Increase In Arterial Blood Pressure Research Articles

Estrogen stimulates fetal vascular endothelial growth factor expression and microvascularization.

We recently showed that the ratio of capillaries/myofibers in skeletal muscle, which accounts for 80% of insulin-directed glucose uptake and metabolism, was reduced in baboon fetuses in which estrogen was suppressed by maternal letrozole administration. Since vascular endothelial growth factor (VEGF) promotes angiogenesis, the present study determined the impact of estrogen deprivation on fetal skeletal muscle VEGF expression and capillary development and long-term vascular and metabolic function in 4-8 year old adult offspring. Maternal baboons were untreated or treated with letrozole or letrozole plus estradiol on days 100-164 of gestation (term = 184 days). Skeletal muscle VEGF protein expression was suppressed by 45% (P < 0.05) and correlated (P = 0.01) with a 47% reduction (P < 0.05) in number of capillaries per myofiber area in fetuses of baboons in which serum estradiol levels were suppressed 95% (P < 0.01) by letrozole administration. The reduction in fetal skeletal muscle microvascularization was associated with a 52% decline (P = 0.02) in acetylcholine-induced brachial artery dilation and 23% increase (P = 0.01) in mean arterial blood pressure in adult progeny of letrozole-treated baboons and restored to normal by letrozole plus estradiol. The present study indicates that estrogen upregulates skeletal muscle VEGF expression and systemic microvessel development within the fetus as an essential programming event critical for ontogenesis of systemic vascular function and insulin sensitivity/glucose homeostasis after birth in primate offspring.

Evaluation of the inter-arm blood pressure difference in subjects with hypertension in Nnewi North Local Government Area, Anambra state

Hypertension is defined as a sustained elevated blood pressure with a systolic blood pressure (SBP) of 140mmHg or more and a diastolic blood pressure of 90mmHg or more. The evaluation of the inter-arm blood pressure difference in subjects with hypertension in Nnewi North Local Government Area, Anambra state was done via sampling techniques. The study population was obtained using convenience sampling method and comprised of male and female hypertensive patients aged 25 to 90 years, from the cardiology unit NAUTH Nnewi. Normotensive subjects of the same age range and gender were used as control. The sample size was determined to be 70 subjects using this formula: n= (z2pq)/d2). The result of the finding showed that there was a significant increase in the mean age when the control was compared to the hypertensive group, and no significant difference in their weight, height and BMI. Furthermore, the findings of this research also supported a significant increase in the left arterial systolic and diastolic blood pressure in the control compared to the hypertensive groups. Also, the mean right systolic and diastolic blood pressure showed a significant increase when the control was compared to the hypertensive group. The inter-arm systolic and diastolic blood pressure had no significant difference when control was compared to the hypertensive group.

Estimation of Systolic and Diastolic Blood Pressure for Hypertension Identification from Photoplethysmography Signals

Continuous monitoring plays a crucial role in diagnosing hypertension, characterized by the increase in Arterial Blood Pressure (ABP). The gold-standard method for obtaining ABP involves the uncomfortable and invasive technique of cannulation. Conversely, ABP can be acquired non-invasively by using Photoplethysmography (PPG). This non-invasive approach offers the advantage of continuous BP monitoring outside a hospital setting and can be implemented in cost-effective wearable devices. PPG and ABP signals differ in scale values, which creates a non-linear relationship, opening avenues for the utilization of algorithms capable of detecting non-linear associations. In this study, we introduce Neural Model of Blood Pressure (NeuBP), which estimates systolic and diastolic values from PPG signals. The problem is treated as a binary classification task, distinguishing between Normotensive and Hypertensive categories. Furthermore, our research investigates NeuBP’s performance in classifying different BP categories, including Normotensive, Prehypertensive, Grade 1 Hypertensive, and Grade 2 Hypertensive cases. We evaluate our proposed method by using data from the publicly available MIMIC-III database. The experimental results demonstrate that NeuBP achieves results comparable to more complex models with fewer parameters. The mean absolute errors for systolic and diastolic values are 5.02 mmHg and 3.11 mmHg, respectively.

