Temporary perfusion arrest maximally activated metabolic vasodilation, demonstrating that coronary resistance vessels show little distensibility between 20 and 60 mm Hg perfusion pressure.
The study demonstrates that coronary resistance is primarily modulated by metabolic factors rather than vessel distensibility, with venous blood perfusion inducing significant vasodilation beyond oxygen delivery effects.
This study was designed to define more accurately the respective influences of perfusion pressure and flow on coronary resistance. Resistance in a coronary branch, perfused at constant flow, was reduced immediately following temporary perfusion arrest. Large epicardial arteries did not appear to take part in this reaction. In the first 10 to 15 seconds after flow was restored, resistance for that flow was uninfluenced by the duration of the preceding perfusion arrest. That mechanism which caused coronary resistance to fall as a result of metabolic factors, such as reduced availability of oxygen, was thus maximally activated. By observing the relationship of coronary resistance to perfusion pressure at this time, it could be shown that resistance vessels and their surrounding structures showed little evidence of distensibility (resistance constant from 20 to 60 mm Hg). The difference between resistance at steady state and resistance at maximal vasodilatation defines the extent of vasomotion attributable at any flow rate to metabolic factors. Perfusion with venous blood caused a fall of resistance which was greater at any flow rate than could be accounted for by the differences in oxygen delivery rate.
Fam et al. (Mon,) conducted a other in Coronary circulation physiology. Temporary perfusion arrest and venous blood perfusion vs. Steady state flow was evaluated on Coronary resistance. Temporary perfusion arrest maximally activated metabolic vasodilation, demonstrating that coronary resistance vessels show little distensibility between 20 and 60 mm Hg perfusion pressure.