Abstract
The effects of insulin on glucose uptake and lactate release in the perfused working rat heart were investigated in 3 types of preparation: a control low-workload preparation (I); an increased-pressure-workload preparation, simulating conditions of aortic pressure encountered in vivo (II); and an increased-volume-workload preparation (III) where pumping work done is approximately the same as II but coronary flow is restricted because of the decreased aortic pressure. Insulin stimulated glucose uptake and lactate release in preparations (I) and (II), but failed to do so in preparation (III). It was considered possible that preparation (III) was hypoxic, necessitating a maximal stimulation of glucose uptake. This was confirmed by improving cardiac oxygenation by addition of stroma-free Hb to the perfusate in preparation (III). Under these conditions in the absence of insulin, glucose uptake and lactate release were decreased compared with perfusions in the absence of Hb. Insulin stimulation of both processes was restored. The failure of other workers to observe insulin effects on glucose uptake and lactate release under physiological workloads [preparation (II)] may be a consequence of intracellular hypoxia in their preparations.

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