Left ventricular compliance in the DOCA-salt model of hypertension in the rat. Effects of propranolol.
The aim of this study was to see if an enhanced myocardial stiffness is an inevitable consequence of the increase in cardiac mass and to analyze the effects of beta-adrenergic blockade on this parameter. The DOCA-salt model of hypertension was used to induce cardiac hypertrophy in the rat. After 6 weeks, the hearts of the DOCA-salt-treated animals were hypertrophied by 67%, and the left ventricular weight, the left ventricular/body weight ratio and the left/right ventricular weight ratio were similarly increased. Isolated hearts were retrogradely perfused at a constant flow of 15 ml/min/g tissue. Contractile parameters were recorded using an intraventricular balloon whose volume was manually adjusted. For each heart, a sequence of three systolic and diastolic pressure-volume curves were constructed: in Krebs alone, after addition of 10(-6) M of propranolol, and after KCl-arrest. In spite of a pronounced degree of hypertrophy, the DOCA-salt hearts had a normal diastolic pressure-volume curve and both the chamber and tissue stiffness constants were not modified. This result indicates that a depressed compliance does not necessarily accompany hypertrophy, especially in a DOCA-salt model in which the collagen content of the heart is unchanged. The systolic pressure-volume curve was greatly modified and shifted to the left indicating an enhanced capacity of the hypertrophied heart to generate force. This increase persisted even when the systolic pressure has been divided by the heart weight. beta-Blockade slightly depressed the contractility of the isolated heart at pharmacological concentrations. At high concentrations, cardiac dilatation was induced. This enhancement in ventricular distensibility had no consequences on diastolic compliance constants. It is thus concluded that, during cardiac hypertrophy, the changes in passive stiffness of the ventricle are more related to collagen content than to the cardiac mass and that beta-adrenergic blockade has no effect on the passive properties of the ventricle.
Cheav
S L
SL
U 127 INSERM, Hôpital Lariboisière, Paris, France.
Delcayre
C
C
Besnard
J C
JC
Paolaggi
F
F
Mouas
C
C
Swynghedauw
B
B
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D006332:Cardiomegaly / Q000503:physiopathology; D003094:Collagen / Q000378:metabolism; D003187:Compliance; D003900:Desoxycorticosterone; D004305:Dose-Response Relationship, Drug; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000473:pathology; D006973:Hypertension / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D010477:Perfusion; D011189:Potassium Chloride / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D016276:Ventricular Function
D003900:Desoxycorticosterone; D011189:Potassium Chloride; D003094:Collagen; D011433:Propranolol