Load dependence of mammalian heart relaxation during cardiac hypertrophy and heart failure.
Mechanical properties of relaxation were studied in left ventricular rat papillary muscle during cardiac hypertrophy induced by chronic pressure and/or volume overload. Maximum velocity of isotonic lengthening was linearly related to total extent of isotonic shortening and to maximum velocity of isotonic contraction and depended on the type of chronic overloading without correlation with the degree of cardiac hypertrophy. Time to peak shortening was significantly increased in each group of hypertrophied heart muscles as compared to controls. The sensitivity of cardiac relaxation to the loading conditions was determined by the time course of relaxation. To quantify the degree of load sensitivity, we measured the ratio of isotonic area to isometric area, which was the area limited by the afterloaded force vs. time at 50% of the isometric peak tension divided by the area of the force vs. time trace in the isometric twitch below the same level of load. The value of this ratio was about 0.81 in normal rat and did not show any significant differences in hypertrophied heart muscles even at the terminal stage of congestive heart failure. During acute hypoxia the load sensitivity of relaxation disappeared both in normal and in hypertrophied hearts. Thus inadequacy in oxygen supply has more drastic effects, as compared with those induced by chronic overload, probably by affecting the sarcoplasmic reticulum uptake of activating calcium.
D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology*; D006321:Heart / Q000033:anatomy & histology; D006333:Heart Failure / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology; D009200:Myocardial Contraction; D009929:Organ Size; D010101:Oxygen Consumption; D010210:Papillary Muscles / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors