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Transmural heterogeneity of postjunctional alpha 2 adrenergic coronary vasoconstriction in hypoperfused cat left
J Westby1, S Birkeland, J Lekven
1Department of Surgery, University of Bergen, Haukeland Hospital, Norway.
Insights
In hypoperfused myocardium, coronary alpha-2 adrenergic vasoconstriction primarily occurs in the epicardium, worsening blood flow to the endocardium. This vasoconstriction is postjunctional and counteracts distal hypoperfusion.
Area of Science:
- Cardiovascular Physiology
- Adrenergic Receptor Pharmacology
Background:
- Coronary blood flow regulation is crucial for myocardial function.
- Alpha-adrenergic vasoconstriction plays a role in coronary circulation, but its specific contribution in hypoperfusion is not fully understood.
- Understanding transmural blood flow distribution is key to managing ischemic conditions.
Purpose of the Study:
- To investigate the role of postjunctional alpha-1 and alpha-2 adrenergic vasoconstriction in hypoperfused myocardium.
- To determine the influence of these receptors on the transmural distribution of coronary blood flow.
Main Methods:
- Hypoperfusion of the left coronary artery was induced in open-chest cats.
- Beta-adrenergic antagonism was followed by selective alpha-1 and alpha-2 adrenergic antagonism.
- Regional myocardial blood flow was measured using radiolabelled microspheres.
Main Results:
- Hypoperfusion reduced endocardial blood flow, while epicardial flow remained unchanged.
- Alpha-1 adrenergic antagonism had no significant effect on myocardial blood flow.
- Subsequent alpha-2 adrenergic antagonism worsened endocardial flow and increased epicardial flow, decreasing overall coronary vascular resistance.
Conclusions:
- Postjunctional alpha-2 adrenergic vasoconstriction is primarily localized epicardially in hypoperfused myocardium.
- This vasoconstriction exacerbates endocardial hypoperfusion distal to a stenosis.
- The findings highlight the specific role of alpha-2 adrenergic receptors in modulating coronary blood flow during ischemia.
Objective:
The aim was to analyse the influence of coronary postjunctional alpha 1 and alpha 2 adrenergic vasoconstriction in hypoperfused myocardium with special emphasis on transmural distribution of blood flow.
Methods:
The left coronary artery was hypoperfused by means of a clamped shunt line. Sequential selective postjunctional alpha 1 (doxazosin) and alpha 2 (SK&F 104078) adrenergic antagonism was established following beta adrenergic antagonism with propranolol. Regional myocardial blood flow was measured with radiolabelled microspheres during equal coronary perfusion pressures. Experimental subjects were nine pentobarbitone anaesthetised open chest cats.
Results:
Left coronary hypoperfusion decreased endocardial blood flow, whereas epicardial flow was unaltered. In this situation alpha 1 adrenergic antagonism did not affect myocardial blood flow. Subsequent alpha 2 antagonism impaired endocardial blood flow, whereas epicardial blood flow was augmented. Mean coronary vascular resistance declined following combined alpha 1 and alpha 2 adrenergic antagonism.
Conclusions:
Coronary alpha adrenergic vasoconstriction is localised mainly epicardially in hypoperfused myocardium and counteracts endocardial hypoperfusion distal to a fixed coronary stenosis. Furthermore, this vasoconstriction is of the postjunctional alpha 2 adrenergic subtype.