Sevoflurane-induced Hypotension Research Articles

Sevoflurane-induced hypotension causes cognitive dysfunction and hippocampal inflammation in mice

Sevoflurane commonly adopted for anesthetic in clinical practice, however, its influences on cerebral blood flow and cognitive function remain controversial. Herein, the sevoflurane-induced hypotension on arterial blood pressure, cerebral blood flow, cognitive function, and hippocampal inflammation was investigated in mice. A significant decrease in arterial blood pressure and cerebral blood flow was indicated by the sevoflurane anesthesia treatment. Moreover, sevoflurane-induced hypotension was associated with the impaired cognitive function and the increased levels of NLRP3 inflammasome activation and oxidative stress in hippocampus. These findings suggest that sevoflurane-induced hypotension may lead to the cognitive dysfunction and hippocampal inflammation.

Invasive and non-invasive assessment of macro- and micro-circulatory effects of vasopressors during sevoflurane anesthesia in a pediatric experimental model: A randomized trial.

While non-invasive assessment of macro- and micro-circulation has the promise to optimize anesthesia management, evidence is lacking for the relationship between invasive and non-invasive measurements of cardiac output and microcirculatory indices. We aimed to compare the abilities of non-invasive techniques to detect changes in macro- and micro-circulation following deep anesthesia and subsequent restoration of the compromised hemodynamic by routinely used vasopressors in a randomized experimental study. A 20%-25% drop in mean arterial pressure was induced by sevoflurane in anesthetized mechanically ventilated just-weaned piglets (n=12) prior to the administration of vasopressors in random order (dopamine, ephedrine, noradrenaline, and phenylephrine). Simultaneous transpulmonary thermodilution cardiac output assessment with the invasive pulse index continuous contour (PiCCO) method was compared with non-invasive estimates obtained with electrical conductivity (ICON) and echo Doppler (Cardio Q). Changes in microcirculation were characterized by sublingual red blood cell velocity, jugular cerebral venous oxygen saturation, and arterial lactate. Cardiac output indices obtained by invasive and non-invasive methods. Changes in cardiac output measured invasively and non-invasively correlated significantly after sevoflurane (r=.78, p=.003 and r=.76, p=.006 between PiCCO and ICON or Cardio Q, respectively). Following the administration of vasopressors, invasive and non-invasive cardiac output assessments were unrelated with significant correlations observed only between PiCCO and ICON after dopamine and ephedrine. Sevoflurane-induced hypotension decreased jugular cerebral venous oxygen saturation significantly and was recovered by all vasopressors. Sevoflurane and vasopressors had no effect on red blood cell velocity, which increased only after dopamine. No consistent changes in lactate were observed during the study period. The results of this study suggest that non-invasive cardiac output measurements may not accurately reflect changes in macrocirculation after hemodynamic optimization by vasopressors. Due to the incoherence between macro- and micro-circulation, monitoring microcirculation is essential to guide patient management.

Evaluation of gastric and bladder tonometry as indicators of tissue perfusion in induced hypotension in dogs.

To evaluate the use of gastric (PgCO2 ) and bladder (PbCO2 ) tonometry for assessing tissue hypoperfusion in dogs during sevoflurane-induced hypotension, and to compare these measurements with delivery of oxygen, arterial oxygen content, and plasma lactate concentration. Prospective experimental trial. University veterinary teaching hospital. Fourteen adult Beagle dogs. Anesthetic induction was performed by mask with sevoflurane and oxygen. Heart rate, direct arterial pressures, respiratory rate, and end-tidal carbon dioxide were recorded; arterial blood samples were taken to measure blood gases, and venous samples were sampled to measure plasma lactate. A tonometric catheter was introduced into the stomach to measure PgCO2 . Samples of saline from the balloon of a Foley catheter placed in the bladder were collected every 10 minutes and used to measure PbCO2 by gas analysis. Tonometry measurements, plasma lactate, and oxygen delivery and consumption were compared at 3 time points: at baseline, during hypotension, and during treatment periods. A hypotensive period (mean arterial pressure (MAP) < 60 mm Hg) of 15 minutes was induced by an overdose of sevoflurane, whereas during the treatment period, a constant-rate infusion of dopamine (10 μg/kg/min) was administered intravenously for 40 minutes. Values for PgCO2 and PbCO2 increased significantly during the hypotensive period, and correlations were found between these values and the delivery of oxygen. Gastric tonometry values had stronger correlations compared with bladder tonometry values. Gastric and bladder tonometry can be used to detect hypoperfusion. Further studies are warranted to determine the potential use of gastric and bladder tonometry in assessing dogs in clinical situations.

