Dilazep and dipyridamole significantly enhance the coronary vasodilating action of adenosine in dogs, primarily by inhibiting its degradation in the lung and myocardium.
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Potentiation seen in dogs should not guide human adenosine use; leaves open translation of uptake inhibition to clinical coronary vasodilation.
The mechanism of the augmentation of adenosine action by 1, 4-bis-[3-(3, 4, 5-trimethoxybenzoyl-oxy)-propyl] perhydro-1, 4-diazepine (dilazep I, N, N,) and dipyridamole on the coronary vessel was examined in the dog. Cororary blood flow was measured by applying a Morawitz cannula to the in vivo heart. It was found that the ratio of coronary vasodilating activity of adenosine administered into saphenous vein, right atrium, and left atrium was 1:1.5: 30, and that coronary vasodilating actions of adenosine administered into saphenous vein, right atrium, and left atrium after dilazep (10 μg/kg, i.v.) were 15.6, 10.8, and 3.3 times greater than those without dilazep, respectively. After dipyridamole coronary vasodilating actions of adenosine administered into saphenous vein, right atrium, and left atrium were 17.5, 14.3, and 5.4 times greater. These results indicate that augmentation of coronary vasodilating action of intravenously administered adenosine by dilazep or dipyridamole was mainly exerted at the lung and myocardium, and slightly in the blood, and was due to inhibition of the disappearance of adenosine.
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Nobuyuki Sano (1974) studied this question.
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