Manohar M, Parks C M
J Pharmacol Exp Ther. 1984 Dec;231(3):640-8.
Effects of sevoflurane anesthesia on organ blood flow were examined in nine healthy isocapnic pigs using 15-mumol diameter radionuclide-labeled microspheres that were injected into the left atrium. Minimum alveolar concentration (MAC) of sevoflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was found to be 2.66 +/- 0.20%. Hemodynamic measurements were made on each pig during the following five conditions: awake (control); 1.0 MAC of sevoflurane anesthesia; 2.66% (1.0 MAC) sevoflurane + 50% N2O anesthesia; 1.5 MAC of sevoflurane anesthesia; and 3.99% (1.5 MAC) sevoflurane + 50% N2O anesthesia. Dose-related decrease in cardiac output, mean aortic pressure and left ventricular work occurred with sevoflurane anesthesia but heart rate was unchanged. Addition of 50% N2O to either of the pre-established sevoflurane concentrations did not change heart rate or the cardiac output, but with 3.99% sevoflurane mean aortic pressure decreased further. Unlike isoflurane and halothane which increase porcine brain blood flow, cerebral blood flow decreased to a similar level with both levels of sevoflurane anesthesia. Whereas cerebellar perfusion was unaltered with both levels of sevoflurane anesthesia, brain-stem blood flow decreased to a similar level from the control value. However, during 3.99% sevoflurane anesthesia, brain-stem blood flow exceeded that at 2.66% sevoflurane anesthesia. Addition of N2O to pre-established concentrations of sevoflurane increased regional brain blood flow but cerebral and brain-stem blood flow exceeded awake value only during 2.66% sevoflurane + 50% N2O anesthesia. Transmural myocardial blood flow decreased in a dose-dependent manner during sevoflurane anesthesia but the subendocardial/subepicardial perfusion ratio remained at control value.(ABSTRACT TRUNCATED AT 250 WORDS)