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Query: UNIPROT:P06889 (Mol)
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Control ( F1B ) and cardiomyopathic (Bio 14.6) hamsters have been studied over an 11 month time interval, in an attempt to relate alterations in liver function with the onset of progressive heart damage. In most instances the parameters measured (e.g., liver weight, liver polysome content, in vitro polysome driven protein synthesis) were similar for both groups of animals. The exceptions appeared to be two Bio 14.6 animals that had liver hypertrophy, coupled with severe necrosis and liver damage. These livers had very low levels of virtually inactive polysomes and depicted many of the histopathological characteristics of hepatic ischemic injury known in humans to be associated with congestive heart failure. Our biochemical and histological data suggests that for the Bio 14.6 hamsters, progressive cardiomyopathy is associated with severe liver damage for only a few animals.
Virchows Arch B Cell Pathol Incl Mol Pathol 1984
PMID:Changes in hamster liver albumin synthesis during the development of cardiomyopathy. 614 43

In experiments of 4 and 8 months duration, blood pressure (BP) and heart rate (HR) were measured periodically in streptozotocin-diabetic (D) rats of normotensive (WKY) and hypertensive (SHR) strains and in corresponding controls (C). BP and HR of D were lower than those of C. In both experiments body length, heart weight and the heart weight/body length ratio (W/L) of D were reduced at autopsy. The number of myocardial cell nuclei per test area was increased in D, indicating a reduced myocardial cell size. No specific change was found at any time in the coronary arteries of rats from any of the groups examined. At 4 months, the retinal capillary basement membrane (BM) of the SHR strain was significantly thicker than that of the WKY strain. At 8 months the BM of D rats was significantly thicker than that of C, but there was no difference between strains. Our results demonstrate that long-term diabetes promotes BM thickening in both normotensive and hypertensive animals. Hypertension does not seem to potentiate diabetes in inducing microangiopathy. Diabetes, however, by causing a lower heart weight and by reducing the heart rate may influence negatively the development of hypertension in the SHR strain. It also appears that there is no direct relationship between increased retinal capillary BM thickness and myocardiopathy.
Virchows Arch B Cell Pathol Incl Mol Pathol 1984
PMID:Morphometric studies on retinal microangiopathy and myocardiopathy in hypertensive rats (SHR) with induced diabetes. 615 Dec 90

Previous reports have documented a cardiomyopathy in rats resulting from streptozotocin-induced diabetes. In order to determine the reversibility of streptozotocin-induced cardiomyopathy to insulin therapy, hearts from rats made diabetic by streptozotocin for 6 weeks and then treated with insulin for 3 weeks were compared with untreated diabetic rats and control rats not injected with streptozotocin. When perfused in an isolated working heart apparatus with 5.5 mM glucose as substrate, hearts from untreated diabetic rats when compared to hearts from either streptozotocin-injected rats treated with insulin or control rats showed significant depressions in peak left ventricular pressure, maximal positive and negative dP/dt, oxygen extraction, lactate production and effluent lactate; pyruvate ratio. Ca2+-actomyosin ATPase was also depressed in untreated diabetics. As left atrial pressure was raised in untreated diabetic rats, a decline in cardiac output was observed, whereas in insulin-treated or control groups there was no such negative response. Indices of cardiac performance were significantly greater in insulin-treated rats when compared to control rats suggesting overcorrection with insulin therapy. To explore whether insulin treatment may have a beneficial effect on the myocardium control rats were made hyperinsulinemic for 6 to 7 weeks. Shorter isovolumic relaxation times and elevated values for Ca2+-actomyosin ATPase were observed in hearts from hyperinsulinemic animals when compared to hearts from control animals. These results demonstrate complete reversibility of streptozotocin-induced cardiomyopathy and confirm that this condition is due to insulin deficiency and not to a primary cardiotoxic effect of streptozotocin.
J Mol Cell Cardiol 1983 Jul
PMID:Left ventricular function after chronic insulin treatment in diabetic and normal rats. 622 76