The use of dexmedetomidine in suppressing cardiovascular response due to intubation in general anesthesia

Endotracheal intubation is commonly used to maintain a safe airway during general anesthesia. This intubation action can trigger a dangerous response for the patient, one of which is the cardiovascular system. Increases in arterial blood pressure, plasma catecholamine levels, and heart rate are responses that can occur during intubation. Therefore, various methods and treatments have been used to control this cardiovascular response, including dexmedetomidine. Dexmedetomidine is a highly selective α2-adrenergic receptor agonist that has analgesic, sympatholytic, and sedative effects with minimal depression of ventilation. Much research has been done on how well dexmedetomidine works to stop the cardiovascular response to intubation. Dexmedetomidine was significantly associated with reductions in heart rate, systolic blood pressure, and MAP.

Interindividual variability in cold-pressor pain sensitivity is not explained by peripheral vascular responding and generalizes to a C-nociceptor-specific pain phenotype.

Pain sensitivity of healthy subjects in the cold-pressor (CP) test was proposed to be dichotomously distributed and to represent a pain sensitivity trait. Still, it has not been systematically explored which factors influence this pain sensitivity readout. The aim of this study was to distinguish potential contributions of local tissue-related factors such as perfusion and thermoregulation or gain settings in nociceptive systems. Cold-pressor-sensitive and CP-insensitive students screened from a medical student laboratory course were recruited for a CP retest with additional cardiovascular and bilateral local vascular monitoring. In addition, comprehensive quantitative sensory testing according to Deutscher Forschungsverbund Neuropathischer Schmerz standards and a sustained pinch test were performed. Cold pressor was reproducible across sessions (Cohen kappa 0.61 ± 0.14, P < 0.005). At 30 seconds in ice water, CP-sensitive subjects exhibited not only more pain (78.6 ± 26.3 vs 29.5 ± 17.5, P < 0.0001) but also significantly stronger increases in mean arterial blood pressure (12.6 ± 9.3 vs 5.6 ± 8.1 mm Hg, P < 0.05) and heart rate (15.0 ± 8.2 vs 7.1 ± 6.2 bpm, P < 0.005), and lower baroreflex sensitivity, but not local or vasoconstrictor reflex-mediated microcirculatory responses. Cold-pressor-sensitive subjects exhibited significantly lower pain thresholds also for cold, heat, and blunt pressure, and enhanced pain summation, but no significant differences in Aδ-nociceptor-mediated punctate mechanical pain. In conclusion, differences in nociceptive signal processing drove systemic cardiovascular responses. Baroreceptor activation suppressed pain and cardiovascular responses more efficiently in CP-insensitive subjects. Cold-pressor sensitivity generalized to a pain trait of C-fiber-mediated nociceptive channels, which was independent of local thermal and vascular changes in the ice-water-exposed hand. Thus, the C-fiber pain trait reflects gain setting of the nociceptive system.

Antihypertensive Medications Can Prevent Fostamatinib-Induced Blood Pressure Elevation

Fostamatinib is a tyrosine kinase inhibitor that has been shown in clinical trials to be effective against spleen tyrosine kinase in patients suffering from rheumatoid arthritis. Fostamatinib medication was linked in clinical trials to a slight increase in systemic arterial Blood Pressure (BP). This observation is consistent with other kinase inhibitors, particularly those that obstruct VEGFR2 signaling. In conscious rats, we examined the relationship between the elevation of blood pressure caused by fostamatinib and the plasma levels of the fostamatinib-active metabolite R940406. We discovered that there was a strong correlation between changes in R940406 plasma concentration and the time course of the blood pressure effect, suggesting a direct pharmacological relationship. The experiments yielded free plasma levels of R940406 up to 346 nmol/L, which is greater than the mean peak free plasma concentration of 49 nmol/L that has been recorded in clinical settings. We beyond the clinically noted mean peak free plasma concentration of 49 nmol/L, up to 346 nmol/L. We’ve shown that there are several effective ways to reduce the blood pressure elevation caused by fostamatinib dosing, including simple drug withdrawal or condoning with a variety of common antihypertensive medications like atenolol, captopril, and nifedipine. These results provide credence to prospective strategies for preserving patient safety during fostamatinib therapy. Additionally, we have shown—using nifedipine as an example drug—that this blood pressure control was not brought about by a decrease in R940406’s plasma exposure, indicating that potential pharmacological benefits of the investigational drug may be preserved while blood pressure control is managed with the use of conventional medications.

