Anoxia-induced changes in ventricular diastolic compliance in two models of hypertension in rats.
OBJECTIVE
The effects of a brief period of anoxia upon myocardial distensibility and coronary vascular resistance (CVR) were evaluated in two models of pressure overload in the rat.


METHODS
A similar degree of left ventricular hypertrophy was obtained by using deoxycorticosterone acetate (DOCA)-salt treatment and abdominal aortic stenosis (AS). The study was performed using an isolated, isovolumic cardiac preparation perfused at a constant coronary flow of approximately 20 ml/min per g left ventricular weight.


RESULTS
In response to a 10-min period of anoxia, hypertrophied hearts manifested an exaggerated decrease in left ventricular diastolic chamber distensibility. Left ventricular diastolic blood pressure (DBP) rose in control, AS and DOCA-salt hearts, with no significant difference between the two hypertrophied groups. The anoxia-induced increase in left ventricular DBP correlated with the left ventricular weight: body weight ratio in all animals, but was higher in the two hypertrophied groups compared with controls when expressed per unit tissue mass. In response to anoxia, CVR increased in both groups of hypertrophied hearts and was correlated with enhanced left ventricular DBP. In addition, CVR increased in proportion to the degree of hypertrophy. Partial correlation analysis showed that this relationship depends upon the level of left ventricular DBP and disappears when this pressure is constant.


CONCLUSIONS
The anoxia-induced increase in myocardial stiffness is exaggerated in two different models of cardiac hypertrophy. This exaggeration is primarily related to the degree of hypertrophy and results in a more pronounced limitation of the coronary flow in hypertrophied hearts.
Callens-el Amrani
F
F
U 127 INSERM, Hôpital Lariboisière, Paris, France.
Snoeckx
L
L
Swynghedauw
B
B
D000704:Analysis of Variance; D000818:Animals; D001012:Aorta, Abdominal; D006332:Cardiomegaly / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology; D003187:Compliance; D003251:Constriction, Pathologic / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology; D003900:Desoxycorticosterone; D003971:Diastole / Q000502:physiology*; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006973:Hypertension / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D000860:Hypoxia / Q000150:complications* / Q000453:epidemiology / Q000503:physiopathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D003900:Desoxycorticosterone