Mean Systemic Arterial Blood Pressure Research Articles

The hearts of large mammals generate higher pressures, are less efficient and use more energy than those of small mammals.

A prevailing assumption in the cardiovascular field is that the metabolic rate of the heart is a constant proportion of a mammal's whole-body aerobic metabolic rate. In this Commentary, we assemble previously published cardiovascular, metabolic and body mass data from matched terrestrial mammalian species, at rest and during heavy exercise, and reveal scaling relationships that challenge this assumption. Our analyses indicate that the fractional metabolic cost of systemic perfusion compared with whole-body metabolic rate increases significantly with body size among resting mammals, from ∼2.5% in a mouse to ∼10% in an elephant. We propose that two significant body size-dependent effects contribute to this conclusion; namely, that larger species generate higher mean systemic arterial blood pressure and that their myocardium operates with lower external mechanical efficiencies compared with those of smaller species. We discuss potential physiological and mechanical explanations, including the additional energy needed to support the arterial blood column above the heart in larger species, especially those with long necks, as well as the possible sources of greater internal energy losses from the heart of larger species. Thus, we present an updated view of how increasing blood pressure and decreasing efficiency of the myocardium result in an increasing fractional metabolic cost of perfusion as body size increases among resting mammals.

The haemodynamic effects of phenylephrine after cardiac surgery.

Phenylephrine increases systemic- and pulmonary resistances and therefore may increase blood pressures at the expense of blood flow. Cardio-pulmonary bypass alters vasoreactivity and many patients exhibit chronotropic insufficiency after cardiac surgery. We aimed to describe the haemodynamic effects of phenylephrine infusion after cardiac surgery. Patients in steady state after low-risk cardiac surgery received incremental infusion rates of phenylephrine up to 1.0 μg/kg/min with the aim of increasing systemic mean arterial blood pressure 20 mmHg. Invasive haemodynamic parameters, including pulmonary wedge pressures, were captured along with echocardiographic measures of biventricular function before, during phenylephrine infusion at target systemic blood pressure, and 20 min after phenylephrine discontinuation. Thirty patients were included. Phenylephrine increased mean arterial pressure increased from 78 (±9) mmHg to 98 (±10) mmHg with phenylephrine infusion. Also, pulmonary blood pressure as well as systemic- and pulmonary resistances increased. The ratio between systemic- and pulmonary artery resistances did not change statistically significantly (p = .59). Median cardiac output was 4.35 (interquartile range [IQR] 3.6-5.4) L/min at baseline and increased significantly with phenylephrine infusion (median Δcardiac output was 0.25 [IQR 0.1-0.6] L/min) (p = .012). Pulmonary artery wedge pressure increased from 10.2 (±3.0) mmHg to 11.9 (±3.4) mmHg (p < .001). This was accompanied by significant increases in central venous pressure. Phenylephrine infusion increased left ventricular end-diastolic volume from 105 (±46) mL to 119 (±44) mL (p < .001). All results of phenylephrine infusion were reversed with discontinuation. In haemodynamically stable patients after cardiac surgery, phenylephrine increased PVR and SVR, but did not change the PVR/SVR ratio. Phenylephrine increased biventricular filling pressures and left ventricular end-diastolic area. Consequently, CO increased as ejection fraction was maintained. These findings do not discourage the use of phenylephrine after low-risk cardiac surgery. clinicaltrial.gov (identifier NCT04419662).

CrossTalk opposing view: Barometric pressure, independent of , is not the forgotten parameter in altitude physiology and mountain medicine.

CrossTalk opposing view: Barometric pressure, independent of , is not the forgotten parameter in altitude physiology and mountain medicine.