Hypertension effects of the COVID-19 lockdowns: Evidence from a repeated cross-sectional survey in Peru

Using data from Peru and a quasi-experimental approach, we document significant increases in arterial blood pressure and in the incidence of arterial hypertension caused by the restrictive measures employed by the Peruvian authorities during the COVID-19 pandemic. The effects are more pronounced for women, older respondents, and urban residents. The effects are statistically significant and high in magnitude relative to the pre-pandemic incidence of disease in the Peruvian population. A main channel of disease propagation seems to be the changes in dietary habits and physical activity imposed by the COVID-19 lockdowns, which affected several anthropometric measurements that are common risk factors for hypertension.

Changes in Cardiac Structure and Function Following Fistula Ligation in Kidney Transplant Recipients (Cohort Study)

Purpose: International guidelines recommend that haemodialysis access is provided by an arteriovenous fistula (AVF), which enables frequent, reliable access to the circulation, but there are no guidelines to suggest whether these AVFs need to be ligated after kidney transplantation. Cardiovascular morbidity and mortality remain high in recipients of a kidney transplant, the persistence of a patent arteriovenous fistula (AVF) after transplantation may contribute to ongoing maladaptive cardiovascular remodelling. The ability to reverse this maladaptive remodelling by ligation of this AVF is unknown. We conducted this trial to evaluate the effect of AVF ligation on cardiac structure and function in stable kidney transplant recipients. Also we studied the ability of preoperative echocardiographic and non-invasive hemodynamic measurements, including the effects of acute temporary occlusion of the fistula, to predict postoperative left ventricular diameter and mass reduction, by the closure of the fistula.&#x0D; Materials and Methods: Nonrandomized controlled trial. kidney transplant recipients (&gt;12 months after transplantation with stable graft function) were divided into 2 groups. The first referred for surgical arteriovenous fistula closure. The second group didn’t receive Fistula closure (control). Standard echocardiographic parameters, heart rate, and blood pressure were assessed preoperatively (fistula closure) at baseline. These measurements were repeated 6 months after surgical closure.&#x0D; Findings: Seventeen kidney transplant patients were prospectively studied with 11 case and 6 controls with no fistula closure. Surgical fistula closure decreased left ventricular end-diastolic diameter and mass indexes (29.9_2.4to 27.4_2.1 mm/m2, P&lt;0.001, and 141_37 to 132_39 g/m2, P&lt;0.05, respectively), whereas no changes were seen in controls after a similar delay. Postoperative left ventricular end-diastolic diameter and mass reductions correlated best with the increases in total peripheral resistance (r_0.85, P&lt;0.0001) and mean arterial blood pressure (r_0.64, P_0.006), respectively.&#x0D; Conclusions. Surgical closure of arteriovenous fistula reduces left ventricular diameter and mass in kidney transplant recipients. The best predictors of those morphological changes are the rise in blood pressure and total peripheral resistance induced by temporary occlusion of the fistula.&#x0D; Implications to Theory, Practice and Policy: Surgical closure of persistent AV fistula after renal transplantation to correct LV geometry and improve symptoms in terms of exertional dyspnea and palpitations.