Cardiovascular Effects of Dobutamine and Phenylephrine Infusion in Sevoflurane-anesthetized Thoroughbred Horses

ABSTRACTTo determine dose-dependent cardiovascular effects of dobutamine and phenylephrine during anesthesia in horses, increasing doses of dobutamine and phenylephrine were infused to 6 healthy Thoroughbred horses. Anesthesia was induced with xylazine, guaifenesin and thiopental and maintained with sevoflurane at 2.8% of end-tidal concentration in all horses. The horses were positioned in right lateral recumbency and infused 3 increasing doses of dobutamine (0.5, 1.0 and 2.0 µg/kg/min) for 15 min each dose. Following to 30 min of reversal period, 3 increasing doses of phenylephrine (0.25, 0.5 and 1.0 µg/kg/min) were infused. Cardiovascular parameters were measured before and at the end of each 15-min infusion period for each drug. Blood samples were collected every 5 min during phenylephrine infusion period. There were no significant changes in heart rate throughout the infusion period. Both dobutamine and phenylephrine reversed sevoflurane-induced hypotension. Dobutamine increased both mean arterial blood pressure (MAP) and cardiac output (CO) as the result of the increase in stroke volume, whereas phenylephrine increased MAP but decreased CO as the result of the increase in systemic vascular resistance. Plasma phenylephrine concentration increased dose-dependently, and these values at 15, 30 and 45 min were 6.2 ± 1.2, 17.0 ± 4.8 and 37.9 ± 7.3 ng/ml, respectively.

The Effects of Hypotension and Norepinephrine on Microvascular Flap Perfusion

Microvascular flap surgery is a common technique in reconstructive surgery. The wide indications and variable patients provide challenge also for anesthesiologist. Both hypotension and hypoperfusion can be harmful to the flap. Hypotensive patients are treated with fluid resuscitation and vasopressors (e.g., norepinephrine), if needed. As vasoconstrictors, vasopressors might impair microvascular flap perfusion. In this experimental pig model we studied the effect of sevoflurane-induced hypotension on the perfusion of microvascular and superiorly pedicled rectus abdominis myocutaneous flaps. In addition, we evaluated the effect of norepinephrine on flap perfusion when it was used for correction of hypotension. Microdialysis (MD) was used to detect metabolic changes, as it is a sensitive method to detect early changes of tissue metabolism and ischemia in different tissue components of soft tissue flaps. The main finding of this study was that moderate degree of normovolemic hypotension or the use of norepinephrine for the correction of this hypotension did not affect flap perfusion as assessed by MD. More studies are clearly needed to confirm the safety of norepinephrine in clinical use in microsurgery.

Middle cerebral artery flow velocity and CO2 reactivity during the combination of hemodilution and sevoflurane-induced hypotension in elderly patients

Middle cerebral artery flow velocity and CO2 reactivity during the combination of hemodilution and sevoflurane-induced hypotension in elderly patients

The effect of sevoflurane-induced hypotension in combination with acute hypervolaemic haemodilution on middle cerebral artery flow velocity in surgical patients

This study was carried out to clarify the effect of the combination of acute hypervolaemic haemodilution and hypotensive anaesthesia induced with sevoflurane on human middle cerebral artery flow velocity using transcranial Doppler ultrasonography. Thirty patients who were maintained with N2O-O2-sevoflurane anaesthesia undergoing hip surgery were randomly divided into two groups (no controlled hypotension group, Group A, and controlled hypotension group, Group B). Haemodilution was produced by acute preoperative infusion of 1000 mL of hydroxyethylstarch without removing blood in both groups. Mean arterial pressure was maintained at approximately 95 mmHg in Group A and at 55 mmHg for 80 min by increasing the inspired concentration of sevoflurane in Group B. Middle cerebral artery flow velocity was measured before haemodilution, after haemodilution, 80 min after starting hypotension, and 60 min after recovery from hypotension. Middle cerebral artery flow velocity significantly increased in both groups after haemodilution; by 28%, in Group A, P < 0.05 vs. before haemodilution and by 30% vs. before haemodilution in Group B, P < 0.05). During controlled hypotension, it decreased towards the pre-haemodilution value (P < 0.05 vs. after haemodilution). Sevoflurane-induced hypotension to a mean arterial pressure of 55 mmHg would reduce middle cerebral artery flow that had been increased by acute hypervolaemic haemodilution, such as haematocrit value of 26%, whereas it could preserve the flow in pre-haemodilution condition during normocapnia.

