Basal inotropic state in rats with renal hypertension: influence of coronary flow and perfusion pressure
Kazumasa Shimamatsu, Fetnat M. Fouad-Tarazi
Abstract
Kazumasa Shimamatsu, Fetnat M. Fouad-Tarazi
Abstract
Cardiac performance in renal hypertensive animals has been variously reported as normal, increased, or decreased. Because of the many factors that can alter cardiac function in vivo ventricular contractility was investigated in isolated, paced, isovolumic heart preparations (modified Langendorff). Twenty one hypertensive rats (2 kidney, 1 clip Goldblatt) and 21 matched sham operated controls, were studied. Mean(SD) blood pressure and left ventricular weight were significantly higher in the study rats (228(5) vs 125(2) mmHg and 4.16(0.12) vs 2.35(0.04) mg·kg−1respectively). In the first experiment performed at 50 mmHg perfusion pressure left ventricular +dP/dt and myocardial flow rate were lower in 12 study rats (mean(SD) 1782(79) vs 2270(105) mmHg·s−1, 5.8(0.4) vs 14.0(1.0) ml·g−1 LV weight·min−1, respectively) than in the controls. In a second experiment performed at 80 mmHg perfusion pressure (nine study hearts and seven controls) the increased myocardial flow rate resulted in a higher left ventricular +dP/dt in both groups, but the study hearts still had a lower mean(SD) myocardial flow rate than the controls (12.5(0.9) vs 19.8(2.2) ml·g−1 LV weight·min−1; the difference in left ventricular +dP/dt became non-significant (2646(186) vs 2951(136) mmHg·s−1). Similarly, at equal myocardial flow rates (study hearts at 80 mmHg perfusion pressure and controls at 50 mmHg perfusion pressure) ventricular performance was similar in the two groups (mean(SD) left ventricular +dP/dt 2270(105) in controls vs 2646(186) mmHg·s−1 in study hearts). In addition, beta blockade by propranolol (10−7 mol·litre−1) did not affect the results obtained in non-blocked preparations as regards either left ventricular +dP/dt or myocardial flow rate. These results indicate that coronary perfusion pressure significantly influences ventricular contractility and that left ventricular performance in hypertensive left ventricular hypertrophy depends on a balance between left ventricular mass, perfusion pressure, and myocardial flow rate.
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Cardiac performance in renal hypertensive animals has been variously reported as normal, increased, or decreased. Because of the many factors that can alter cardiac function in vivo ventricular contractility was investigated in isolated, paced, isovolumic heart preparations (modified Langendorff). Twenty one hypertensive rats (2 kidney, 1 clip Goldblatt) and 21 matched sham operated controls, were studied. Mean(SD) blood pressure and left ventricular weight were significantly higher in the study rats (228(5) vs 125(2) mmHg and 4.16(0.12) vs 2.35(0.04) mg·kg−1respectively). In the first experiment performed at 50 mmHg perfusion pressure left ventricular +dP/dt and myocardial flow rate were lower in 12 study rats (mean(SD) 1782(79) vs 2270(105) mmHg·s−1, 5.8(0.4) vs 14.0(1.0) ml·g−1 LV weight·min−1, respectively) than in the controls. In a second experiment performed at 80 mmHg perfusion pressure (nine study hearts and seven controls) the increased myocardial flow rate resulted in a higher left ventricular +dP/dt in both groups, but the study hearts still had a lower mean(SD) myocardial flow rate than the controls (12.5(0.9) vs 19.8(2.2) ml·g−1 LV weight·min−1; the difference in left ventricular +dP/dt became non-significant (2646(186) vs 2951(136) mmHg·s−1). Similarly, at equal myocardial flow rates (study hearts at 80 mmHg perfusion pressure and controls at 50 mmHg perfusion pressure) ventricular performance was similar in the two groups (mean(SD) left ventricular +dP/dt 2270(105) in controls vs 2646(186) mmHg·s−1 in study hearts). In addition, beta blockade by propranolol (10−7 mol·litre−1) did not affect the results obtained in non-blocked preparations as regards either left ventricular +dP/dt or myocardial flow rate. These results indicate that coronary perfusion pressure significantly influences ventricular contractility and that left ventricular performance in hypertensive left ventricular hypertrophy depends on a balance between left ventricular mass, perfusion pressure, and myocardial flow rate.
Key concepts: Internal medicine, Perfusion, Medicine, Cardiology, Contractility, Ventricular pressure, Coronary perfusion pressure, Inotrope