Adenosine deaminase attenuates canine coronary vasodilatation during regional non-ischaemic myocardial hypoxia

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Abstract
To test the hypothesis that adenosine contributes to the coronary hyperaemia produced by regional non-ischaemic myocardial hypoxia coronary blood flow and myocardial oxygen extraction and consumption were continuously monitored in 21 anaesthetised open chest dogs under the following conditions: control 1 — postinstrumentation, steady state control; hypoxia 1 — 3–5 min of regional (LAD) hypoxaemia (partial pressure of oxygen, Po2, 21.4(2.0) mmHg (3.1(0.2) kPa), coronary arterial oxygen content, Cao2, 3.9(0.4) ml·100 ml−1 (39(4) ml·litre−1): control 2 — repeat steady state control; and hypoxia 2 — 3–5 min repeat regional hypoxaemia (Po2 18.9(2.4) mmHg (2.5(0.3) kPa); Cao2 3.6(0.6) ml·100 ml−1 (36(6) ml·litre−1) blood). Left anterior descending artery perfusion pressure was held constant for all conditions. Control 2 and hypoxia 2 were performed in the presence of locally infused adenosine deaminase (n= 16) or saline vehicle (n=5). The 16 dogs given adenosine deaminase were further subdivided into those perfused with blood deoxygenated by a donor canine lung (group 1, n= 11) and those perfused with blood from a paediatric oxygenator (group 2, n=5). Systemic haemodynamics, heart rate, and coronary arterial Po2 and 02 contents were similar during the two control periods and during the two exposures to hypoxia in all three groups. Left anterior descending artery blood flow increased by approximately 400% (p<0.05) in all three groups during the first exposure to hypoxia. Myocardial oxygen consumption was unchanged. During the second exposure to hypoxia left anterior descending artery blood flow increased by 400% in the saline vehicle group, whereas the response was significantly attenuated (p<0.05) to 241(30)% and 294(61)% in group 1 and group 2 respectively. Regional myocardial oxygen consumption was significantly attenuated (p<0.05) in group 1 but unaffected in group 2 during the second exposure to hypoxia. These results indicate a prominent role for endogenous adenosine in the coronary vasodilatation of canine regional myocardial hypoxia.