P: 18 Impaired Cerebral Oxygenation, but Preserved Cerebrovascular reactivity, in an Animal Model of Hepatic Encephalopathy

BACKGROUND: We have recently obtained evidence of energy deficiency, in the form of impaired lactate release, in the brains of cirrhotic animals with hepatic encephalopathy (HE). Previous reports of cerebral hypoperfusion in patients with HE indicated that cerebral oxygen supply could also be compromised (Dam et al., 2013). Decreased lactate and reduced oxygen supply may lead to CNS energy deficiency and have important neurological consequences, particularly in patients with advanced cirrhosis. In this study we assessed cerebral tissue oxygen tension and CO2 cerebrovascular reactivity in an animal model of HE. METHODS: HE was induced by bile duct ligation (BDL) and after 4 weeks rats were anesthetized with α-chloralose (100 mg·kg−1), instrumented for arterial blood pressure recording and artificially ventilated. 7 BDL and 6 sham-operated animals were treated daily for one week with an ammonia lowering treatment, ornithine phenylacetate (OP) in order to investigate the role of ammonia on brain oxygenation. Blood gas tensions and pH were maintained within physiological ranges in all animal groups. Cerebral tissue PO2 was monitored by fluorescence method (Oxylite™). After a small craniotomy, optical sensors were placed in the somatosensory cortex and sealed. PO2 at baseline and in response to systemic hypercapnia (10% CO2, 5 min) was recorded. RESULTS: BDL resulted in high plasma ammonia concentrations which was lowered with OP treatment. At similar levels of blood PO2 and PCO2, BDL rats had a significantly lower brain PO2 (15.3 ± 2 mm Hg; n = 10) compared to sham controls (26 ± 2 mm Hg; n = 6; P = 0.001). BDL rats treated with OP showed a significant improvement in cerebral PO2 (22 ± 1 mm Hg, n = 6, P = 1), increasing the oxygen tension to levels similar to that recorded in OP treated sham rats (27 ± 2 mm Hg, n = 7), when blood PO2 and PCO2 were constant. Systemic hypercapnia resulted in similar increases in cerebral PO2 in BDL and sham-operated animals (ΔPO2 21 ± 2 vs. 24 ± 2 mm Hg; P = 0.6). Additionally, under anaesthesia, the mean systemic arterial blood pressure was found to be significantly lower in BDL animals (60 ± 3 vs. 84 ± 8 mm Hg; P = 0.04). Cerebral oxygenation did not recover when the blood pressure was normalised via infusion of phenylephrine, but it significantly improved with infusion of acetazolamide which increases cerebral blood flow. CONCLUSIONS: In the BDL model of HE, cerebral tissue oxygen tension is compromised but cerebrovascular reactivity to CO2 appears to be preserved. The cause of the low basal PO2 remains unknown however; high ammonia concentrations and hypoperfusion could be contributing factors.

Reduction of circulating renin‐angiotensin following unilateral nephrectomy signals kidney hypertrophy via increase in renal blood flow

RationaleThe compensatory hypertrophy of a remaining kidney after nephrectomy has long been recognized and the molecular and functional responses to these events have been well characterized. However, the signal that triggers these events is unknown. Recent studies have found that nephrectomy of the right kidney in rats results in a rapid increase of renal blood flow of the remaining kidney within the first 30 minutes and activation of the mTOR pathway with consequent hypertrophy. In the present study, we hypothesized that a reduction of circulating renin would immediately occur with removal of the right kidney which could produce an immediate peripheral vasodilation and increase of renal blood flow within the remaining left kidney.MethodsSprague Dawley rats (male; 7 wk age) were anesthetized, the left kidney was denervated and then the right kidney was removed while monitoring immediate changes of systemic mean arterial blood pressure (MAP), left renal arterial blood flow (RBF), and left urine volume (V). Three groups were studied: 1) No drug treatment (n=5); 2) Pretreated with the AT1 receptor blocker Losartan (n=4); 3) Pretreated with Losartan and Angiotensin II administered to return aortic pressure and RBF to normal before removing the right kidney (n=2).ResultsLeft RBF gradually increased from 3.8 to 4.7 ml/min and became stable 30 minutes following removal of the right kidney. A slight decrease of MAP occurred during that time (~4 mmHg) and urine volume nearly doubled from 2.7 to 5.3 μl/min. Rats treated with Losartan exhibited a reduced baseline level of MAP and increased level of RBF but the changes in MAP and RBF following right nephrectomy were abolished. Rats treated with Losartan with Angiotensin II infused to normalize baseline levels of RBF and MAP, also exhibited no increases of RBF following removal of the right kidney.ConclusionWe conclude that rapid reductions of circulating renin‐angiotensin following right kidney nephrectomy produce increased RBF in the remaining kidney which in turn may trigger the compensatory hypertrophy.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Corrigendum to "Total Intravenous Anaesthesia with High-Dose Remifentanil Does Not Aggravate Postoperative Nausea and Vomiting and Pain, Compared with Low-Dose Remifentanil: A Double-Blind and Randomized Trial".

