Adenosine (10 μg kg-1 min-1, infused into the lumen of the left ventricle) and dipyridamole (0.25 mg kg-1 intravenously, a dose that potentiated markedly the fall in arterial pressure in response to bolus doses of adenosine) each reduced the number of extrasystoles which occurred during the first 30minutes following coronary artery occlusion in anaesthetised greyhound dogs (from 786 ± 115 in control dogs to 156 ± 44 in those treated with adenosine and to 388 ± 167 with dipyridamole. Intracoronary adenosine (1 μg kg kg-1 min-1, infused into the ischaemic area) however appeared to increase the number of extrasystoles to 1230 ± 214. Left ventricular infusion of adenosine reduced the incidence of ventricular fibrillation (from 88 to 43%) when the ischaemic myocardium was perfused at the end of a 40 min occlusion period. In the dose used in this study (10 μg kg-1 min-1) adenosine caused a sustained fall in blood pressure but did not alter blood gases. In control dogs the levels of purine derivatives in blood draining the myocardium rendered ischaemic by coronary artery occlusion (local coronary venous samples) increased gradually during the ischaemic period (from 9 ± 3 μM pre-occlusion to 25 ± μM post-occlusion). Dipyridamole increased the resting plasma concentration of purines prior to occlusion by approximately 90%; these remained raised for the occlusion period. These results support the suggestion that adenosine may act as a locally produced endogenous antiarrhythmic agent.
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