Cardiovascular measurements were performed in rats 3–4 days, 1 week, 2 weeks, 5–6 weeks, and 4–5 months after the subcutaneous injection of 40 mg/kg isoproterenol on two consecutive days. Up to 1 week after the injections severe histological damage of the myocardium was accompanied by cardiac enlargement and impaired function: blood pressure, cardiac output and work were in the normal range under basal conditions but the maximum cardiac output and work measured during infusion of polyvinylpyrrolidone into the right side of the heart were well below normal. During the following weeks histological repair took place and the cardiovascular parameters measured were not different from those found in normal rats. This period was followed by a third stage which occurred without further interference with the heart. It consisted of thinning of the ventricular wall and aneurysm formation. All cardiovascular values (maximum and basal as well) were below normal without development of cardiac enlargement.

Cardiac output, reserve force of the heart, total peripheral resistance and weights of the heart and other organs were determined in normal rats, and in rats at different times after their aortas were narrowed just below the diaphragm. Although the output of the hypertrophied heart was normal, its reserve force WHS greater.

BEZVAK, M., KORE.C'KY, B., AND THOMAS, 6. 1969. Regression of cardiac hypcrlrophics of vario~ls origin. Can. J. Physiol. Pharrnacol. 47,[579][580][581][582][583][584][585][586] Enlargement of the heart was prod~rced in rats by four methods: (u) unilateral ncphrectomy with DOC pellet implantation and salt loading, (b) experimental hypcrthyroidism, ( c ) cxpcrimcntal aortic coarctation, and (62') nutritional anemia. All enlargements proved to be reversible if the provoking stirnul~~s was removed. In laearts enlarged by anemia elp to 80-100 %, the extra protein and RNA synthesized during the process of accelerated growtln of the heart disappcarcd as the size of the heart revcrtcd to nor~nal. In this way, the concentration of these two n~acromolecules remained the same, in spite of the claanges in the s i~e sf the heart. On tkc other hand, a Large part of the new DNA was not rernovcd during regression. BEZYAK, hf., KORECKY, B., AND THOMAS, G. L969. ~egressiorm of cardiac hypestrophics of various origin. Can. J . Physiol. Phannacal. 47, 579-586.Une augmentation du poids du coee~r a Cte obtenue chez B c rat par qualre mktI1odes differentes: ((1) B a nCphrectomie uniBatCrale suivie de I'implantation dc pellets de IIOC ct de la substitution d'une solution B ", de NaCl A la boisson norinale, (b) I'hyperthyroi'die cxptirimentale, (c) la coarctation experimcntale de l'aorte et (dl I'anCmie provoquke par un rkgime alimcntaire pauvre en fer. Dams tous les cas, le poids du meur rcvint a la normale lorsque l'anin~al cessa d'etre sous l'influencc dc I'agertt dCclenc11ant. Chcz Ics anima~ax andanies ou l'on observe une augmentation du poids du cseur pouvarra allcr de 869 a loo%, I'on note que le surplus de protkines et de K N A synlhetisks de~rant cette croissance acceldrke du nsusclc cardiaque dirninue jusqu'k disparaitre ii rnesure que le poids du coeur redevient normal. De cette faqon la concentration de ces macromolecules dans le muscle cardiaque demeurc la m6me et independante des variations du paids de I'organe. Par cantre, une importante fraction du DNA ClaborC durant cette augmentation de poids se retrouve encore dans B e cseur aprits Is retour A la normale. IntroductionThe heart sf rats can undergo quick changes in weight (Walter and Addis 1939). During restricted food intake the loss of body weight is followed by a corresponding decrease in the weight of the heart with a lag of only 1-2 days (Beznak 1954). Hall et al. (1953) showed that cardiac hypertrophy produced by a constricting ligature on one renal artery or by the subcutaneous implantation of a desoxycorticosterone (DOC )I pcllet regressed after the ligated kidney or the DOC pellst was renaoved.

Metabolic rate, blood pressure, weight and rate of the heart, cardiac output, and work were determined at weekly intervals in groups of normal rats receiving thyroxine. The measurements were made before and during the infusion of polyvinylpyrrolidone into the right side of the heart. The maximum values of cardiac output and work obtained during infusion were considered to be an approximate measure of the strength of the heart. Cardiac output and work in thyroxine-treated rats far exceeded the normal values before as well as during infusion. The greater strength was not merely the consequence of the greater size of the heart which developed in the course of thyroxine treatment. Hearts of similar size — coming from larger normal rats or from smaller normal rats with cardiac hypertrophy due to aortic constriction — did significantly less work than the hearts of thyroxine-treated rats.

Metabolic rate, blood pressure, weight and rate of the heart, cardiac output, and work were determined at weekly intervals in groups of normal rats receiving thyroxine. The measurements were made before and during the infusion of polyvinylpyrrolidone into the right side of the heart. The maximum values of cardiac output and work obtained during infusion were considered to be an approximate measure of the strength of the heart. Cardiac output and work in thyroxine-treated rats far exceeded the normal values before as well as during infusion. The greater strength was not merely the consequence of the greater size of the heart which developed in the course of thyroxine treatment. Hearts of similar size — coming from larger normal rats or from smaller normal rats with cardiac hypertrophy due to aortic constriction — did significantly less work than the hearts of thyroxine-treated rats.