[This corrects the article DOI: 10.1155/2014/724753.].

Physiologically based cord clamping stabilises cardiac output and reduces cerebrovascular injury in asphyxiated near-term lambs

BackgroundPhysiologically based cord clamping (PBCC) has advantages over immediate cord clamping (ICC) during preterm delivery, but its efficacy in asphyxiated infants is not known. We investigated the physiology of PBCC...

Impaired Cerebral Oxygenation, But Preserved Cerebrovascular Reactivity, In An Animal Model of Hepatic Encephalopathy

Introduction: We have recently obtained evidence of energy deficiency, in the form of impaired lactate release, in the brains of cirrhotic animals with hepatic encephalopathy (HE). Previous reports of cerebral hypoperfusion in patients with HE indicated that cerebral oxygen supply could also be compromised [[1]Philips B.J. Armstrong I.R. Pollock A. Lee A. Cerebral blood flow and metabolism in patients with chronic liver disease undergoing orthotopic liver transplantation.Hepatology. 1998; 27: 369-376Crossref PubMed Scopus (43) Google Scholar]. Decreased lactate and reduced oxygen supply may lead to the CNS energy deficiency and have important neurological consequences, particularly in patients with advanced cirrhosis. Objectives: In this study we assessed cerebral tissue oxygen tension and CO2 cerebrovascular reactivity in an animal model of HE. Methods: HE was induced by bile duct ligation (BDL) and after 4 weeks rats were anesthetized with α-chloralose (100 mg kg−1), instrumented for arterial blood pressure recording and artificially ventilated. Blood gas tensions and pH were monitored and maintained within the physiological ranges in both BDL (n = 10) and sham operated (n = 6) rats. Cerebral tissue PO2 was monitored by fluorescence method (Oxylite™, Oxford Optronics). After a small craniotomy, optical sensors were placed in the somatosensory cortex and sealed. PO2 at baseline and in response to systemic hypercapnia (10% CO2; 5 min) was recorded. Results: At the similar levels of blood PO2 (120 ± 4 vs. 113 ± 4 mmHg) and PCO2 (34 ± 1 vs. 35 ± 2 mmHg), BDL rats had a significantly lower brain PO2 (15.3 ± 2 mmHg; n = 10) compared to the shams (26 ± 2 mmHg; n = 6; P = 0.001). Systemic hypercapnia resulted in similar increases in cerebral PO2 in BDL and sham animals (ΔPO2 21 ± 2 vs. 24 ± 2 mmHg; P = 0.6). However, the peak increases in parenchymal PO2 was significantly smaller in BDL rats when compared to sham-operated animals; 36 ± 4 ± 2 vs. 50 ± 3 mmHg (P = 0.03). Additionally, under anesthesia, the mean systemic arterial blood pressure was found to be significantly lower in BDL animals (60 ± 3 vs. 84 ± 8 mmHg; P = 0.04). Conclusion: In the BDL model of HE, cerebral tissue oxygen tension is compromised but cerebrovascular reactivity to CO2 appears to be preserved. The cause of the low basal PO2 remains unknown however; low systemic arterial blood pressure could be a contributing factor considering the maximum increase in PO2 induced by hypercapnia was lower in BDL animals indicating decreased brain perfusion. The authors have none to declare.

Antidiuretic and antinatriuretic response to high salt load in normotensive Wistar-Kyoto rats: Role of alpha-1A-adrenoreceptors

Altered renal adrenergic responses have been recognized as pathophysiological responses to high salt intake. This study aims to investigate the influence of 6weeks of high salt diet on α1A -adrenoceptor regulation of renal tubular antinatriuretic and antidiuretic response in normal Wistar Kyoto rats. To achieve the above objective, antinatriuretic and antidiuretic response to phenylephrine was measured in the absence and presence of 5-methylurapidil (5-MeU) using the inulin clearance method. Systemic mean arterial blood pressure and renal haemodynamics were also measured simultaneously. Six weeks of high salt intake in Wistar-Kyoto (WKY) rats did not bring any significant increase in mean arterial blood pressure. WKY rat on high salt diet (WKYHNa) showed an exaggerated increase in absolute and fractional sodium excretion. There was a significant involvement of α1A -adrenoceptor in carrying out renal tubular antinatriuretic and antidiuretic response in Wistar Kyoto rats on normal sodium diet (WKYNNa). However, α1A -adrenoceptor played a minimal role in handling the tubular reabsorptive response in WKY rats on high salt diet.