The purpose of this study was to examine the density of intramembrane particles in the cardiac sarcolemma of normal and myopathic Syrian hamsters in a search for a morphological marker of a putative membrane defect. Hereditary cardiomyopathy in hamsters is manifested by progressive multifocal skeletal and cardiac muscle necrosis. Although pharmacological and biochemical data suggest a molecular defect in the cardiac sarcolemma, there has been no morphological observation that would substantiate this suggestion. We quantified numerical densities of intramembrane particles in freeze-fractured sarcolemmal membrane protoplasmic and extracellular faces from the left and right ventricular myocardium of female 25-day-old hamsters of the U.M.-X 7.1 cardiomyopathic line compared with sex- and age-matched randomly bred Syrian hamsters. Intramembrane particle numerical densities significantly increased above control values in cardiomyopathic hamsters for protoplasmic face (from 2188 +/- 61 to 2454 +/- 89 microns-2 in left ventricle (P less than 0.025) and from 2255 +/- 83 to 2574 +/- 56 microns-2 in right ventricle (P less than 0.001]. There was no significant difference between intramembrane particle densities of normal and cardiomyopathic hamsters for extracellular face (707 +/- 45 and 687 +/- 49 microns-2 in the left ventricle and 742 +/- 41 and 746 +/- 28 microns-2 in the right ventricle). These results implicate an increase of protoplasmic face-associated integral proteins in the sarcolemmal membrane of cardiomyopathic hamster. The significance of this finding is not known. It may represent an adaptive change related to a molecular defect in the sarcolemmal membrane of cardiomyopathic hamster.
J Mol Cell Cardiol 1983 Aug
PMID:Numerical densities of intramembrane particles in the cardiac sarcolemma of normal and myopathic Syrian hamsters. 632 23

The role of cardiac lysosomal and nonlysosomal protease alterations in the development of the cardiomyopathy that occurs in genetically diabetic C57BL/KsJ db/db mice has been examined. The db/db mice and age-matched controls were sacrificed between 7 and 24 weeks of age. Cathepsin D activity, myofibrillar alkaline protease (MAP) activity (including serine protease activity), and Ca2+-activated protease activity were determined by using [3H]acetyl-casein as substrate. There is a significant decrease in cathepsin D, MAP, and serine protease activities in the myocardium of 7- to 20-week old diabetic mice with a rebound of these activities toward normal levels by 24 weeks of age. Cathepsin D and MAP activities are inversely related to heart weight in diabetic mice with the higher levels being recorded in association with the most pronounced decrease in heart weight. In contrast, Ca2+-activated protease activity in the hearts of diabetic mice does not differ significantly from controls throughout the period of observation. The results suggest that both lysosomal cathepsin D and nonlysosomal MAP may mediate the accelerated cardiac muscle degradation that occurs in the late stage of diabetic cardiomyopathy in the db/db mice.
Exp Mol Pathol 1984 Jun
PMID:Lysosomal and nonlysosomal proteolytic activities in experimental diabetic cardiomyopathy. 632 62

Mild (not harmful) stress may initiate an adaptive mechanism, protecting the heart from harmful consequences of a more severe stress. There are at least three known types of cardiac adaptation to stress, such as: a) the gradually developing, long lasting adaptation to chronic mechanical overload, leading to cardiac hypertrophy, later to cardiomyopathy and heart failure, b) the rapidly developing adaptation to moderate stress initiated by 'preconditioning' brief coronary occlusion(s) or brief periods of rapid cardiac pacing, protecting for less than 1 h against consequences of a subsequent, severe stress, c) the later appearing, more prolonged cardio-protective adaptation, described by us in 1983, induced by various forms of more severe but not injurious stimuli, such as an optimal dose of prostacyclin or its stable analogues; or a series of brief periods of rapid pacings. This form of cardiac adaptation to stress protects for 24-48 h against consequences of a more severe stress such as: 1. myocardial ischaemia; 2. early and late postocclusion and reperfusion arrhythmias; 3. early morphologic changes secondary to ischaemia and reperfusion; 4. ischaemia induced myocardial loss of K+ and accumulation of Na+ and Ca++; 5. it may increase the tolerance to the toxic effects of cardiac glycosides. A reduced response to beta-adrenergic stimuli and a concomitant increase in activity and amount of PDE I and IV was shown by us earlier.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Biochem
PMID:On the mechanism and possible therapeutic application of delayed adaptation of the heart to stress situations. 749 39

