PORCINE SYSTEMIC AND REGIONAL ORGAN BLOOD-FLOW DURING 1.0 AND 1.5 MINIMUM ALVEOLAR CONCENTRATIONS OF SEVOFLURANE ANESTHESIA WITHOUT AND WITH 50-PERCENT NITROUS-OXIDE

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  • 1 January 1984
    • journal article
    • research article
    • Vol. 231  (3) , 640-648
Abstract
Effects of sevoflurane anesthesia on organ blood flow were examined in 9 healthy isocapnic pigs using 15 .mu.m diameter radionuclide-labeled microspheres that were injected into the left atrium. Minium alveolar concentration (MAC) of sevoflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was 2.66 .+-. 0.20%. Hemodynamic measurements were made on each pig during the following 5 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. 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. Addition of N2O to sevoflurane did not alter myocardial perfusion. Neither renal nor adrenal perfusion were affected by either dose of sevoflurane. Splenic and hepatic arterial blood flows increased with both levels of sevoflurane anesthesia. Blood flow to the thyroid gland, pancreas and the gastrointestinal tract decreased with sevoflurane anesthesia. The effects of sevoflurane anesthesia on myocardial, renal, adrenal gland and splanchnic organ blood flows were quite similar to those caused by equipotent isoflurane anesthesia in swine.