Release of two vasodilators, adenosine and prostacyclin, from isolated rabbit hearts during controlled hypoxia.

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Abstract
The release of 2 locally formed vasodilators, adenosine and prostacyclin (PGI2), from hearts subjected to different degrees of hypoxia was investigated. Isolated rabbit hearts were perfused according to Langendorff with Tyrode solution, saturated with gas mixtures containing 8-95% O2 and 5% CO2 in N2. Coronary flow rate, O2 extraction and uptake, cardiac production of lactate, purines and 6-keto-PGE1.alpha. (the stable metabolite of PGI2) were determined. During perfusion of the hearts with a solution saturated with 95% O2, release of lactate, 6-keto-PGF1.alpha. and purines was very low: lactate was liberated at a rate of about 5 .mu.mol/100 g .cntdot. min, purine release corresponded to 2% of the total adenosine nucleotide content of the heart per hour and the release of 6-keto-PGF1.alpha. was about 150 .mu.mol/100 g .cntdot. min. During hypoxia there was a graded release of lactate and purines from the heart, as well as a liberation of 6-keto-PGF1.alpha.. Mild hypoxia (60% O2 in the gas mixture) elicited a 160% increase in the formation of lactate and a 40% increase in the release of purines. During severe hypoxia (8% O2 in the gas mixture) the release of lactate and purines increased by > 2000%. In contrast, the release of 6-keto-PGF1.alpha. never increased > 80% at any degree of hypoxia, neither did it correlate to the severity of the hypoxia. Evidently, of the 2 vasodilating agents formed in the heart, adenosine and prostacyclin, the former is probably more important in the regulation of coronary flow.