Effects of Sevoflurane Anesthesia on Carotid-Cardiac Baroreflex Responses in Humans

Sevoflurane depresses cardio-vagal baroreflex gain (ability of vagally mediated R-R interval response to arterial blood pressure change). We examined the effects of sevoflurane anesthesia on maximum buffering capacity of vagally mediated hemodynamic control (baroreflex range) by examining the entire stimulus-response baroreflex relation. Electrocardiogram and invasive arterial blood pressure were monitored in 11 healthy volunteers. Carotid-cardiac baroreflex responses were elicited by increasing neck chamber pressure (external pressure applied over the bilateral carotid sinuses) to 40 mm Hg for 5 heartbeats followed by decreasing chamber pressure by successive 15-mm Hg R-wave triggered decrements to -65 mm Hg during held expiration. R-R intervals were plotted as functions of preceding carotid distending pressure. Range, maximum gain, and operational point (relative position of the resting set point within the entire baroreflex response curve) were determined at conscious baseline, during 2% (end-tidal) sevoflurane anesthesia, without and with phenylephrine infusion to maintain conscious arterial blood pressure, and at 30, 60, 120, and 180 min after emergence from anesthesia. Sevoflurane anesthesia significantly depressed maximum gain (from 3.84 +/- 0.99 to 1.04 +/- 0.40 ms/mm Hg [mean +/- sd]; P < 0.001) and range (from 207 +/- 43 to 52 +/- 19 ms; P < 0.001) of the reflex relation, both of which recovered at 120 and 180 min after emergence. Phenylephrine infusion only partially restored these variables. The operational point was unchanged throughout the study. Our results indicate that maximum cardio-vagal compensatory response to buffer hemodynamic perturbation is depressed during sevoflurane anesthesia. Sevoflurane-induced hypotension, which produced vagal withdrawal, did not play an important role in depressing cardio-vagal reflex function.

Haemodynamic and splanchnic organ blood flow responses during sevoflurane-induced hypotension in dogs

Haemodynamic and splanchnic organ blood flow responses during sevoflurane-induced hypotension in dogs

Haemodynamic and splanchnic organ blood flow responses during sevoflurane-induced hypotension in dogs

The safety of hypotension induced by sevoflurane and splanchnic organ blood flow remains to be clarified. The aim was to investigate the effects of sevoflurane-induced hypotension on systemic haemodynamics and splanchnic organ blood flows in dogs. Mean arterial pressure was maintained at 60 mmHg by increasing sevoflurane concentrations. The renal, hepatic and pancreatic blood flows were measured by using the hydrogen clearance method. Hypotension induced by sevoflurane resulted in a 50% decrease of mean arterial pressure due to a 30% reduction in systemic vascular resistance associated with a 30% decrease in cardiac index. The mechanisms causing the lower cardiac index were produced by the decreases in heart rate and left ventricular dP/dt(max). Renal, hepatic and pancreatic blood flow were reduced, but the whole-body oxygen consumption did not change during the hypotensive period. The haemodynamic changes induced by sevoflurane were caused by the suppression of arterial baroreflexes and myocardial depression, but splanchnic organ blood flows, though reduced, could provide adequate peripheral perfusion to meet the decrease in oxygen supply.

Differential vascular reactivity of canine mesenteric arteries and veins to sevoflurane.

The aim of this study was to compare the vascular reactivities of canine mesenteric arteries and veins to sevoflurane and to elucidate the underlying mechanism that is responsible for sevoflurane-induced hypotension. Vascular rings of canine mesenteric arteries and veins were suspended in organ baths, and the effect of 2.3% and 4.6% sevoflurane on the contractile responses to transmural electrical stimulation (ES) and to norepinephrine (NE) were determined by recording isometric tension changes. The rings were contracted to a stable tension by the addition of NE and then exposed to increasing concentrations of sevoflurane (0%-5.1%). Sevoflurane attenuated the contractile responses to transmural ES in veins but not in arteries. The concentration responses to NE were not affected by sevoflurane in arteries or in veins. At stable precontraction induced by NE, when sevoflurane was placed in the bathing medium, arteries with intact endothelium had significant contraction at 1.7% and 3.4% sevoflurane, followed by relaxation at 5.1%. On the contrary, sevoflurane produced dose-dependent relaxation in endothelium-denuded arteries and endothelium-intact veins CONCLUSION: It is suggested that the relaxation of the veins by sevoflurane may be due to the inhibition of NE release from sympathetic nerve endings and to the direct inhibition of the contractile mechanisms of vascular smooth muscle. In arteries, sevoflurane causes endothelium-dependent vasocontraction, probably by inhibiting the release of basal endothelium-derived relaxing factor (EDRF).