Myocardial oxygen utilization has been shown to be impaired following prolonged global ischemia in experimental and clinical studies. The precise nature of this defect in O2 utilization has not been well defined and the present study was designed in an attempt to elucidate the defect. Forty-six isolated, isovolumic feline heart preparations were utilized and three groups of 10 hearts each were subjected to 60 min of normothermic ischemic arrest. Left ventricular function, assessed by developed pressure (DP) and dP dt, coronary blood flow (CBF), myocardial oxygen consumption (M V ̇O2), and oxygen extraction (O2E) were measured before and after ischemia. One group (I) had unmodified reperfusion; the second group (II) received epinephrine during reperfusion to increase contractility, and the third group (III) received nitroprusside post-ischemia to increase CBF. The remaining hearts, none of which underwent ischemic arrest, were divided into two groups, one of which (IV) was subjected to a period of reduced perfusion pressure with the above parameters examined, and in the final group (V) a period of epinephrine infusion was performed. In Group I hearts after ischemia, dP dt, CBF, M V ̇O2, and O2E were all significantly reduced when compared to preischemic levels. Epinephrine infusion postarrest (Group II), although increasing dP dt, CBF, and M V ̇O2, did not change the postischemic depression of O2E. With nitroprusside infusion to postischemic depression of oxygen extraction was still apparent. By contrast, epinephrine infusion in the nonarrested hearts (V) increased oxygen extraction as well as dP dt, CBF, and M V ̇O2. These data suggest that the primary defect in postischemic oxygen utilization after prolonged ischemia is an impairment in oxygen extraction. Furthermore, the data demonstrate that oxygen extraction remains depressed following arrest in spite of changes in CBF and ventricular function.
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