Sevoflurane Anesthesia In Patients Research Articles

Perfusion and metabolism of liver and splanchnic nerve area under sevoflurane anesthesia

In common with other halogenated volatile anaesthetics, sevoflurane causes a dose-related cardiovascular depression and therefore the affection of blood flow of different organ systems is suggested. So far known, sevoflurane is not different compared to isoflurane in affecting liver and splanchnic blood flow. Concluded from former published studies there was no case of hepatic toxicity of sevoflurane been published so that this substance can be used in patients with reduced hepatic function. The primary organic metabolite of sevoflurane is hexafluorisopropanol (HFIP), which is readily and rapidly conjugated with glucuronic acid. No reactive intermediates are formed and HFIP appears to be an unlikely compound to form liver protein adducts. For this reasons sevoflurane "hepatitis" is not expected. Like most other inhalation agents sevoflurane increase the neuromuscular blockade after treatment with muscle relaxants in anaesthesia. The MAC values of Sevoflurane where reduced after the application of nitrous oxide, benzodiazepines and opiates. From human studies we know that chronic drug therapy with isoniazid induces the metabolism of sevoflurane, enflurane and isoflurane, markedly increasing peak plasma fluoride concentrations. However, barbiturates as well as phenytoin do not influence the metabolism of sevoflurane because these agents do not induce the major hepatic defluorinating enzyme cytochrome P450 2E1. Obesity, untreated diabetes mellitus and alcohol abuse increase the hepatic content and activity of cytochrome P450 2E1 and therefore enhanced anaesthetic defluorination is to be suspected. Until now, there are no studies about sevoflurane anaesthesia in patients after liver transplantation but the extremely low hepatotoxic potential as compared to isoflurane provides no argument to avoid this substance for anesthesia in liver transplanted patients.

Control of hypertension during isoflurane or sevoflurane anesthesia with continuous infusion of nicardipine hydrochloride

In a multicenter study, the efficacy and tolerability of nicardipine hydrochloride (NIC) were examined when the drug was used to control hypertension during isoflurane or sevoflurane anesthesia in patients with or without a preoperative history of hypertension. Retrospectively, the 124 study patients were divided into four groups: patients without (group 1) or with (group 2) a preoperative history of hypertension who received isoflurane anesthesia, and those without (group 3) or with (group 4) a preoperative history of hypertension who received sevoflurane anesthesia. NIC infusion was started when systolic pressure exceeded 160 mm Hg or 30% above the control value determined before the induction of anesthesia. The ability of NIC to control hypertension was analyzed for 30 minutes after starting the infusion. Arterial pressure, heart rate, and urine volume were examined in each group. Mean doses of NIC infused during the 30-minute study period in groups 1, 2, 3, and 4 were 2.23, 2.13, 2.43, and 2.19 μg · kg −1 · min −1, respectively. There were no significant differences between the four groups in the amount of NIC infused. In the four groups, no significant changes were seen in heart rate, and blood pressure was effectively controlled (group 1: 149.5/86.4 mm Hg and 113.3/63.0 mm Hg before and after the 30-minute study period, respectively; group 2: 156.6/91.2 mm Hg and 118.2/71.0 mm Hg; group 3: 153.4/90.1 mm Hg and 119.0/71.1 mm Hg; and group 4: 160.6/98.7 mm Hg and 124.1/76.8 mm Hg). The final blood pressure measurements were considered within normal ranges for the patients studied. A decrease in blood pressure was slightly delayed in both sevoflurane groups (groups 3 and 4) and in the isoflurane group with a preoperative history of hypertension (group 2). While urine output tended to increase in all groups, a significant increase was found only in group 1 (from 0.019 ± 0.011 mL · kg −1 · min −1 before treatment to 0.087 ± 0.041 mL · kg −1 · min −1 after treatment). In conclusion, NIC was effective and well tolerated in controlling hypertension during isoflurane or sevoflurane anesthesia

Effects of Sevoflurane on Cerebral Circulation and Metabolism in Patients with Ischemic Cerebrovascular Disease

Sevoflurane is a newly developed volatile anesthetic that has a low blood-gas partition coefficient. The effects of sevoflurane on the cerebral circulation or metabolism in humans have not been studied. The authors examined the cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) during sevoflurane anesthesia. The carbon dioxide response and autoregulation of cerebral circulation were also examined. Ten patients with ischemic cerebrovascular disease undergoing extra-intracranial artery anastomosis were studied. Cerebral blood flow and CMRO2 were determined by the Kety-Schmidt method using argon. These procedures were performed during the inhalation of 33% N2O, 33% argon, and oxygen with 1.5% sevoflurane (0.88 minimum alveolar concentration). To examine the relationship of CBF to a change in PaCO2, CBF was measured repeatedly at steady state PaCO2, of 40, 35, and 45 mmHg. Furthermore, CBF was measured before and after an increase in mean arterial pressure (MAP) caused by intravenous infusion of methoxamine to determine the relationship between CBF and MAP. Cerebral blood flow and CMRO2 were 28 +/- 4 ml x 100 g-1 x min-1 and 1.34 +/- 0.23 ml x 100 g-1 x min-1, respectively. Cerebral blood flow was found to vary directly with PaCO2 alteration. The slope of the regression line between PaCO2 and CBF was 1.29 ml x 100 g-1 x min-1 x mmHg-1. On the other hand, CBF was constant throughout the elevation of MAP with vasopressor. Both carbon dioxide response and cerebral autoregulation were well maintained under 0.88 MAC sevoflurane anesthesia in patients with ischemic cerebrovascular disease.