Summary. To study the t-ITects of certain vasodilator drugs on tho c-oronary viLsculatun; of the trnnsplantud heart, dog hearts wore inipiantcd inlo tht-necks of recipient dofis and connected to the circulation so that L-oronary ]ilt)o' blood flow and reiliiccd tiironary va.M.ular resistance in thf transpl^intcd heart; dipyridamolt jjn'atly potentiated tlie vniiodilator actions of adenosine. Propranolol. in a beta adrenerKif hlockinK dose, did not alter coronan blood How or coronary vascular rcsistiincc cr influents the actions of (lipyridaniole or adenosine. l^)w dose infusions of luninophyltitic iintfonnly reduced cxironary blood flow and incrciised corontiry vascular re.si.staiut! mid iilso tilocked the actions of dipyridantolc ami adenosinr'. The blocking cirect was similar witli hi^jher doses of aiuinophylline whicli temporarily increascruiiary vastiilar rcacUvity to dipyridainole and adenosine is maintained up to at le^st six hours after transplantation, und siiRgest that dipyridamolc acts largely through aderostne. Propranolol tlm-s imt increase conmar>' vascular resistance in the dencr\ated heart. The aniinophylliiiemediated increase in coronarv" vascular resistance couhl resntt from a bItK-king of the vasodilator effects of adenosine locally produced in non-ischuemie myocardium.
Summary
Using chronically implanted electromagnetic flow transducers, we examined the effects of dipyridamole (1 mg/kg) and aminophylline (10 mg/kg) on reactive hyperaemic responses induced by four‐second and eight‐second occlusions of the circumflex branch of the left coronary artery in conscious dogs. Reactive hyperaemia was not affected by either dipyridamole or aminophylline when pre‐occlusion coronary blood flow heart rate and mean blood pressure were the same as during control observations. Two to four hours after dipyridarmole, when pre‐occlusion coronary blood flow was increased but blood pressure and heart rate had returned to control values, reactive hyperaemic responses were significantly reduced. At these times dipyridamole markedly potentiated, and aminophylline greatly reduced, the coronary vasodilator effects of adenosine injected into either the superior vena cava or left atrium. Since dipyridamole and aminophylline both move out of the intravascular compartment after intravenous injection, these results do not support the hypothesis that release of adenosine into the extracellular space is essential for die production of reactive hyperaemia induced by brief coronary artery occlusions.
Summary. Using electromagnetic flow transducers, we examined the efFects of close arterial infusions of dipyritlaniole (1 HK/niiTinte) anti aminophylliiie (200 ng/minute) on repcinses to adenosine, and on the rt-active hv-penieniic responses induced by GO-second occlusions of thf circuniflex branch of the left coronary artery in anaesthetised dogs. Results were analysed only when preocclusion coronary blood ilow values and blood pressure and heart rate before, during and after coronary artery occlusion in pre-and post-drug responses did not var>-by more than 5%.Dip>Hdamo!e niarkediy increased the coronary blood flow response to adenosine (from + 32% ± 3-1 to + 82?> ± 7; means ±: S.E.), while aininophylliiu! reduced this response (from + 46% ± 6-2 to + 0% ±; 2; means ± S.E.). Despite this, reactive h>'peraemic responses were not changed during either dipyridamole or aminophyliine. These Bndings suggest that adenosine-induced vasodilatation is not essential for the reactive h>'peraemia resulting from 60-second coronar\' artery occlusions.INTRODUCTION.
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