Pediatric acute kidney injury: Appraisal of predictors and prognostic indicators

Acute kidney injury (AKI) is a major contributor to childhood morbidity and mortality worldwide. In spite of the advances in renal replacement therapy, there has been a minimal reduction in AKI-related morbidity and mortality. Identifying the prognostic indicators and the risk factors that predict disease onset and progression, and instituting appropriate measures will lead to better survival outcomes. This narrative review seeks to appraise the predictors and prognostic indicators of pediatric AKI. Several biomarkers clearly stand out as predictors and prognostic indicators of the acute disease. Some of them are urine angiotensinogen, fibroblast growth factor-23, cystacin C, neutrophil gelatinase-associated lipocalin, tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-binding protein 7. Combining few of these biomarkers with clinical prediction models has improved their predictive and prognostic utility for AKI. Hemodynamic parameters such as indexed systemic oxygen delivery and mean arterial blood pressure have been proved to be reliable in predicting the occurrence and progression of the disease and its outcomes. Miscellaneous predictors and prognostic indicators like AKI definition criteria, presence of co-morbidities, and health-related quality of life assessment have also been documented from evidence-based studies. An understanding and application of these indices will obviously help to reduce AKI mortality in children.

Hemodynamic and metabolic effects of a new pediatric dobutamine formulation in hypoxic newborn pigs.

The aim of our study was to measure drug-related changes in hemodynamics and oxygen metabolism in response to different doses of an age-appropriate dobutamine formulation in hypoxic pigs. A secondary aim was to validate superior vena cava flow (SVCF) as a marker of cardiac index (CI) for subsequent clinical trials of this formulation in humans. Newborn pigs (n = 18) were exposed to 2-h hypoxia (10-15% oxygen) followed by reoxygenation (21-30% oxygen 4 h). After 1-h reoxygenation, pigs were randomized to: control group (no treatment), dobutamine infusion at a rate of 10-15 or 15-20 µg/kg/min. Dobutamine groups received two dobutamine doses during 30 min with a 60 min washout period between doses. Cardiovascular profile and oxygen metabolism were monitored. In four animals, an ultrasonic perivascular flow probe was placed around superior vena cava to measure SVCF. Hypoxia significantly decreased CI, systemic vascular resistance and mean arterial blood pressure (MABP). Dobutamine doses significantly increased heart-rate, CI, and oxygen-delivery without changes in stroke-volume and MABP. Only 10-15 µg/kg/min increased oxygen consumption and peripheral tissue oxygenation measured by Near-infrared spectroscopy. A positive correlation was observed between SVCF and CI. The new pediatric dobutamine formulation improved hemodynamic status, with dose-specific differences in metabolic response. SVCF may be a useful surrogate for CI in subsequent clinical trials.

A prospective, randomized study of inhaled prostacyclin versus nitric oxide in patients with residual pulmonary hypertension after pulmonary endarterectomy

ObjectivesPulmonary endarterectomy (PEA) is an effective treatment for chronic thromboembolic pulmonary hypertension (CTEPH), but postoperative residual hypertension leads to in-hospital mortality. Inhaled epoprostenol sodium (PGI2) and NO are administered for pulmonary hypertension after cardiothoracic surgery. This prospective study provides the first comparative evaluation of the effects of inhaled PGI2 and NO on pulmonary hemodynamics, systemic hemodynamics, and gas exchange in patients developing residual pulmonary hypertension after PEA.MethodsThirteen patients were randomized to receive either NO (n = 6) or PGI2 (n = 7) inhalation when pulmonary hypertension persisted after weaning from cardiopulmonary bypass. Hemodynamic and respiratory variables were measured before inhalation of the agent (T0); 30 min (T1), 3 h (T2), and 6 h after inhalation (T3); and the next morning (T4). The NO dose was started at 20 ppm and gradually tapered until extubation, and PGI2 was administered at a dose of 10 ng kg−1 min−1.ResultsIn both groups, mean pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) significantly decreased over time until T4 (mean PAP: p < 0.0001; PVR: p = 0.003), while mean systemic arterial blood pressure significantly increased (p = 0.028). There were no significant between-group differences in patient characteristics, cardiac index, left atrial pressure, or ratio of arterial oxygen tension to fraction of inspired oxygen. There were no in-hospital deaths.ConclusionsBoth inhaled PGI2 and NO significantly reduced PAP and PVR without adverse effects on systemic hemodynamics in patients who developed residual pulmonary hypertension after PEA. Inhaled PGI2 can be offered as alternative treatment option for residual pulmonary hypertension.

