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The hypothesis that isoflurane causes coronary steal was investigated in a canine model of chronic coronary occlusion. An ameroid constrictor was implanted in dogs to stimulate the development of intercoronary collateral vessels. During an acute experiment 3–4 weeks following implantation, heart rate, mean arterial pressure, and total coronary flow were held constant, and flow distribution was measured with microspheres in the presence and absence of isoflurane. Contractile function of the collateral-dependent zone and myocardial lactate extraction were also measured. Isoflurane produced a decrease in collateral flow and a decrement in collateral zone contraction, while, at the same time, enhancing flow in the normally perfused zone. In a second series of animals, isoflurane was found to have effects similar to those of adenosine, an arteriolar dilator known to produce coronary steal. In contrast, neither halothane nor nitrous oxide caused flow alterations or dysfunction of the collateral-dependent zone.