Role of adenosine in mediating the coronary vasodilative response to acute hypoxia

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Abstract
To test the hypothesis that adenosine is required to mediate the coronary vasodilative response to acute hypoxia haemodynamic indices, regional myocardial blood flow, and oxygen and lactate metabolism were measured in nine closed chest anaesthetised domestic swine at control, after 3–5 min of 100% nitrogen inhalation, at second control, and after 3–5 min of 100% nitrogen inhalation plus adenosine deaminase infusion in the left anterior descending coronary artery. Cardiac lymph adenosine deaminase concentration was also measured in a separate group of four animals previously reported on. Heart rate was held constant by atrial pacing during the study. Aortic mean pressure did not change. Changes in arterial and anterior interventricular vein pH, PO2, Pco2, and oxygen content were similar for each intervention. Transmural left anterior descending artery zone flow increased significantly (p −1·g−1; mean(SD)) in response to hypoxia (2.73(0.92)). Intracoronary adenosine deaminase infusion (167 nmol·s−1), however, failed to blunt the flow response to hypoxia (1.33(0.30) to 2.79(1.32); second control to hypoxia plus adenosine deaminase respectively, p −1) in cardiac lymph was 105(85) at the end of 10 min of intracoronary infusion (167 nmol·s−1) and 203 (148) nmol·s−1 at the end of 15 min. Even at considerably accelerated rates of myocardial adenosine production (for example, 2 μmol·min−1·litre−1 interstitial fluid), interstitial fluid adenosine deaminase activity of 105 nmol·s−1 resulted in steady state adenosine concentrations at least 10-fold lower than generally accepted base values (0.1–0.2 μmol·litre−1). Accordingly, the data indicate that coronary vasodilatation in response to acute hypoxia is not uniquely dependent on adenosine.