Excessive release or administration of beta-mimetic catecholamines may induce cardiomegaly, necrotic lesions and accumulation of connective tissue in the heart of adult homoiotherms. It was examined here whether similar changes can also be observed at different stages of evolution of the cardiovascular system, i.e. in poikilotherms and in homoiotherms during embryonic life. Sensitivity of the poikilothermic hearts (carp, frog, turtle) to isoproterenol (IPRO) was significantly lower than in the homoiotherms. Necrotic lesions, if present, were localized in the inner spongious musculature which has no vascular supply but which exhibits higher activities of enzymes connected with aerobic oxidation. Moreover, the IPRO-induced decrease of the phospholipid content was also significantly more expressed in the spongious layer. IPRO treatment did not influence the total weight of the fish heart but the proportion of the outer compact layer was significantly higher. These changes were accompanied by an increase of collagen, higher water content and an increase of isomyosin with a lower ATPase activity. The response of the poikilothermic heart to IPRO-induced overload thus differs significantly from that in the homoiotherms. The administration of IPRO during embryonic life of homoiotherms (chick) induces serious cardiovascular disturbances, including cardiomegaly and cellular oedema. Necroses of myofibrils, characteristic of IPRO-induced lesions of adults, were, however, rather exceptional. IPRO did not elevate the concentration of 85Sr (as a calcium homologue) in the immature myocardium; it seems, therefore, that IPRO-induced changes of the embryonic heart are not necessarily due to an intracellular calcium overload. It may be concluded that the character of catecholamine-induced cardiomyopathy is not uniform and depends strictly on the stage of cardiac development.
Mol Cell Biochem
PMID:Structural and biochemical remodelling in catecholamine-induced cardiomyopathy: comparative and ontogenetic aspects. 749 59

Adriamycin (doxorubicin) is a broad spectrum anti-tumor antibiotic used to treat cancer patients. However, the potential usefulness of this drug is currently limited by the development of a dose-dependent cardiomyopathic process terminating in severe heart failure. Although several mechanisms have been suggested to explain the pathogenesis of adriamycin-induced cardiomyopathy, free-radical induced oxidative stress appears to play an important role. A concise description of adriamycin-induced cardiomyopathy is provided. Various combination therapies which have been attempted in the past to modulate the adriamycin-induced cardiomyopathy are also discussed. Recently, it has been discovered that probucol, a lipid lowering agent and potent antioxidant, provides complete protection against adriamycin-induced cardiomyopathy in rats without interfering with the anti-tumor properties of this antibiotic. Clinical trials employing adriamycin therapy in combination with probucol are needed to determine the applied value of these laboratory findings.
J Mol Cell Cardiol 1995 Apr
PMID:Combination therapy with probucol prevents adriamycin-induced cardiomyopathy. 756 2

End stage heart failure due to ischemic (ICM) or dilated (DCM) cardiomyopathy is characterized by a dilated, relatively thin-walled ventricle. The hypothesis has been proposed that the structural basis of ventricular expansion is due to side-to-side slippage of myocytes within the wall. Although this represents one potential mechanism for the observed phenomena of chamber dilatation and subsequent wall thinning, the degree of slippage claimed is not necessarily in harmony with the magnitude of chamber enlargement and mural thinning. Moreover, sarcomere extension was not examined in the base to the apical regions of the heart, leaving open the question as to the role of changes in resting sarcomere length in acute chamber dilatation. In this regard, an alternative etiology for the detrimental cardiac architectural rearrangement seen in dilated failure can be supplied by postulating the occurrence of maladaptive remodeling of cardiac myocyte morphology. In this model, myocytes increase in length by an increase in the number of sarcomeres in series, thus increasing chamber diameter in an attempt to maintain cardiac output. However, these cells do not enlarge to any significant degree in the transverse diameter preventing the heart from developing adequate force. This hypothesis is supported by recent evidence from patients with ICM and DCM indicating that myocyte lengthening alone could account for all the dilatation observed. Furthermore, it appears that the thinning of the ventricular wall in failure is due to inadequate transverse growth of cardiac myocytes coupled with scattered myocyte cell loss throughout the ventricular wall.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Cell Cardiol 1995 Mar
PMID:Structural remodeling and mechanical dysfunction of cardiac myocytes in heart failure. 760 3

Light microscopic and ultrastructural findings in patients suffering from chloroquine-induced cardiomyopathy are reviewed. Based on our own observations in an autopsy case, functional and morphological similarities between chloroquine effects and hereditary lysosomal storage diseases are discussed.
J Mol Med (Berl) 1995 Feb
PMID:Histological and ultrastructural findings in chloroquine-induced cardiomyopathy. 762 32


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