hypertensive rats. However, there was an increase in expression TGF‐β, an index of fibrosis, in DOCA‐hypertensive rats, which was paradoxically increased in fumarate‐treated rats (P&gt;0.05). In conclusion, fumarate attenuated the hypertension and renal injury but not the fibrosis in DOCA/salt hypertension by mechanisms involving selective reduction of L‐arginine metabolism in the medulla and amelioration of renal oxidative stress.Support or Funding InformationNational Institute of Health grant HL03674 and G12 MD0076056Mean arterial blood changes after 21‐day administration of fumarate to DOCA/salt induced hypertensive rats. Control (n=8), DOCA (n=8), fumarate (n=8). a=P&lt;0.001 when compared to control; b=P&lt;0.01 when compared to DOCA group.Figure 1Nitric oxide produced in homogenized kidneys (cortex and medulla) of DOCA salt induced hypertensive rats after 21‐day fumarate (1 mg/kg) administrationa=P&lt;0.05 when compared to control.Figure 2

Acute hypotensive effect of EET‐A, a stable analog of epoxyeicosatrienic acid (EET), in spontaneously hypertensive rats: dependence on endogenous EETs activity

IntroductionArterial hypertension and related disorders are one of the main mortality causes world‐wide. Recent evidence points to epoxyeicosatrienoic acids (EETs) as significant factors in blood pressure regulation. These cytochrome P‐450 dependent metabolites of arachidonic acid, exhibit vasodilator and natriuretic activity. Therefore EETs might contribute to reduction of elevated blood pressure and have therapeutic potential. In our spontaneously hypertensive rats (SHR), potential hypotensive efficiency was examined of EET‐A (disodium (S)‐2‐(13‐(3‐entyl)ureido)‐tridec‐8(Z)‐enamido) succinate), a stable 14,15‐EET analog. EET‐A effects were studied in animals that were or were not pretreated with c‐AUCB (cis‐4‐[4‐(3‐adamantan‐1‐yl‐ureido)‐ cyclohexyloxy]‐benzoic acid), an inhibitor of soluble epoxide hydrolase (sEH) which prevents degradation of EETs. Inhibition of sEH increases endogenous EETs levels.MethodsAnesthetized SHR aged 16 weeks (established hypertension) received 1‐hour infusion of EET‐A (5 mg/kg BW iv) or its solvent. These acute experiments were performed in rats pretreated for 14 days with oral c‐AUCB (8.5 mg/kg/24 h, in drinking water) or in untreated rats receiving c‐AUCB solvent. Throughout experiments mean arterial blood pressure (MABP) and left kidney total blood flow (RBF, renal artery probe) and perfusion of the cortex, outer‐ and inner medulla (CBF, OMBF, IMBF; laser‐Doppler fluxes) were measured, along with renal excretion of water (V), total solute (UosmV), and sodium (UNaV).ResultsBasal MABP measured after chronic treatments tended to be lower after c‐AUCB compared to solvent‐treated group; otherwise no meaningful between‐group differences in renal hemodynamics and excretion parameters were seen. In control group pretreated with c‐AUCB‐solvent, EET‐A administration was followed by a delayed significant progressive decrease in MABP, down to a value 6% below control (p=0.01). In AUCB‐pretreated group no significant post‐EET‐A change in MABP was seen. During EET‐A infusion RBF and CBF significantly and fairly rapidly increased, to 130% and 124% of the control levels, respectively, comparably in untreated and c‐AUCB pretreated group and became almost always significant within the first 30 minutes of EET‐A infusion.SummaryIn acute experiments with anesthetized SHR, administration of EET analog (EET‐A) caused a significant delayed reduction of MABP. Not unexpectedly, previous enhancement of endogenous EETs activity after sEH blockade tended to reduce baseline MABP and virtually abolished the pressure reduction in response to exogenous EET analog. Irrespective of the baseline endogenous EET activity, EET‐A invariably induced renal vasodilation. The data indicate that in adult SHR a hypotensive effect can be obtained both by administration of EET analog and by enhancing endogenous EETs activity. On the other hand, only EET‐A treatment was found to improve renal hemodynamics.Support or Funding InformationNational Science Centre 2017/26/M/NZ5/00367

White mulberry fruit polysaccharides enhance endothelial nitric oxide production to relax arteries in vitro and reduce blood pressure in vivo

Mulberry fruit polysaccharides have demonstrated excellent anti-inflammatory, antioxidant, hypolipidemic, and hypoglycemic properties. This study tested the effect of white mulberry fruit polysaccharides (WMFPs) on blood pressure. WMFPs induced endothelium-dependent relaxation in rat mesenteric arteries and NO production in endothelial cells, both of which were reversed by the NO synthase inhibitor Nω-nitro-l-arginine methyl ester hydrochloride, a phosphoinositide 3-kinase inhibitor LY294002, a cell-permeable Ca2+ chelator (1,2-bis (o-aminophenoxy) ethane-N,N,N’,N’-tetraacetic acid (acetoxymethyl ester)), and inhibitors of molecules downstream of NO, including the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, the potassium channel inhibitor tetraethylammonium chloride, the large conductance calcium-activated potassium channel-specific inhibitor iberiotoxin, and the KATP channel inhibitor glibenclamide. Intravenous injection of WMFPs reduced mean arterial blood pressure in both normotensive Sprague-Dawley and spontaneously hypertensive rats through enhanced endothelial NO production. This study demonstrated that WMFPs induce endothelium-dependent relaxation in rat mesenteric arteries to regulate blood pressure, suggesting that development of WMFPs as a novel antihypertensive agent is warranted.