Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat.
This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.
D000818:Animals; D001834:Body Water / Q000032:analysis; D001835:Body Weight; D006332:Cardiomegaly / Q000150:complications / Q000503:physiopathology*; D002415:Cats; D003250:Constriction; D004558:Electric Stimulation; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006352:Heart Ventricles / Q000032:analysis / Q000033:anatomy & histology; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D009929:Organ Size; D011312:Pressure; D011651:Pulmonary Artery / Q000502:physiology; D013997:Time Factors
D009638:Norepinephrine