Compensatory changes of the distal coronary vascular bed during progressive coronary constriction.
The degree and effectiveness of compensatory changes in the distal coronary vascular bed during progressive proximal coronary stenosis have not been described. In this study, coronary vascular bed resistance and pressure gradient-flow relationships were determined for 157 different stenoses in nine opened-chest dogs by measuring coronary flow, aortic pressure, and coronary pressure distal to a coronary constrictor while flow was varied from resting to maximal values by the intracoronary injection of Hypaque-M, 75% (previously shown to cause transient, maximal vasodilatation comparable to ten second occlusion). This approach provided a means of hemodynamically characterizing coronary stenoses in a standary, experimental manner for quantitative analysis of different arteries at different flow rates as found in the intact coronary circulation. The results show that 1) pressure gradient-flow characteristics or hydraulic resistance of stenoses do not become abnormal enough to alter normal resting coronary flow nor to elicit compensatory changes for stenoses up to constriction of approximately 60% of the diameter, 2) compensatory vasodilatation of the distal coronary vascular bed maintains near normal resting flow for lesions between 60% and 85% diameter stenosis but adaptive vasodilatation fails to compensate for the high resistance of lesions greater than 85% diameter stenosis, and 3) there is vasodilator reserve still present when total coronary artery flow is reduced below normal by a stenosis. This vasodilator reserve probably exists in the epicardium since the endocardium is characteristically underperfused due to the low coronary pressure caused by stenosis and is therefore likely to be maximally vasodilated with no remaining vasodilator reserve.
D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism / Q000503:physiopathology; D001794:Blood Pressure; D003201:Computers; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D003973:Diatrizoate / Q000494:pharmacology; D004285:Dogs; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D012044:Regression Analysis; D014655:Vascular Resistance
D003973:Diatrizoate