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Recovery of Function and Adenosine Triphosphate Metabolism Following Myocardial Ischemia Induced in the Presence of Volatile Anesthetics

Department of Anesthesiology, Centre of Experimental Surgery and Anesthesiology, Katholieke Universiteit Leuven, Leuven, Belgium *Department of Anesthesiology, University of Wisconsin, Madison, Wisconsin

Abstract

Using a normothermic isolated working rabbit heart model, experiments were performed to determine whether exposure to halothane or isoflurane prior to ischemia improved postischemic recovery of myocardial function and the preservation of myocardial high energy phosphates. After 30 min of Langendorff perfusion, hearts were perfused for 30 min in the working mode. Three groups were studied: 1) the blank undergoing no pretreatment during an additional 15 min of working mode; 2) hearts exposed to 1.5% halothane; and 3) hearts exposed to 2.3% isoflurane during the additional 15 min of working mode. Subsequently, all hearts underwent 15 min of global normothermic ischemia, followed by 5 min of Langendorff reperfusion and 15 min of working heart mode using a perfusate devoid of volatile anesthetic. Adenosine triphosphate (ATP) and catabolites were determined after 15 min exposure to volatile anesthetics or blank, after 15 min global ischemia and at the end of the recovery phase. Myocardial function was determined after 30 min of working mode, after exposure to volatile anesthetics, and at the end of the recovery phase. In nonischemic hearts, 15-min treatment with 1.5% halothane or 2.3% isoflurane resulted in a significant decrease in positive LVdP/dt, from 1858 ± 286 to 1316 ± 180 mm Hg·s^–1and from 1888 ± 304 to 1541 ± 226 mm Hg·s^–1, respectively. Coronary flow was increased significantly after isoflurane but not after halothane. After 15 min of global ischemia followed by 5 min of Langendorff reperfusion and 15 min of working mode, left ventricular contractility assessed by positive LVdP/dt was depressed significantly (P < 0.05, paired t-test) in all three groups. Recovery, expressed as a percentage of control value at 30 min working heart, was not significantly higher in both groups pretreated with anesthetics compared to the blank group (P > 0.05 two-way ANOVA for repeated measures): recovery was 80 ± 6% in the blank group, 88 ± 9% in the halothane 1.5% group, and 86 ± 7% in the isoflurane 2.3% group. The myocardial content of ATP and catabolites remained unchanged during the exposure to volatile anesthetics under normoxic preischemic conditions. The catabolism of ATP to ADP and AMP induced by 15 min of global ischemia was similar in the three groups. During reperfusion, there was a fast resynthesis of ATP such that ATP levels were not different from control values. Again, there was no significant difference in high energy phosphate content between the blank and the pretreated hearts. We conclude that depressed cardiac function during exposure to halothane and isoflurane is not related to any change in myocardial ATP content, and that ATP catabolism during ischemia is not influenced by halothane and isoflurane. Further, treatment with halothane or isoflurane preceding ischemia has no effect on functional indices of recovery after myocardial stunning, which is in concert with unaltered myocardial tissue content of high energy phosphates.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999