Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart.
The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.
D000818:Animals; D002216:Captopril / Q000008:administration & dosage; D002307:Cardiography, Impedance; D004285:Dogs; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D010656:Phenylephrine / Q000008:administration & dosage; D010992:Plethysmography, Impedance; D012083:Renin / Q000097:blood; D013318:Stroke Volume; D013722:Teprotide / Q000008:administration & dosage; D014661:Vasoconstriction
D010656:Phenylephrine; D002216:Captopril; D013722:Teprotide; D012083:Renin