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Normalization of impaired coronary circulation in hypertrophied rat hearts
F Sato1, S Isoyama, T Takishima
1First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Insights
Pressure overload in hypertrophied hearts impairs coronary autoregulation and flow reserve, but these deficits fully reverse after pressure relief. This study demonstrates the reversibility of cardiac dysfunction in hypertension models.
Area of Science:
- Cardiovascular Physiology
- Cardiac Hypertrophy
- Renal Physiology
Background:
- Coronary arterial hypertension can lead to myocardial hypertrophy and impaired cardiac function.
- The reversibility of coronary autoregulation and reactive hyperemia after pressure overload relief is not well understood.
Purpose of the Study:
- To investigate whether impaired coronary autoregulation, flow reserve, and reactive hyperemia in hypertrophied hearts are reversible after relieving pressure overload.
Main Methods:
- Ascending aortic banding in rats induced pressure overload and myocardial hypertrophy.
- Coronary perfusion pressure-flow relations were assessed in isolated hearts under resting and vasodilated conditions.
- Reactive hyperemia was measured after a 40-second ischemic period.
Main Results:
- Banded rats exhibited significantly increased left ventricular pressure and hypertrophy compared to controls.
- Hearts from banded rats showed impaired coronary autoregulation, reduced flow reserve, and diminished reactive hyperemia.
- Four weeks after debanding, cardiac hypertrophy and pressure normalized, with complete reversal of the observed functional deficits.
Conclusions:
- Pressure overload-induced impairments in coronary autoregulation, flow reserve, and reactive hyperemia are fully reversible.
- Relief of pressure overload can restore normal coronary microvascular function in hypertrophied hearts.
Abstract:
We tested the hypothesis that impaired coronary autoregulation, decreased flow reserve, and diminished reactive hyperemic response in hypertrophied hearts with coronary arterial hypertension may be reversible after relief of pressure overload. In 4-week ascending aortic banded rats, in vivo peak systolic left ventricular pressure increased to 178 +/- 8 mm Hg (103 +/- 6 mm Hg in sham-operated control group). This increased pressure produced myocardial hypertrophy, and the left ventricular weight/body weight ratio was 46% above that of the control group. After the rats were killed, the coronary perfusion pressure-flow relations were obtained during resting conditions and maximal vasodilation after a 40-second period of ischemia in beating but nonworking isolated hearts perfused with Tyrode's solution with bovine red blood cells and albumin. In hearts from control rats, coronary autoregulation (i.e., a slight decrease in flow with reduction of pressure) was observed in the range of 50-100 mm Hg of perfusion pressure. A pronounced reactive hyperemic response was observed: a peak flow/resting flow ratio of 2.9 +/- 0.1 and a repayment ratio of 1.7 +/- 0.2 at 100 mm Hg of perfusion pressure. In hearts of banded rats the resting pressure-flow relation was rectilinear in the range of 25-175 mm Hg of perfusion pressure. Flow reserve and the time of reactive hyperemia to one half peak flow decreased at 50, 100, and 150 mm Hg of perfusion pressure compared with values in control rat hearts. Four weeks after debanding, peak systolic left ventricular pressure and cardiac hypertrophy had normalized. The impaired autoregulation, decreased flow reserve, and diminished reactive hyperemic response had completely reversed.(ABSTRACT TRUNCATED AT 250 WORDS)