Deep Parasternal Intercostal Plane Block for Intraoperative Pain Control in Cardiac Surgical Patients for Sternotomy: A Prospective Randomized Controlled Trial

Sternotomy pain is common after cardiac surgery. The deep parasternal intercostal plane (DPIP) block is a novel technique that provides analgesia to the anterior chest wall. The aim of this study was to investigate the analgesic effect of bilateral DPIP blocks on intraoperative pain control in cardiac surgery. This is a double-blinded, prospective randomized controlled trial (Oct 2020-Dec 2022). This study was conducted in a single institution, which is an academic university hospital. Eighty-six elective cardiac surgical patients with median sternotomy were recruited. Patients were randomly divided into DPIP or control group. Either 20ml 0.25% levobupivacaine or 0.9% normal saline was injected for the DPIP under ultrasound guidance after induction of general anaesthesia. The primary outcome was intraoperative opioids consumption and hemodynamic changes at sternotomy. Secondary outcomes included postoperative morphine consumption, postoperative pain and time to tracheal extubation. Intraoperative opioids requirement was reduced from a median (IQR) intravenous morphine equivalence of 21.4mg (13.8-24.3mg) in control group to 9.5mg (7.3-11.2mg) in the DPIP group (P<0.001). Hemodynamic parameters were more stable in DPIP group at sternotomy, as evidenced by lower percentage increase in systolic, diastolic and mean arterial blood pressure from baseline. No difference was observed in time to tracheal extubation, postoperative morphine consumption, postoperative pain score and spirometry. Bilateral DPIP block provides effective intraoperative analgesia and opioid-sparing. It may be included as part of the multimodal analgesia for enhanced recovery in cardiac surgery.

Functional knockout of the TRPV1 channel has no effect on the exercise pressor reflex in rats.

The role played by the transient receptor potential vanilloid 1 (TRPV1) channel on the thin fibre afferents evoking the exercise pressor reflex is controversial. To shed light on this controversy, we compared the exercise pressor reflex between newly developed TRPV1+/+ , TRPV1+/- and TRPV1-/- rats. Carotid arterial injection of capsaicin (0.5μg), evoked significant pressor responses in TRPV1+/+ and TRPV1+/- rats, but not in TRPV1-/- rats. In acutely isolated dorsal root ganglion neurons innervating the gastrocnemius muscles, capsaicin evoked inward currents in neurons isolated from TRPV1+/+ and TRPV1+/- rats but not in neurons isolated from TRPV1-/- rats. The reflex was evoked by stimulating the tibial nerve in decerebrated rats whose femoral artery was either freely perfused or occluded. We found no difference between the reflex in the three groups of rats regardless of the patency of the femoral artery. For example, the peak pressor responses to contraction in TRPV1+/+ , TRPV1+/- and TRPV1-/- rats with patent femoral arteries averaged 17.1 ± 7.2, 18.9 ± 12.4 and 18.4 ± 8.6mmHg, respectively. Stimulation of the tibial nerve after paralysis with pancuronium had no effect on arterial pressure, findings which indicated that the pressor responses to contraction were not caused by electrical stimulation of afferent tibial nerve axons. We also found that expression levels of acid-sensing ion channel 1 and endoperoxide 4 receptor in the L4 and 5 dorsal root ganglia were not upregulated in the TRPV1-/- rats. We conclude that TRPV1 is not needed to evoke the exercise pressor reflex in rats whose contracting muscles have either a patent or an occluded arterial blood supply. KEY POINTS: A reflex arising in contracting skeletal muscle contributes to the increases in arterial blood pressure, cardiac output and breathing evoked by exercise. The sensory arm of the reflex comprises both mechanoreceptors and metaboreceptors, of which the latter signals that blood flow to exercising muscle is not meeting its metabolic demand. The nature of the channel on the metaboreceptor sensing a mismatch between supply and demand is controversial; some believe that it is the transient receptor potential vanilloid 1 (TRPV1) channel. Using genetically engineered rats in which the TRPV1 channel is rendered non-functional, we have shown that it is not needed to evoke the metaboreflex.

Increased Oxygen Saturation in Retinal Venules During Isometric Exercise Is Accompanied With Increased Peripheral Blood Flow in Normal Persons.

