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Ultrasound Based Assessment of Coronary Artery Flow and Coronary Flow Reserve Using the Pressure Overload Model in Mice
Published on: April 13, 2015
Coronary circulation in hypertension and aging: an experimental study
Dinko Susic1, Jasmina Varagic, Edward D Frohlich
1Division of Research, Ochsner Clinic Foundation, New Orleans, Louisiana.
Ochsner Journal
|May 24, 2011
Summary
Hypertension, aging, and high salt intake impair coronary blood flow in rats, even without atherosclerosis. Myocardial fibrosis contributes to this coronary vascular impairment, but therapies can improve outcomes.
Area of Science:
- Cardiovascular physiology
- Hypertension research
- Aging studies
Background:
- Essential hypertension in humans shares similarities with spontaneously hypertensive rats (SHR).
- Atherosclerosis can confound studies on coronary hemodynamics, necessitating models like SHR that do not develop this condition.
Purpose of the Study:
- To investigate adverse changes in coronary hemodynamics linked to hypertension, aging, and excessive salt intake.
- To evaluate the role of perivascular fibrosis in myocardial impairment.
- To assess the efficacy of antihypertensive and angiotensin II receptor blocker therapies.
Main Methods:
- Systemic and coronary hemodynamics, left ventricular mass, and collagen content were measured in normotensive Wistar-Kyoto rats and SHR.
- Studies included rats of various ages and different salt intake and treatment conditions.
- Rats were used to avoid the confounding effects of atherosclerosis.
Main Results:
- Spontaneously hypertensive rats (SHR) exhibited lower coronary blood flow reserve and higher minimal coronary vascular resistance compared to normotensive rats.
- Both rat strains showed age-related decreases in coronary flow reserve and increases in minimal vascular resistance.
- In aged SHR, increased left ventricular collagen correlated with coronary insufficiency, which was improved by antihypertensive therapy.
- Excessive salt intake in SHR worsened hypertension, increased myocardial fibrosis, and impaired coronary circulation, effects mitigated by angiotensin II receptor blocker therapy.
Conclusions:
- Coronary insufficiency can occur due to hypertension, aging, and salt overload, independent of atherosclerotic changes.
- Perivascular fibrosis in the myocardium is a significant factor contributing to coronary vascular impairment.
- Therapeutic interventions can ameliorate hypertension-induced coronary dysfunction and fibrosis.
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