PERFUSION OF ISCHEMIC MYOCARDIUM DURING ANESTHESIA WITH SEVOFLURANE

Background: Sevoflurane produces direct vasodilation of coronary arter ies in vitro and decreases coronary vascular resistance in vivo pharma cologic properties that may contribute to the development of ''coronar y steal.'' This investigation examined the effects of sevoflurane on t he distribution of regional myocardial perfusion in chronically instru mented dogs with steal-prone coronary artery anatomy. Methods: Dogs we re chronically instrumented for measurement of aortic and left ventric ular pressure, diastolic coronary blood flow velocity and subendocardi al segment length. After recovery from surgery, dogs underwent repetit ive, brief, left anterior descending coronary artery (LAD) occlusions via an implanted hydraulic vascular occluder to enhance collateral dev elopment. A progressive left circumflex coronary artery (LCCA) stenosi s was also obtained using an ameroid constrictor. After development of LCCA stenosis, the LAD was totally occluded to produce a model of mul tivessel coronary artery disease. Systemic hemodynamics, regional cont ractile function and myocardial perfusion measured with radioactive mi crospheres were assessed in the conscious state and during sevoflurane anesthesia at 1.0 and 1.5 MAC with and without restoration of arteria l blood pressure and heart rate to conscious levels. Results: Total LA D occlusion with simultaneous LCCA stenosis increased heart rate, mean arterial pressure, left ventricular systolic and end-diastolic pressu res, end-diastolic segment length, and rate-pressure product in consci ous dogs. Subsequent administration of sevoflurane caused dose-related decreases in arterial pressure, left ventricular systolic pressure, d ouble product, and peak rate of increase of left ventricular pressure at 50 mmHg. Perfusion of normal myocardium was unchanged during sevofl urane anesthesia. In contrast, sevoflurane caused dose-dependent decre ases in blood flow to myocardium supplied by the stenotic LCCA, which returned to control levels after restoration of heart rate and arteria l pressure. No reduction in collaterally derived blood flow to the occ luded region was produced by 1.0 or 1.5 MAC sevoflurane. No redistribu tion of blood flow away from the occluded LAD region to normal or sten otic myocardium occurred during sevoflurane anesthesia. In fact, incre ases in the ratio of blood flow between occluded and normal zones or o ccluded and stenotic zones were observed in the subepicardium during 1 .5 MAC sevoflurane with maintenance of the heart rate and arterial pre ssure at conscious levels. Conclusions: The results demonstrate that s evoflurane does not reduce or abnormally redistribute myocardial blood flow derived from coronary collateral vessels in a chronically instru mented canine model of multivessel coronary artery obstruction.