A recent study has shown that an increase in the arterial blood pressure of approximately 10 mm Hg in healthy persons can increase the oxygen saturation in venules from the retinal periphery but not from the macular area. The purpose of the present study was to investigate whether a higher increase in blood pressure has further effects on oxygen saturations and whether this is accompanied with changes in retinal blood flow. In 30 healthy persons, oxygen saturation, diameter, and blood flow were measured in arterioles to and venules from the retinal periphery and the macular area. The experiments were performed before and during an experimental increase in arterial blood pressure of (mean ± SD) 18.3 ± 6.2 mm Hg. A higher number of venules than arterioles branching from the temporal vascular arcades to the macular area was balanced by a smaller diameter of the venules. Isometric exercise induced significant contraction of both peripheral and macular arterioles (P<0.01 for both comparisons) and significant increase in oxygen saturation in both peripheral and macular venules (P<0.001 for both comparisons). This was accompanied with a significant increase in the blood flow in the peripheral arterioles and venules (P=0.4 for both comparisons), but not in their macular counterparts (P>0.06 for both comparisons). Increased systemic blood pressure leading to arterial contraction and increased venous oxygen saturation in the retina in normal persons can increase peripheral blood flow without significant effects on macular blood flow. This may contribute to explaining regional differences in the response pattern of retinal vascular disease.

TCD assessment in fulminant hepatic failure: Improvements in cerebral autoregulation after liver transplantation

Introduction and ObjectivesAcute liver failure, also known as fulminant hepatic failure (FHF), includes a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction and hepatic encephalopathy. The objective of this study was to assess cerebral autoregulation (CA) in 25 patients (19 female) with FHF and to follow up with seventeen of these patients before and after liver transplantation. Patients and MethodsThe mean age was 33.8 years (range 14–56, SD 13.1 years). Cerebral hemodynamics was assessed by transcranial Doppler (TCD) bilateral recordings of cerebral blood velocity (CBv) in the middle cerebral arteries (MCA). ResultsCA was assessed based on the static CA index (SCAI), reflecting the effects of a 20–30 mmHg increase in mean arterial blood pressure on CBv induced with norepinephrine infusion. SCAI was estimated at four time points: pretransplant and on the 1st, 2nd and 3rd posttransplant days, showing a significant difference between pre- and posttransplant SCAI (p = 0.005). SCAI peaked on the third posttransplant day (p = 0.006). Categorical analysis of SCAI showed that for most patients, CA was reestablished on the second day posttransplant (SCAI > 0.6). ConclusionsThese results suggest that CA impairment pretransplant and on the 1st day posttransplant was re-established at 48–72 h after transplantation. These findings can help to improve the management of this patient group during these specific phases, thereby avoiding neurological complications, such as brain swelling and intracranial hypertension.

Physiological Mechanisms of Dietary Salt Sensing in the Brain, Kidney, and Gastrointestinal Tract.

Excess dietary salt (NaCl) intake is strongly correlated with cardiovascular disease and is a major contributing factor to the pathogenesis of hypertension. NaCl-sensitive hypertension is a multisystem disorder that involves renal dysfunction, vascular abnormalities, and neurogenically-mediated increases in peripheral resistance. Despite a major research focus on organ systems and these effector mechanisms causing NaCl-induced increases in arterial blood pressure, relatively less research has been directed at elucidating how NaCl is sensed by various tissues to elicit these downstream effects. The purpose of this review is to discuss how the brain, kidney, and gastrointestinal tract sense NaCl including key cell types, the role of NaCl versus osmolality, and the underlying molecular and electrochemical mechanisms.

Abstract 061: Continuous And Cyclic Components Of Blood Pressure Profile Have Impact On Different Brain Areas In Controlled Hypertensive Patients

Increase in arterial blood pressure consistently damages the connectivity and function of the brain. While this evidence is becoming more widely accepted, the effects of daily fluctuations and variability in blood pressure levels on the brain are still not well understood. Our study investigated the impact of blood pressure variability (BPV) on cognitive function and white matter brain structure in a cohort of hypertensive patients under optimal BP control. We used diffusion tensor imaging (DTI-MRI) to assess white matter injury, neuropsychological tests such as the Montreal Cognitive Assessment (MoCA) to evaluate cognitive function, and 24-hour ambulatory blood pressure monitoring to measure BPV. Spectral analysis of BPV allowed us to measure both the cyclic and the continuous components of arterial blood pressure profile. We found that the Fractional Anisotropy of the Middle Cerebellar Peduncle was correlated with the cyclic component of both diastolic and systolic blood pressure. Additionally, a significant association between the continuous component of both diastolic and systolic blood pressure and the Anterior Thalamic Radiation was detected.. Finally, cognitive functions measured by MoCA were correlated with the continuous component of both diastolic and systolic blood pressure (Table). Our results suggest that the continuous component of blood pressure negatively impacts white matter regions associated with cognitive impairment, while the cyclic component is associated with alterations in brainstem regions where nervous vagal control is coordinated.

