Anesthetic influences on regional hemodynamics in normal and hemorrhaged rats.

Forty-six male Sprague-Dawley rats were divided in five groups: awake animals and those receiving ketamine, halothane, enflurane, or isoflurane anesthesia. Cannulae were inserted into the left femoral artery and vein and the left ventricle. Inspired concentrations of the volatile anesthetics were adjusted to achieve the minimal alveolar concentration (MAC) of each drug. Ketamine, 125 mg . kg-1, was injected intraperitoneally and then infused at a rate of 1 mg . kg-1 . min-1. All animals breathed spontaneously throughout the experiment (FIO2 = 0.3). Following a 2-h stabilization period, 30% of estimated blood volume was withdrawn gradually over 10 min. Immediately before and 20 min after hemorrhage, cardiac output and regional blood flows were measured by the microsphere method (85Sr, 141Ce-labeled 15-microns microspheres, respectively). Arterial blood samples were analyzed for PO2, PCO2, pH, lactate, and pyruvate at these times also. Prior to hemorrhage, cardiac output (CO) values were similar in awake rats and those receiving ketamine or isoflurane, but CO was reduced moderately by enflurane and to a greater extent by halothane. After hemorrhage, CO was greatest in awake animals and those receiving isoflurane, and awake rats tended to have the greatest organ blood flows. Values of lactate/pyruvate and excess lactate were least in awake animals. Overall results suggested that, in terms of cardiac output and regional blood flows, ketamine approximates the awake state most closely in normovolemic animals, whereas isoflurane anesthesia is most like the awake condition after hemorrhage.