Studies about the coronary vasodilating properties of isoflurane indic
ate that this drug induces coronary vasodilation. No work has examined
isoflurane-induced vasodilation in known stunned myocardium. This stu
dy was conducted to determine isoflurane's coronary vasodilation poten
cy in stunned myocardium and to compare the results obtained with norm
al myocardium. We determined the vasodilating properties of isoflurane
in regionally perfused swine myocardium. Six domestic swine were anes
thetized with pentobarbital and fentanyl. The left anterior descending
artery (LAD) was cannulated and perfused with blood drawn from the ca
rotid artery and passed thorough a membrane oxygenator. LAD arterial f
low was controlled by a calibrated roller pump with continuous digital
readout, and LAD arterial pressure was measured directly. The anterio
r interventricular vein was cannulated and dimension crystals placed i
n the LAD-perfused myocardium. Myocardial stunning was induced by redu
ction of coronary blood flow (CBF) to 30% of control flow for 20 minut
es. One hour after reperfusion, the vasodilatory response to 0%, 1%, a
nd 2% isoflurane administered via the membrane oxygenator was determin
ed and compared to maximum vasodilatation produced by regional intraco
ronary administration of adenosine. Systemic blood pressure and heart
rate remained constant throughout the experiment. At 2% isoflurane, sy
stolic shortening and regional myocardial oxygen consumption decreased
53% and 17%, respectively. The same concentration increased CBF by 33
% and reduced coronary vascular resistance (CVR) by 25%. One percent i
soflurane affected neither CBF nor CVR. Regional coronary administrati
on of adenosine produced much greater changes in CBF (+509) and CVR (-
89.5%). We conclude that isoflurane is a mild dose dependent coronary
vasodilator in the stunned myocardium. At 1% isoflurane concentration
the coronary vasodilating properties of isoflurane are minimal.