Abstract P384: Cytochrome P450 1B1-Testosterone Metabolite 6β-Hydroxytestosterone Promotes Ang II-induced Hypertension And Neuroinflammation Via Group IV Cytosolic Phospholipase A 2 α In Paraventricular Nucleus Of Male Mice

We reported previously that Ang (angiotensin) II-induced hypertension depends on the activation of group IV cPLA 2 α (cytosolic phospholipase A 2 α). Moreover, we showed that testosterone (T) metabolite 6β-hydroxytestosterone (6β-OHT) generated by CYP1B1 (cytochrome P450 1B1) in the paraventricular nucleus (PVN) promotes Ang II-induced hypertension and neuroinflammation in male mice. This study determined the relationship of cPLA 2 α and CYP1B1-T derived 6β-OHT in the PVN to Ang II-induced hypertension and neuroinflammation in male mice. cPLA 2 α knockdown in the PVN by transduction with adenovirus (Ad)-cPLA 2 α-short hairpin (sh)RNA (200 nL, bilaterally, 5.4X10 11 pfu/mL) but not its control Ad-scrambled (Scr)-shRNA (2.5X10 11 pfu/mL) in wild-type (WT) male mice, inhibited Ang II (700 ng/kg/min, s.c., two weeks)-induced increase in systolic blood pressure (Day 12- SBP mmHg, tail-cuff) (126±4 vs 167±4, respectively, P&lt;0.05, n=4/group). Moreover, reconstitution of cPLA 2 α in the PVN by Ad-cPLA 2 α-DNA (5.5X10 9 pfu/mL), but not its control Ad-GFP-DNA (1.0X10 11 pfu/mL) in cPLA 2 α -/- mice restored the increase in SBP (153±6 vs 117±4, respectively, P&lt;0.05, n=4/group). Ang II-induced increase in mean arterial blood pressure (MAP mmHg, radiotelemetry) that was minimized in WT-orchidectomized (ORX) or intact Cyp1b1 -/- mice were restored by ICV injections of 6β-OHT (1.5 μg/2 μL/alternate day), but it was attenuated by ICV (2 μL, single injection) Ad-cPLA 2 α-shRNA, but not its control Ad-Scr-shRNA (114±4 vs 150±7, and 121±2 vs 154±9, respectively, P&lt;0.05, n=4-6/group). Ang II-induced increase in MAP was restored by 6β-OHT, but not its vehicle (2-hydroxypropyl-β-cyclodextrin in CSF, 2 μL/alternate day) in Ad-cPLA 2 α-DNA transduced ORX- cPLA 2 α -/- mice (165±6 vs 121±2, respectively, P&lt;0.05, n=4/group). The number of TMEM119 + microglia and GFAP + astrocytes in PVN, markers of neuroinflammation, followed the changes in BP in the above groups produced by Ang II. In conclusion, T-CYP1B1 metabolite 6β-OHT promotes Ang II-induced hypertension and neuroinflammation by a mechanism dependent on cPLA 2 α in the PVN. Therefore, agents that reduce CYP1B1 or cPLA 2 α activity could be useful for treating Ang II/T-dependent hypertension and neuroinflammation in males.

