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Stenosis differentially affects subendocardial and subepicardial arterioles in vivo
D Merkus1, I Vergroesen, O Hiramatsu
1Department of Medical Physics, Cardiovascular Research Institute Amsterdam, Academic Medical Center, University of Amsterdam, 1100 DE Amsterdam, The Netherlands.
Insights
Coronary stenosis impairs blood flow, causing greater subendocardial arteriole constriction and reduced dilation. This explains why the subendocardium is more vulnerable to ischemia during stenosis.
Area of Science:
- Cardiovascular Physiology
- Myocardial Ischemia Research
Background:
- Coronary stenosis reduces coronary perfusion pressure and flow pulsations.
- Subendocardial ischemia is a primary consequence of coronary stenosis.
Purpose of the Study:
- To compare the autoregulatory responses of subendocardial and subepicardial arterioles to reduced coronary pressure.
- To investigate the impact of stenosis on arteriolar dilation and coronary flow.
Main Methods:
- In vivo canine model (n=9) with a coronary perfusion system.
- Stepwise reductions in coronary arterial pressure (100 to 30 mmHg) with and without stenosis.
- Measurement of maximal arteriolar diameter and coronary inflow, with nitric oxide inhibition.
Main Results:
- Subendocardial arterioles showed a larger initial diameter decrease with pressure reduction compared to subepicardial arterioles.
- Stenosis significantly impaired the dilatory response of subendocardial arterioles.
- Nitric oxide inhibition abrogated the stenosis-induced reduction in coronary flow.
Conclusions:
- Coronary stenosis exacerbates the pressure-induced decrease in subendocardial arteriole diameter.
- Stenosis selectively diminishes the dilatory capacity of subendocardial arterioles, increasing vulnerability to ischemia.
Abstract:
The presence of a coronary stenosis results primarily in subendocardial ischemia. Apart from the decrease in coronary perfusion pressure, a stenosis also decreases coronary flow pulsations. Applying a coronary perfusion system, we compared the autoregulatory response of subendocardial (n = 10) and subepicardial (n = 12) arterioles (<120 microm) after stepwise decreases in coronary arterial pressure from 100 to 70, 50, and 30 mmHg in vivo in dogs (n = 9). Pressure steps were performed with and without stenosis on the perfusion line. Maximal arteriolar diameter during the cardiac cycle was determined and normalized to its value at 100 mmHg. The initial decrease in diameter during reductions in pressure was significantly larger at the subendocardium. Diameters of subendocardial and subepicardial arterioles were similar 10--15 s after the decrease in pressure without stenosis. However, stenosis decreased the dilatory response of the subendocardial arterioles significantly. This decreased dilatory response was also evidenced by a lower coronary inflow at similar average pressure in the presence of a stenosis. Inhibition of nitric oxide production with N(G)-monomethyl-L-arginine abrogated the effect of the stenosis on flow. We conclude that the decrease in pressure caused by a stenosis in vivo results in a larger decrease in diameter of the subendocardial arterioles than in the subepicardial arterioles, and furthermore stenosis selectively decreases the dilatory response of subendocardial arterioles. These two findings expand our understanding of subendocardial vulnerability to ischemia.