A structure-function analysis of the left ventricle.

This study presents a structure-function analysis of the mammalian left ventricle and examines the performance of the cardiac capillary network, mitochondria, and myofibrils at rest and during simulated heavy exercise. Left ventricular external mechanical work rate was calculated from cardiac output and systemic mean arterial blood pressure in resting sheep (Ovis aries; n = 4) and goats (Capra hircus; n = 4) under mild sedation, followed by perfusion-fixation of the left ventricle and quantification of the cardiac capillary-tissue geometry and cardiomyocyte ultrastructure. The investigation was then extended to heavy exercise by increasing cardiac work according to published hemodynamics of sheep and goats performing sustained treadmill exercise. Left ventricular work rate averaged 0.017 W/cm3 of tissue at rest and was estimated to increase to ∼0.060 W/cm3 during heavy exercise. According to an oxygen transport model we applied to the left ventricular tissue, we predicted that oxygen consumption increases from 195 nmol O2·s-1·cm-3 of tissue at rest to ∼600 nmol O2·s-1·cm-3 during heavy exercise, which is within 90% of the oxygen demand rate and consistent with work remaining predominantly aerobic. Mitochondria represent 21-22% of cardiomyocyte volume and consume oxygen at a rate of 1,150 nmol O2·s-1·cm-3 of mitochondria at rest and ∼3,600 nmol O2·s-1·cm-3 during heavy exercise, which is within 80% of maximum in vitro rates and consistent with mitochondria operating near their functional limits. Myofibrils represent 65-66% of cardiomyocyte volume, and according to a Laplacian model of the left ventricular chamber, generate peak fiber tensions in the range of 50 to 70 kPa at rest and during heavy exercise, which is less than maximum tension of isolated cardiac tissue (120-140 kPa) and is explained by an apparent reserve capacity for tension development built into the left ventricle.

Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress.

Noise pollution has been realized as an environmental stressor associated with modern life style that affects our health without being consciously aware of it. The present study investigated the effect of acute, chronic intermittent and chronic continuous exposure to noise of intensity 80-100 dB on heart rate and mean systemic arterial blood pressure in rats and the possible underlying mechanisms. Noise stress causes significant increase in heart rate, mean systemic arterial blood pressure as well as significant increase in plasma levels of corticosterone, adrenaline, noradrenaline, endothelin-1, nitric oxide and malondialdehyde with significant decrease in superoxide dismutase and these values are significantly more worse in chronic continuous exposure to noise than acute or chronic intermittent exposure. These findings suggest that noise stress has many adverse effects on cardiovascular system via increasing plasma levels of stress hormones, oxidative stress and endothelial dysfunction. These findings have major implication in the management of adverse cardiovascular reactions of people subjected to daily noise stress.

Inhaled Desflurane vs. Propofol for Postoperative Sedation Guided with Patient State Index of SEDline in Mechanically Ventilated Liver Transplant Recipient