The Effect of Classical Music Therapy and Deep Breathing Relaxation Therapy on Lowering Blood Pressure in Hypertension Sufferers in RW 001 Samba Danum Village, Katingan Tengah District, Central Kalimantan Year 2022

Background: Hypertension is an abnormal increase in arterial blood pressure. Non-pharmacological therapeutic interventions can be performed such as classical music therapy and deep breathing relaxation therapy. Classical music therapy is to improve physical and mental quality with sound stimulation, melody, harmony, rhythm and slow style forms. The deep breathing relaxation technique is a therapy to regulate breathing in the abdomen with a slow and slow frequency, rhythmic and comfortable by closing your eyes when inhaling. Objective: To determine the effect of classical music therapy and deep breathing relaxation therapy on reducing blood pressure in hypertensive patients. Methods: The research design was a quasi-experimental (quasi-experimental) design with one group pretest-posttest design. The sample used was 15 respondents who met the inclusion and exclusion criteria. The data collection for this study used observation sheets and standard operating procedures for classical music therapy and deep breathing relaxation therapy (SOP). Results: The results of the study using the Wilcoxon Sign Rank Test with the results of systolic and diastolic blood pressure before and after being given classical music therapy and deep breathing relaxation therapy showed a p-value = 0.000 &lt; ɑ = 0.05. Conclusion: The results showed that there was an effect of classical music therapy and deep breathing relaxation therapy on reducing blood pressure in hypertension sufferers in RW 001 Samba Danum Village, Katingan Tengah District, Central Kalimantan.

A Preliminary Feasibility Study on Hemodynamic Changes Following Feyh-Kastenbauer Retractor Insertion During Transoral Robotic Surgeries.

Introduction Transoral robotic surgery (TORS) has become increasingly popular for the removal of pharyngeal and laryngeal cancers with the objective to improve functional and aesthetic outcomes. Feyh-Kastenbauer (FK) retractor is one such routinely used retractor during TORS. The setting up of this retractor has been seen to be accompanied by hemodynamic fluctuations. Methodology This prospective observational study was carried out on 30 patients undergoing TORS. All patients were administered general anesthesia using a pre-defined anesthesia protocol. The primary outcome was to compare hemodynamic fluctuations following endotracheal intubation with that after FK retractor insertion. Any requirement of a bolus dose of sevoflurane and fentanyl was recorded in response to hemodynamic fluctuations recorded in secondary outcomes. Results There was no statistically significant increase in mean heart rate, systolic, diastolic, and mean arterial blood pressure from baseline to endotracheal intubation and following retractor insertion (p=0.810, p=0.2, p=0.6, p=0.3 respectively). On subgroup analysis, hypertensive patients reported a greater rise in blood pressure following two minutes post FK retractor insertion compared to non-hypertensive patients (p=0.03). Out of 30 patients, five patients required a bolus dose of sevoflurane. Conclusion FK retractor insertion had a comparable hemodynamic response as endotracheal intubation during TORS. Hypertensive patients showed a rise in blood pressure at both endotracheal intubations and at FK retractor insertion.

Intravenous injection of fentanyl in adult awake goats increases arterial blood pressure and reduces heart rate without affecting metabolic rate or temperature

At high doses, synthetic opioids are thought to slow heart rate and reduce mean arterial blood pressures in humans and rodents and could create a life-threatening situation. Herein, we report dose-dependent effects of intravenous (IV) injection of fentanyl on systolic (SYS), diastolic (DIA), and mean (MAP) arterial blood pressure, heart rate (HR) metabolic rate and body temperatures in adult female goats (n=7). Variables were measured 30 min before, during and up to 90 min after IV injection of vehicle (saline) or 25, 50, 75, 100, and 125 mcg/kg fentanyl. Baseline averages for SYS, DIA, MAP was 102, 73, 83 mmHg, respectively, and HR was 84 beats/minute (bpm). There were no significant changes in these values over 90 minutes when saline was injected. Between 8 and 10 minutes after fentanyl injection, SYS, DIA, and MAP increased substantially from control by about 40, 25, and 30 mmHg, respectively. These increases did not appear dose independent, but by 90 minutes post-injection SYS, DIA, and MAP decreased toward control at the lowest dose (25 mcg/kg). The fentanyl induced arterial hypertension was partially compensated by a ~15 bpm decrease in heart rate which changed minimally between 10 and 90 minutes after fentanyl injection. The sustained increase in arterial blood pressure indicates a sustained excitatory effect of fentanyl consistent with the excitatory effect of fentanyl on tidal volume and respiratory muscle activity (see additional abstracts from our group). This excitatory effect is not due to changes in metabolic rate and/or body temperature as we found no consistent effect of fentanyl injections on these variables. This excitatory effect of fentanyl appears species-dependent as opioid agonists injected into rats and humans typically induces arterial hypotension. Species dependency of fentanyl may reflect species variation in effects of fentanyl on vagal nerve endings, brainstem control centers, and/or cardiac receptors (J. Car.Pharm, 1985), or alternatively may reflect differences in fentanyl metabolism whereby metabolites may have differential effects on blood pressure among these species. NIH DA050571 This is the full abstract presented at the American Physiology Summit 2023 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.

