In a hereditary cardiomyopathy of the Syrian hamster, changes in water and electrolyte metabolism were investigated. Four age groups were differentiated histopathologically. Body weight of cardiomyopathic animals was initially decreased but later exceeded that of controls. The total extracellular fluid volume was larger than in controls, with a decreased haematocrit; these changes were especially pronounced in the oldest hamsters. The myocardial extracellular space and water content underwent similar changes to those in total extracellular volume. Besides a tendency to hyponatraemia there were no alterations of the serum potassium and sodium levels in the youngest three groups. However, in animals with congestive heart failure, serum potassium was decreased and serum sodium increased. Initially serum calcium was increased and the magnesium value was normal. In prenecrotic tissue myocardial magnesium was markedly decreased but calcium only slightly increased. In the necrotizing myocardium, however, calcium was greatly elevated; in the later stages, calcium tended to decrease. Surprisingly, magnesium was unchanged in necrotizing tissue, and decreased later. Myocardial sodium and potassium did not exhibit changes during the prenecrotic but in the following stages, when potassium was lowered and sodium was elevated. A distinct rise of the extracellular sodium concentration was observed in animals with obvious congestive heart failure.

Oxidative phosphorylation and calcium transport were measured in mitochondria isolated from cardiomyopathic hamster hearts. In the presence of glutamate, a small increase in respiratory control was noted in mitochondria isolated from moderately enlarged hearts of hamsters without peripheral signs of failure. These mitochondria also tended to exhibit lower oxygen consumption rates. Mitochondria isolated from hearts of hamsters showing severe peripheral manifestations of congestive failure were depressed with respect to respiratory control and exhibited diminished rates of electron transport. Mitochondria isolated from hearts of the cardiomyopathic animals accumulated less calcium than mitochondria from control animals. This alteration parallels the changes in electron transport. The magnitude of the changes in both electron transport and calcium uptake appear to be related to the severity of failure.

Cardiac relaxing system (CRS) was isolated from control (BIO-RB) and cardiomyopathic (BIO 14.6, BIO 82.62 and BIO 40.54) hamsters. Both dual-beam spectrophotometric and Millipore filter methods were employed to study calcium binding by CRS. The four groups (control and cardiomyopathic hamsters) were killed at three ages: Age I = 60 ± 9 days, Age II = 216 ± 7 days, and Age III = 262 ± 12 days. The latter two ages were in congestive heart failure. CRS isolated from Age I did not demonstrate diminished capacity or rate of calcium binding, whereas both Ages II and III revealed a decrease in rate and maximal capacity of calcium binding compared to controls. It is suggested that an aberration of intracellular calcium metabolism is characteristic of congestive heart failure associated with the cardiomyopathic process.

Focal myocardial degeneration occurs spontaneously in all members of an inbred strain of Syrian hamsters (BIO 14.6 line). The underlying metabolic defect is transmitted by an autosomal recessive gene. The progressive, chronic cardiac condition results in the appearance of all the known features of congestive heart failure. Cardiomyopathic hamsters can be produced in large numbers simply by maintaining appropriate colonies through brother-sister matings. The histogenesis and some additional characteristics of this hereditary disease model have been clarified. These and other observations suggest that hamsters of the cardiomyopathic strain offer unique opportunities for investigative cardiology.

Annals of the New York Academy of SciencesVolume 156, Issue 1 p. 396-420 DISSOCIATION OF FACTORS INFLUENCING MYOCARDIAL DEGENERATION AND GENERALIZED CARDIOCIRCULATORY FAILURE* E. Bajusz, E. Bajusz Bio-Research Institute, Cambridge. Mass.Search for more papers by this authorF. Homburger, F. Homburger Bio-Research Institute, Cambridge. Mass.Search for more papers by this authorJ. R. Baker, J. R. Baker Bio-Research Institute, Cambridge. Mass.Search for more papers by this authorP. Bogdonoff, P. Bogdonoff Bio-Research Institute, Cambridge. Mass.Search for more papers by this author E. Bajusz, E. Bajusz Bio-Research Institute, Cambridge. Mass.Search for more papers by this authorF. Homburger, F. Homburger Bio-Research Institute, Cambridge. Mass.Search for more papers by this authorJ. R. Baker, J. R. Baker Bio-Research Institute, Cambridge. Mass.Search for more papers by this authorP. Bogdonoff, P. Bogdonoff Bio-Research Institute, Cambridge. Mass.Search for more papers by this author First published: January 1969 https://doi.org/10.1111/j.1749-6632.1969.tb16742.xCitations: 25 * This work was supported by United States Public Health Service research grant no. HE-09791 (National Heart Institute) and general research support grant no. FR-05525 (Division of Research Facilities and Resources). AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume156, Issue1Experimental "Metabolic" Cardiopathes and their Relationship to Hima Heart DiseaseJanuary 1969Pages 396-420 RelatedInformation