Background: Monitoring sedation depth with appropriate sedative choice can reduce over sedation and associated side effects. Objectives: To compare Desflurane (Des) vs. Propofol (P) sedation with regards to, haemodynamics, recovery profiles, side effects and costs. Design: A prospective randomized hospital based comparative study. Setting: In a single centre between May 2012 and December 2014. Patients: Sixty mechanically ventilated liver recipients were assigned randomly to receive postoperative sedation either with inhalational Des in air/oxygen 1 litre min-1 or intravenous P 4 mg/kg/hr. Interventions: Recovery time and response to eye opening was recorded. Memorization of five words, Trieger dot test, and digit symbol substitution tests were applied. The Patient State Index (PSI) by SEDLine Sedation Monitor (Masimo, Irvin, CA) was used to target adequate depth of sedation (50-75) in both groups. Ramsay sedation score (RSS) was monitored. Fentanyl was used to assist sedation guided with PSI. The Transesophageal Doppler (TED) was recorded hourly; corrected flow time (FTc) of TED was used for fluid optimization. Main outcome measures: Recovery profile was the primary end point.Secondary outcomes were haemodynamic events, side effects and cost. Recovery was faster with Desflurane than Propofol (2.0+1.1 vs. 13.1+4.4 min, P 75), five words recall, trieger dot test and digit symbol substitution test. Required duration of sedation was lower with Desflurane (6.83 ± 2.00 vs. 8.26 ± 1.68 hour, P=0.004). Systemic vascular resistance (SVR) and mean arterial blood pressure (MABP) were better maintained with Desflurane. Under comparable PSI readings between both groups at all measuring points (SVR, MABP and PSI after 2hrs sedation 908.93 ± 139.5 vs. 617.6 ± 104.5 dyn.sec.cm-5, P 0.01). Fentanyl was frequently combined with P to reduce its effect on SVR and MBP. (483.3+168.3 vs. 100 ± 0.00 μg, P<0.05). Total consumption of Des and P were (53.13 ± 10.30 ml vs. 1010.33 ± 205.06 mg). Cost was lower with Desflurane (0.9+0.3 vs. 1.6+0.4) Sterling £/hour, (P=0.000). Conclusion: Postoperative Desflurane sedation guided with PSI enhanced recovery at a lower cost when compared to Propofol as well as preserving better the haemodynamics at a lower cost.

Increased expression of macrophage migration inhibitory factor in the nucleus of solitary tract attenuates the renovascular hypertension

We investigatedwhether hemorrhagic hypotension (HH) altered the sensitivity of vagal pulmonary C-fibers in this study. The fiber activity (FA) of single vagal pulmonary C-fiber was continuously recorded in anesthetized rats before, during, and after HH was induced by bleeding from the femoral arterial catheter into a blood reservoir and lowering the mean systemic arterial blood pressure (MSAP) to ~40 mmHg for 20 min. Our results showed: 1)AfterMSAP reached a steady state of HH, the peak FA response to intravenous injection of capsaicin was elevated by ~5 folds. The enhanced C-fiber sensitivity continued to increase during HH and sustained even after MSAP returned to baseline during the recovery, but slowly returned to control ~20 min later. 2) Responses of FA to intravenous injections of other chemical stimulants of pulmonary Cfibers (phenylbiguanide, lactic acid and adenosine) and a constantpressure lung hyperinflation were all significantly potentiated by HH. 3) Infusion of sodium bicarbonate alleviated the systemic acidosis during HH, and it also attenuated, but did not completely prevent the HHinduced C-fiber hypersensitivity. In conclusion, the pulmonary C-fiber sensitivity was elevated during HH, probably caused by the endogenous release of chemical substances (e.g., lactic acid) that were produced by tissue ischemia during HH. This enhanced C-fiber sensitivity may heighten the pulmonary protective reflexes mediated through these afferents (e.g., J reflex) during hemorrhage when the body is more susceptible to other hazardous insults and pathophysiological stresses. (Supported in part by NHLBI and DoD grants)

Impaired cerebral autoregulation and brain injury in newborns with hypoxic-ischemic encephalopathy treated with hypothermia.

Impaired cerebral autoregulation may contribute to secondary injury in newborns with hypoxic-ischemic encephalopathy (HIE). Continuous, noninvasive assessment of cerebral pressure autoregulation can be achieved with bedside near-infrared spectroscopy (NIRS) and systemic mean arterial blood pressure (MAP) monitoring. This study aimed to evaluate whether impaired cerebral autoregulation measured by NIRS-MAP monitoring during therapeutic hypothermia and rewarming relates to outcome in 36 newborns with HIE. Spectral coherence analysis between NIRS and MAP was used to quantify changes in the duration [pressure passivity index (PPI)] and magnitude (gain) of cerebral autoregulatory impairment. Higher PPI in both cerebral hemispheres and gain in the right hemisphere were associated with neonatal adverse outcomes [death or detectable brain injury by magnetic resonance imaging (MRI), P < 0.001]. NIRS-MAP monitoring of cerebral autoregulation can provide an ongoing physiological biomarker that may help direct care in perinatal brain injury.

