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Observations on the Effect of Changes in Arterial Oxygenation on Adenosine Induced Coronary Vasodilation

1973; Springer Nature; Linguagem: Inglês

10.1007/978-1-4615-9020-0_2

2214-8019

THOMAS W. MOIR, Paul K. Jones,

Electron Spin Resonance Studies

At present there are two general theories that have been proposed to account for the autoregulatory vascular response to decreased coronary arterial flow. One holds that an increased concentration of vasoactive tissue metabolites which accumulate as a result of myocardial hypoxia, most notable among which is the nucleoside adenosine, directly causes vasodilation in the coronary resistance vessels (1, 2, 3, 4). The other states that the low pO2 incident to low coronary flow acts directly on vascular smooth muscles to cause vasodilation, possibly because of depletion of ATP and other oxygen dependent energy substrates necessary to maintain the contractile state (5, 6, 7, 8). Recently, a study of isolated coronary vascular smooth muscle strips has suggested another mechanism in which both the local oxygen tension and adenosine concentration may act in concert to effect coronary vasodilation in the presence of myocardial hypoxia: this in vitro study demonstrated an enhancement of adenosine induced relaxation of vascular smooth muscle when local oxygen tension was reduced to below 40 mm Hg (9).