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Dipyridamole-induced capillary growth in normal and hypertrophic hearts
R J Torry1, D M O'Brien, P M Connell
1Department of Anatomy, University of Iowa, Iowa City 52242.
Insights
Elevated myocardial blood flow, stimulated by dipyridamole, promotes capillary growth in hypertrophied rabbit hearts. This finding suggests a potential therapeutic strategy for heart conditions involving reduced blood flow.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Cardiac Hypertrophy
Background:
- Chronic increases in myocardial blood flow stimulate capillary proliferation in normal hearts.
- The effect of elevated myocardial blood flow on capillary growth in hypertrophied hearts remains unknown.
Purpose of the Study:
- To investigate whether increased myocardial blood flow stimulates capillary growth in the hypertrophied heart.
- To assess the impact of dipyridamole-induced hyperemia on coronary angiogenesis in a rabbit model of renal hypertension.
Main Methods:
- Renal hypertension was induced in rabbits using the Page 1-kidney, 1-wrap model.
- Dipyridamole or vehicle was administered for 2 months to hypertensive and normotensive sham rabbits.
- Coronary vascular resistance and histomorphometric indexes of capillarity were evaluated.
Main Results:
- Dipyridamole increased myocardial blood flow without altering systemic blood pressure or minimal coronary vascular resistance.
- Dipyridamole significantly increased endomyocardial capillary length density in hypertensive rabbits (33%) and sham rabbits (11%).
- Intercapillary distance was significantly reduced in the endomyocardial region of both dipyridamole-treated groups.
Conclusions:
- Elevated myocardial blood flow stimulates capillary growth in the hypertrophied heart.
- Dipyridamole-induced hyperemia promotes angiogenesis in both normotensive and hypertensive rabbit hearts.
- These findings suggest a potential therapeutic role for hyperemia in managing cardiac hypertrophy.
Abstract:
Chronic increases in myocardial blood flow have been shown to stimulate capillary proliferation in normal growing hearts. It is unknown, however, if elevated myocardial blood flow stimulates precapillary and/or capillary growth in hearts undergoing hypertrophy. Accordingly, renal hypertension was produced in rabbits (Page, 1-kidney, 1-wrap model) in which one group of Page (n = 9) and one group of normotensive sham (n = 10) rabbits were given dipyridamole (4.0 mg/kg sc) twice daily for 2 mo. Another group of Page (n = 7) and sham (n = 12) rabbits received vehicle injections. In separate acute studies performed on conscious rabbits, this does of dipyridamole increased myocardial blood flow 35-60% over time without altering transmural distribution of flow or systemic blood pressure. Two months later, minimal coronary vascular resistance (MCVR/100 g) was calculated from perfusion during maximal coronary vasodilation in conscious animals. Histomorphometric methods were then utilized to evaluate various indexes of capillarity in perfuse-fixed hearts. Systolic pressure and left ventricle weight-to-body weight ratios were significantly higher in Page vs. sham rabbits; dipyridamole treatment did not alter these parameters within either group. Similarly, dipyridamole treatment did not significantly alter MCVR/100 g values in either normotensive or hypertensive rabbits. In contrast, dipyridamole treatment increased endomyocardial capillary length density by 33% in the hypertensive group (P less than 0.05) and 11% in the sham group (P not significant) compared with the respective vehicle-treated rabbits. In addition, intercapillary distance was significantly reduced in the endomyocardial region of both groups receiving dipyridamole injections.(ABSTRACT TRUNCATED AT 250 WORDS)