Key points are not available for this paper at this time.
Design
Review
Answers are grounded in this paper and cite their sources.
Physiological responses to occlusion inform ischemia models; leaves open whether collateral modulation improves clinical outcomes.
Coronary occlusion causes increased flow in adjacent arteries due to increased myocardial oxygen consumption in the area of the unoccluded arteries. Interarterial collateral circulation increases after coronary occlusion and is rapidly mobilized with repeat occlusion. There is some collateral flow from the cardiac cavities to the myocardium with coronary occlusion but this is via retrograde perfusion of venous drainage channels in the atria and right ventricle rather than directly from the left ventricular cavity. Endocardial distribution of coronary flow is equal to that of the epicardium in the normal or hypertensive left ventricle but the inner layers of the ischemic left ventricle show a marked restriction of flow. Coronary autoregulatory mechanisms are immediately mobilized by acute myocardial ischemia but the metabolic adenosine hypothesis appears unlikely to be the sole cause of the vasodilatory response.
No takes yet. Share an insight, caveat, or question.
THOMAS W. MOIR (1972) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: