ANESTHESIA AND PRESSOR RESPONSIVENESS IN CHRONIC BILE-DUCT LIGATED DOGS

Cardiovascular homeostasis is compromised under general anesthesia and in jaundice. Because surgery is often performed on jaundiced patients, it is not altogether surprising that the incidence of perioperative complications is higher in such patients than in nonjaundiced ones. In this study we assessed the potential synergistic effects of anesthesia and jaundice on cardiovascular responsiveness of chronic bile‐ductligated dogs. Responsiveness to norepinephrine, angiotensin II and isoproterenol was determined before and after chronic bile‐duct ligation or sham‐operation while the dogs were conscious or under halothane, fentanyl or pentobarbital‐sodium anesthesia. These data have shown that halothane‐ and barbiturate‐induced anesthesia do not alter mean arterial blood pressure in unoperated dogs when compared with conscious dogs before laparoatomy. Furthermore, these two agents did not modify the pressor, dilator and positive inotropic responses to intravenous infusions of norepinephrine, angiotensin II and isoproterenol. Fentanyl, however, reduced mean arterial blood pressure and heart rate without influencing responsiveness to the three vasoactive agents. Blunted responsiveness in the chronic bile‐duct‐ligated dogs to the three vasoactive agents was observed without any marked changes in mean arterial blood pressure or heart rate. The same blunted responses observed in the conscious, chronic bile‐duct‐ligated dogs were also seen in the anesthetized, chronic bile‐duct‐ligated dogs. Halothane caused a marked hypotensive effect in the chronic bile‐duct‐ligated dogs that was not seen in the sham‐operated dogs. Conscious and anesthetized sham‐operated dogs responded in the same manner as the conscious and anesthetized dogs before ligation. Because we could not demonstrate any synergistic or antagonistic effects of anesthesia and jaundice on cardiovascular responsiveness, these results may be useful for researchers using animal models to investigate the pathogenesis of the cardiovascular complications of liver disease.(HEPATOLOGY 1990; 11:551:556.) Copyright © 1990 American Association for the Study of Liver Diseases