Focal myocardial lesions are consistently present in an inbred strain of Syrian hamsters (BIO 14.6 line) suffering from a hereditary primary polymyopathy. The onset and rapid progression of myocardial degeneration play an eliciting or contributory role in the genesis of congestive heart failure, which is also regularly observed during the advanced stages of this hereditary disease. Under the present experimental conditions, variations in calcium and inorganic-phosphorus intake, as well as parathyroidectomy, influenced the secondary calcification of the myocardial lesions but not the extent of focal degeneration itself. Enhancement of dystrophic calcification accelerated the subsequent development of congestive heart failure, while the prevention of calcific deposits afforded a protective effect. Since an inverse relationship was established between the severity of calcification of the degenerating heart-muscle areas and the progression of healing of these lesions, it is postulated that dystrophic calcification influences the development of congestive heart failure by affecting the normal reparative processes in the damaged myocardium. In fact, it was shown that dystrophic calcification interferes with healing not only mechanically, but also qualitatively it alters the normal healing patterns. Calcification appears to be an important conditioning factor in the genesis of heart failure in the hamster.

Annals of the New York Academy of SciencesVolume 156, Issue 1 p. 105-129 SPONTANEOUS, HEREDITARY MYOCARDIAL DEGENERATION AND CONGESTIVE HEART FAILURE IN A STRAIN OF SYRIAN HAMSTERS* E. Bajusz, E. Bajusz Bio-Research Institute, Cambridge, Mass.Search for more papers by this authorJ. R. Baker, J. R. Baker Bio-Research Institute, Cambridge, Mass.Search for more papers by this authorC. W. Nixon, C. W. Nixon Bio-Research Institute, Cambridge, Mass.Search for more papers by this authorF. Homburger, F. Homburger Bio-Research Institute, Cambridge, Mass.Search for more papers by this author E. Bajusz, E. Bajusz Bio-Research Institute, Cambridge, Mass.Search for more papers by this authorJ. R. Baker, J. R. Baker Bio-Research Institute, Cambridge, Mass.Search for more papers by this authorC. W. Nixon, C. W. Nixon Bio-Research Institute, Cambridge, Mass.Search for more papers by this authorF. Homburger, F. Homburger Bio-Research Institute, Cambridge, Mass.Search for more papers by this author First published: January 1969 https://doi.org/10.1111/j.1749-6632.1969.tb16721.xCitations: 109 * This work was supported by United States Public Health Service research grant no. HE-09791 (National Heart Institute) and general research support grant no. FR-05525 (Division of Research Facilities and Resources). AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 ARMSTRONG, T. G. 1940. Quart. J. Exp. Physïol. 30: 263. 2 BARGER, A. C., G. S. RICHARDSON & B. B. ROE. 1950. Proc. Soc. Exp. Biol. Med. 73: 113. 3 HUFNAGEL, C. A., B. B. ROE & A. C. BARGER. 1951. Surgery 29: 77. 4 MUNRO, A., O. J. BALCHUM, J. C. OWENS & H. SWAN. 1955. Surg. Forum 6: 204. 5 VEITH, F. J. & W. B. THROWER. 1959. Surg. Gynec. Obstet. 109: 687. 6 GERTLER, M. M. 1959. Proc. Soc. Exp. Biol. Med. 102: 396. 7 BOR, N. B. & A. P. RIEBEN. 1961. Amer. J. Cardiol. 8: 41. 8 IMAI, H. & R. M. O'NEAL. 1961. Arch. Path. (Chicago) 7: 688. 9 WEIL, M. H. & B. S. MILLER. 1961. J. Lab. Clin. Med. 57: 683. 10 SCHWARTZ, A. & K. S. LEE. 1962. Circ. Res. 10: 321. 11 DONALD, D. E. & H. E. ESSEX. 1954. Amer. J. Physiol. 177: 477. 12 BAKOS, A. C. P. 1950. Circulation 1: 724. 13 JOHNS, T. P. N. & B. J. OLSON. 1954. Ann. Surg. 140: 675. 14 BAJUSZ, E. 1963. Conditioning Factors for Cardiac Necroses. Intercontinental Medical Book Corp. New York , N. Y. 15 CORDAY, E., R. SPITZLER & M. PRINZMETAL. 1949. Ann. Intern. Med. 31: 450. 16 HOMBURGER, F., J. R. BAKER, C. W. 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Summary Prolonged isolation stress of rats was associated with a significant diminution of myocardial potassium and magnesium, and with a marked increase in myocardial sodium, causing a reduction of the K/Na ratio. Restoration of contact with other animals tended to correct these changes within a short period of time. Myocardial calcium was increased during isolation. Histochemical and histological observations revealed a marked aggravation of epinephrine-induced myocardial focal potassium displacement, and the appearance of epinephrine-induced hemorrhages and necroses in the hearts of isolated rats, which could not be elicited in the controls by analogous doses of epinephrine. This type of augmented vulnerability of the heart muscle to catecholamine action is attributed to the well-established principle of exaggerated catecholamine cardiotoxicity under corticoid over-action, in view of the fact that others have observed an increased corticoid production in isolated rats.