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Hypoperfusion of the myocardium relative to myocardial metabolism during delayed coronary constriction
A H Huang1, B D Nearing, R L Verrier
1Department of Pharmacology, Georgetown University School of Medicine, Washington, DC 20007.
Insights
Sympathetic stimulation causes delayed coronary constriction, leading to myocardial hypoperfusion. Coronary blood flow becomes insufficient for the heart
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System
- Coronary Circulation
Background:
- Sympathetic stimulation influences myocardial metabolism and coronary blood flow.
- Delayed coronary constriction is an observed phenomenon after sympathetic stimulation cessation.
Purpose of the Study:
- To test if myocardium is hypoperfused relative to metabolic demands during delayed coronary constriction.
- To investigate the relationship between coronary blood flow and myocardial metabolism post-stimulation.
Main Methods:
- Beat-by-beat analysis of coronary blood flow to myocardial metabolism index (heart rate x systolic blood pressure).
- Experiments conducted in open-chest canine models with left stellate ganglion stimulation.
- Measurements taken before, during, and after sympathetic stimulation.
Main Results:
- Stellate stimulation increased myocardial metabolism and coronary blood flow.
- Delayed coronary constriction occurred 1-3 minutes post-stimulation, with coronary vascular resistance overshooting control levels.
- The ratio of coronary blood flow to myocardial metabolism significantly decreased during delayed constriction, indicating hypoperfusion.
Conclusions:
- Delayed coronary constriction results in a mismatch between myocardial oxygen supply and demand.
- Coronary blood flow becomes inappropriately low for the heart's metabolic needs during this period.
Objective:
The aim was to test the hypothesis that the myocardium becomes hypoperfused, relative to its metabolic demands, during the delayed coronary constriction which is observed following termination of a period of sympathetic stimulation.
Methods:
This was tested by beat by beat analysis of the ratio of coronary blood flow to the product of heart rate and systolic blood pressure (HR x SBP), an index of myocardial metabolism, in acutely instrumented open chest canine preparations, before, during, and after direct electrical stimulation of the left stellate ganglion.
Results:
Myocardial metabolism increased in response to stellate stimulation, as evidenced by increases in heart rate, aortic blood pressure, and HR x SBP. These were accompanied by increased blood flow and decreased vascular resistance in the left anterior descending coronary artery. Delayed coronary constriction, defined as the period with the lowest coronary blood flow observed after the end of the stimulation, occurred 1 to 3 min after stimulation was terminated and was characterised by recovery of heart rate, blood pressure, HR x SBP, and coronary blood flow toward control levels, while coronary vascular resistance overshot to above control levels. The ratio of coronary blood flow to HR x SBP fell progressively in the poststimulation period to significantly less (mean 0.715, range of +/- 1 SEM 0.638 to 0.800, p < 0.05) than control (1.0, by definition) in experiments performed with partial prestenosis of the left anterior descending coronary artery. In a selected subgroup of observations with a mean reduction in coronary blood flow during delayed coronary constriction comparable to that reported previously, the flow/metabolism ratio was even lower (mean 0.239, range of +/- 1 SEM 0.202 to 0.284).
Conclusions:
The phenomenon of delayed coronary constriction clearly involves a mismatch between myocardial supply and demand: coronary blood flow becomes inappropriately low for the prevailing level of myocardial metabolism.
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