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Effects of alpha-1 adrenergic blockade on regional flow in the ischemic heart
1Departamento de Preclínicas, Facultad de Medicina, Universidad de Chile, Santiago.
Insights
Persistent alpha-1 adrenergic receptor activity causes vasoconstriction in ischemic heart muscle. Blocking these receptors with Trimazosin worsened blood flow to the subendocardium in dogs.
Area of Science:
- Cardiovascular Physiology
- Adrenergic Receptor Pharmacology
Background:
- Ischemia triggers coronary vasodilation but leaves some vasoconstrictive tone in the heart muscle.
- The role of alpha-adrenergic receptors in this persistent tone is not fully understood.
Purpose of the Study:
- To investigate if alpha-adrenergic receptors mediate vasoconstrictive tone in the ischemic myocardium.
- To assess the effect of alpha-1 blockade on coronary blood flow distribution.
Main Methods:
- Coronary blood flow was measured using radioactive microspheres in dogs.
- Ischemia was induced by reducing coronary perfusion pressure.
- Alpha-1 blockade was achieved using Trimazosin.
Main Results:
- Trimazosin increased blood flow in normal myocardium, more in the subepicardium than subendocardium.
- In ischemic regions, Trimazosin did not alter total flow but decreased subendocardial flow and increased subepicardial flow.
- The inner/outer flow ratio significantly decreased in both normal and ischemic regions after Trimazosin administration.
Conclusions:
- A vasoconstrictive tone mediated by alpha-1 adrenergic receptors persists in ischemic myocardium.
- Blocking these receptors with Trimazosin is detrimental to subendocardial blood flow in ischemic conditions.
Abstract:
Although ischemia induces strong coronary vasodilation, some vasoconstrictive tone persists in the ischemic myocardium. To assess whether this tone is mediated through alpha adrenergic receptors, coronary blood flow was measured with radioactive microspheres in the normal and in the ischemic left ventricular wall of the dog before and during alpha blockade with Trimazosin. Ischemia was accomplished by decreasing the coronary perfusion pressure to 22 +/- 1.4 mmHg. Heart rate and aortic pressure were kept constant in each experiment. Trimazosin significantly increased flow in the normal left ventricular wall, but to a greater extent in the subepicardium than in the subendocardium with a decrease of the inner/outer flow ratio from 1.38 +/- 0.12 to 1.20 +/- 0.11 (p less than 0.05). In the ischemic region, Trimazosin did not change total transmural flow, but flow decreased in the subendocardium and increased in the subepicardium with a decrease in the inner/outer flow ratio from 0.63 +/- 0.09 to 0.38 +/- 0.06 (p less than 0.01). These results show that a vasoconstrictive tone mediated through alpha-1 adrenergic receptors persists in the ischemic myocardium, the blockade of which is detrimental for the subendocardium.