Epinephrine-induced Effects on Cerebral Microcirculation and Oxygenation Dynamics Using Multimodal Monitoring and Functional Photoacoustic Microscopy.

The administration of epinephrine after severe refractory hypotension, shock, or cardiac arrest restores systemic blood flow and major vessel perfusion but may worsen cerebral microvascular perfusion and oxygen delivery through vasoconstriction. The authors hypothesized that epinephrine induces significant microvascular constriction in the brain, with increased severity after repetitive dosing and in the aged brain, eventually leading to tissue hypoxia. The authors investigated the effects of intravenous epinephrine administration in healthy young and aged C57Bl/6 mice on cerebral microvascular blood flow and oxygen delivery using multimodal in vivo imaging, including functional photoacoustic microscopy, brain tissue oxygen sensing, and follow-up histologic assessment. The authors report three main findings. First, after epinephrine administration, microvessels exhibited severe immediate vasoconstriction (57 ± 6% of baseline at 6 min, P < 0.0001, n = 6) that outlasted the concurrent increase in arterial blood pressure, while larger vessels demonstrated an initial increase in flow (108 ± 6% of baseline at 6 min, P = 0.02, n = 6). Second, oxyhemoglobin decreased significantly within cerebral vessels with a more pronounced effect in smaller vessels (microvessels to 69 ± 8% of baseline at 6 min, P < 0.0001, n = 6). Third, oxyhemoglobin desaturation did not indicate brain hypoxia; on the contrary, brain tissue oxygen increased after epinephrine application (from 31 ± 11 mmHg at baseline to 56 ± 12 mmHg, 80% increase, P = 0.01, n = 12). In the aged brains, microvascular constriction was less prominent yet slower to recover compared to young brains, but tissue oxygenation was increased, confirming relative hyperoxia. Intravenous application of epinephrine induced marked cerebral microvascular constriction, intravascular hemoglobin desaturation, and paradoxically, an increase in brain tissue oxygen levels, likely due to reduced transit time heterogeneity.

Barosensory vessel mechanics and the vascular sympathetic baroreflex: Impact on blood pressure homeostasis.

What is the topic of this review? We review barosensory vessel mechanics and their role in blood pressure regulation across the lifespan. What advances does it highlight? In young normotensive men, aortic unloading mechanics contribute to the resting operating point of the vascular sympathetic baroreflex; however, with advancing age, this contribution is removed. This suggests that barosensory vessel unloading mechanics are not driving the well-documented age-related increase in resting muscle sympathetic nerve activity. An age-associated increase in arterial blood pressure is evident for apparently healthy humans. This is frequently attributed to stiffening of the central arteries and a concurrent increase in sympathetic outflow, potentially mediated by a reduced ability of the baroreceptive vessels to distend. This is supported, in part, by a reduced mechanical component of the vascular sympathetic baroreflex (i.e., a reduction in distension for a given pressure). Previous characterization of the mechanical component has assessed only carotid artery distension; however, evidence suggests that both the aortic and carotid baroreflexes are integral to blood pressure regulation. In addition, given that baroreceptors are located in the vessel wall, the change in wall tension, comprising diameter, pressure and vessel wall thickness, and the mechanics of this change might provide a better index of the baroreceptor stimulus than the previous method used to characterize the mechanical component that relies on diameter alone. This brief review summarizes the data using this new method of assessing barosensory vessel mechanics and their influence on the vascular sympathetic baroreflex across the lifespan.