The protective role of vitamin E and angiotensin II receptor blocker in diabetic cardiomyopathy in male albino rats

Background Diabetic cardiomyopathy is a common complication of diabetes mellitus. There are many pathophysiological mechanisms of diabetic cardiomyopathy, such as apoptosis and oxidative stress. Aim This study was designed to assess the issue of cardiomyocyte apoptosis as a possible cause of diabetic cardiomyopathy and the use of vitamin E as an antioxidant and losartan as an angiotensin II receptor blocker in suppressing this apoptosis. Materials and methods Rats were randomly divided into five groups of 10 animals each: group 1 included healthy control rats; group 2, the diabetic group, included rats that were made diabetic with a single injection of streptozotocin; group 3 included diabetic rats treated with losartan; group 4 included diabetic rats treated with vitamin E; and group 5 included diabetic rats treated with losartan and vitamin E. At the end of the experimental period, plasma glucose and serum lipid profile were evaluated. The heart rate and mean systemic arterial blood pressure were measured in all groups. Oxidative stress as assessed with malondialdehyde and reduced glutathione (GSH-PX) concentrations, as well as caspase-3 activity as an index of apoptosis, was determined in cardiac tissue. In addition, cardiac apoptosis was measured with the BCL-X immunohistochemistry technique. Results Administration of vitamin E and losartan caused significant decrease in apoptosis. In addition, there was significant decrease in malondialdehyde and caspase-3 and significant increase in GSH in cardiac tissue homogenate, with significant decrease in the serum lipid level. The mean systemic arterial blood pressure was significantly decreased, whereas heart rate increased to normal level. Conclusion Vitamin E and losartan have a protective effect on diabetes-induced cardiomyopathy in rats.

Hemodynamic Effects of Sevoflurane versus Dexmedetomidine

Background: Cardiac catheterization procedures produce challenges for the anesthetist because of the increased need to provide support in sedating and/or anesthetizing patients. Objective: To compare pulmonary and systemic hemodynamics of two anesthetic regimens: sevoflurane as volatile induction maintenance anesthesia and dexmedetomidine as total intravenous anesthesia in pediatric patients suffering from congenital heart disease with left-to-right intracardiac shunt. Design: A Prospective Randomized Study. Setting: Mansoura University Children Hospital (MUCH), Egypt. Method: Sixty pediatric patients of both sexes were referred for elective cardiac catheterization. Patients were randomly allocated into two equal groups, consisted of 30 patients. In the first group, the patients received volatile induction maintenance anesthesia (VIMA) with sevoflurane (GS group) while in the second, the patients received total intravenous anesthesia (TIVA) with dexmedetomidine (1 μg/kg) intravenous bolus dose over 10 minutes, anesthesia was maintained by intravenous infusion of dexmedetomidine at a rate of 1-2 μg/kg/hour (GD group). Result: The present study showed that the heart rate (HR), Pulmonary blood flow index (QpI), Systemic blood flow index (QsI) and Qp/Qs ratio were comparable in both groups. Pulmonary vascular resistance index (PVRI) and Systemic vascular resistance index (SVRI) were significantly lower in GS group after induction of general anesthesia (GA) if compared with the basal value maintaining PVR/SVR at baseline value. However, PVRI and SVRI were insignificantly higher in GD group after induction of GA if compared with the basal value; thus, maintaining PVR/SVR. The Systemic Mean arterial blood pressure (MAP) decreased in both groups. Conclusion: Total intravenous anesthesia with dexmedetomidine provided hemodynamic stability. It is comparable to volatile induction and maintenance of anesthesia with sevoflurane when administered to pediatric patients suffering from congenital heart disease with left-to-right intracardiac shunt during cardiac catheterization.

Central retinal venous pulsation pressure in different stages of primary open-angle glaucoma

BackgroundTo evaluate the central retinal venous pulsation pressure (CRVPP) in patients with intraocular pressure (IOP)-controlled early, moderate and advanced open-angle glaucoma and a healthy control group.MethodsCRVPP was measured with a...