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Enhanced coronary vasoconstriction in the Syrian myopathic hamster supports the microvascular spasm hypothesis
R S Conway1, B H Natelson, W H Chen
1Department of Surgery, UMDNJ-Robert Wood Johnson Medical School, New Brunswick 08903.
Insights
Young Syrian cardiomyopathic hamsters show heightened coronary vasoconstriction to arginine vasopressin (AVP). This supports the microvascular spasm theory in cardiomyopathic hearts.
Area of Science:
- Cardiovascular Research
- Animal Models of Disease
- Myocardial Pathophysiology
Background:
- Syrian cardiomyopathic hamsters (CMH) exhibit active myocytolytic necrosis.
- Arteriolar spasm is hypothesized to trigger these cardiac lesions.
Purpose of the Study:
- To investigate if coronary vasoconstriction to arginine vasopressin (AVP) is more pronounced in young, actively necrotizing CMH.
- Compare AVP response in young CMH versus age-matched normal hamsters, older CMH, and older normal hamsters.
Main Methods:
- Utilized an isovolumetric isolated heart preparation.
- Coronary arteries were perfused with Krebs-Henseleit buffer at constant flow.
- Determined coronary vascular resistance via perfusion pressure to flow rate ratio.
Main Results:
- No significant baseline coronary vascular resistance differences were observed across groups.
- AVP infusion caused a significantly greater increase in coronary resistance in young CMH compared to all other groups (p < 0.01).
Conclusions:
- Young CMH coronary vasculature demonstrates increased vasoconstrictive responsiveness.
- Findings suggest a broader coronary abnormality in this myopathic model.
- Results align with the microvascular spasm hypothesis for myocytolytic lesion formation.
Objective:
The heart of the young Syrian cardiomyopathic hamster (CMH) displays discrete patches of active myocytolytic necrosis and it has been hypothesised that these lesions are triggered by arteriolar spasm. Accordingly, we tested the theory that the coronary vasoconstrictor response to arginine vasopressin (AVP) infusion is more vigorous in the actively necrotising young (2-3 month old) CMH than in age matched normal hamsters, 5-6 month old CMHs in the histologically quiescent phase of the disease, or 5-6 month old normal hamsters.
Methods:
An isovolumetric isolated heart preparation was used in which the coronary arteries were perfused with Krebs-Henseleit buffer at constant flow by a syringe pump. Coronary vascular resistance was determined by the ratio of measured perfusion pressure to flow rate during extended diastoles.
Results:
There were no significant differences in baseline coronary vascular resistance among the four groups. The increase in resistance with AVP infusion (0.54 pressor units.min-1) was significantly greater (p < 0.01) in the young CMH [6.66(SEM 4.75) mm Hg.ml-1.min-1] than in the old CMH [1.66(0.78)], the young normal [1.10(1.07)], and the old normal [2.72(1.86)] groups.
Conclusions:
There is increased vasoconstrictive responsiveness in the young CMH coronary vasculature. The results suggest a broader coronary abnormality in this myopathic model and are consistent with the microvascular spasm hypothesis of myocytolytic lesion formation.