The effect of decreased left-ventricular afterload on cardiac performance in the normal and hypertrophied rat heart.
The effect of left-ventricular afterload on cardiac performance was investigated in normotensive Wistar rats and in spontaneously hypertensive rats (10 months old) with a left-ventricular hypertrophy of 54%. The measurements were performed on a modified heart-lung preparation in which left-ventricular afterload could be adjusted arbitrarily. In the heart in situ, left-ventricular afterload limits not only the mechanical conditions of the contraction, but also influences coronary perfusion pressure. With decreasing afterload stroke volume and pressure-volume work initially increases. Simultaneously coronary resistance decreases considerably so that coronary flow increases, although coronary perfusion pressure is reduced. However, when perfusion pressure falls short of a critical value, coronary flow cannot be maintained despite maximal coronary dilatation and stroke volume decreases, i.e., stroke volume, pressure-volume work and coronary flow run through an optimum with decreasing afterload. A reduction in coronary perfusion pressure below a certain value yields acute heart failure in all preparations. The minimal aortic mean pressure without reaching cardiac insufficiency was in the spontaneously hypertensive rats with 65 mm Hg significantly higher than in the control animals with 35 mm Hg, although the minimal coronary resistance was identical in both groups. The elevated critical coronary perfusion pressure of the spontaneously hypertensive rats can be explained by the increased O2-demand of the hypertrophied hearts.
Kissling
G
G
Physiologisches Institut II, Universität Tübingen, FRG.
Brändle
M
M
D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology*; D003331:Coronary Vessels / Q000502:physiology; D003971:Diastole / Q000502:physiology; D006321:Heart / Q000502:physiology*; D006973:Hypertension / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*