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Morphologic changes in the myocardium of hemorrhagic shock resistant dogs
34 BIOCHEMICAL AND MORPHOLOGICAL STUDIES IN DIABETIC RAT HEART. J.H. McNeil1 and C.V. Jackson, Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada. Previous studies in our laboratory have indicated that chemically-induced diabetes can produce functional abnormalities in rat hearts. As early as 6 weeks after the onset of diabetes diabetic hearts do not respond as well as controls to increases in atria1 filling pressure when (+) or (-) dP/dt is monitored on a working heart apparatus. Sarcoplasmic reticulum (SR) prepared from the hearts did not take up Ca++ as rapidly as did SR from control hearts. Changes could be prevented or reversed by insulin treatment. Some pharmacological differences were also noted in diabetic hearts. The response to al agonists was enhanced, the response to ,E agonists was either depressed or not affected and the response to carbachol was initially depressed (3 months) but later enhanced (6 months). We have now examined right ventricular myocardium from both 3 month and 6 month diabetic rats using electron microscopy. Hearts showed an increase in glycogen content, disruption of mitochondria and cellular edema, especially around the nuclear membrane and a decrease in contractile protein. Six month ventricles also contained ischemic zones denoted by large contractile bands of the contractile apparatus. Age matched controls exhibited none of the above features. The morphological changes noted may contribute to the decrease in contractility observed in diabetic rat hearts. (Supported by MRC, Can.Ht.Fdn. and the B.C. Branch of the Can. Diabetes Fdn.)
ISOMYOSINS IN NORMAL AND HYPERTROPHIED HUMAN HEARTS. J.J. Mercadier, D. de la Bastie, P. Bouveret, Ph. Menasche, Ph. Beaufils, K. Schwartz. INSERM Unite 127 and Dept. of Cardiology, Hopital Lariboisiere, Paris, France. Current evidence indicates that adaptation of the adult rat heart to increase in cardiac work is mediated by the synthesis of the V3 isomyosin which is predominant in fetal hearts (i). This isomyosin redistribution (Vl+V3) is characterized by the coexistence of Vl and V3 isofor s in the same cardiac cell (2) and by decreases of total myosin Cay+-stimulated ATPase activity Looking for such modifications durinq human left ventricular hvoertrophv, we have observed on autoosv samples that human myosins were-composed-mostly of a V3 type (HV3),'but contained also some VI isomvosin (HVl, from 0 to 15%). Studies oerformed on 30 per-operative biopsies indicated that in these'conditions; hypertrophic hearts contained exclusively HV3. Cazt-ATPase activities on the other bland were unchanged. This strongly suggests that isomyosin shifts are pos#sible in man, but do not contribute to adaptation to chronic mechanical overload. (1) Schwartz, K. et al. J. Biol. Chem. 1982, 257, 14412 ; (2) Samuel et al. Circ. Res. 1983, 52, 200.
MORPHOLOGIC CHANGES IN THE MYOCARDIUM OF HEMORRHAGIC SHOCK RESISTANT DOGS. E. Mikat, J. Schaper, D. Hackel, P. Cruz. Path. Dept., Duke Univ., Durham, NC 27’710 The objective of this study was to determine the morphologic changes in the myocardium of dogs resistant to a 2-hour period of hemorrhagic hypotension at 36 mm Hg (Shock). Twelve dogs were given either 1 or ‘2 hours of shock, transfused and allowed to recover. This protocol was repeated at 3-week intervals for up to 6 months. Eight dogs survived (resistant) the final 2 hr. shock episode and were sacrificed The non-resistant dogs which died spontaneously had marked subendocardlal hemorrhage, contraction band necrosis, areas of fibrosis and zonal lesion They showed areas of formation; whereas resistant dogs had few such acute changes. hyperconvoluted intercalated discs, increased amounts of Z-band material, and increased interstitial connective tissue. The hypoxia induced hemorrhage and necrosis was detectable to a slight degree in the resistant dogs 24 hours after the final 2-hour shock period. The increased amounts of Z band material and the increased surface area of hyperconvoluted intercalated discs resemble changes found in developing myocardium of newborn-animals, in myocytes grown in tissue culture and in human myocytes of various forms of congenital and acquired heart disease. An increase in the amount of connective tissue was a consistent finding in shock resistant dogs and has been described as a distinctive feature of ischemia associated myocardial hypertrophy. These morphologic changes indicate that the episodes of shock involved enough myocardial injury to lead to fibrosis as well as to signs of regenerative activity in the myocytes.
ISOMYOSINS IN NORMAL AND HYPERTROPHIED HUMAN HEARTS. J.J. Mercadier, D. de la Bastie, P. Bouveret, Ph. Menasche, Ph. Beaufils, K. Schwartz. INSERM Unite 127 and Dept. of Cardiology, Hopital Lariboisiere, Paris, France. Current evidence indicates that adaptation of the adult rat heart to increase in cardiac work is mediated by the synthesis of the V3 isomyosin which is predominant in fetal hearts (i). This isomyosin redistribution (Vl+V3) is characterized by the coexistence of Vl and V3 isofor s in the same cardiac cell (2) and by decreases of total myosin Cay+-stimulated ATPase activity Looking for such modifications durinq human left ventricular hvoertrophv, we have observed on autoosv samples that human myosins were-composed-mostly of a V3 type (HV3),'but contained also some VI isomvosin (HVl, from 0 to 15%). Studies oerformed on 30 per-operative biopsies indicated that in these'conditions; hypertrophic hearts contained exclusively HV3. Cazt-ATPase activities on the other bland were unchanged. This strongly suggests that isomyosin shifts are pos#sible in man, but do not contribute to adaptation to chronic mechanical overload. (1) Schwartz, K. et al. J. Biol. Chem. 1982, 257, 14412 ; (2) Samuel et al. Circ. Res. 1983, 52, 200.
MORPHOLOGIC CHANGES IN THE MYOCARDIUM OF HEMORRHAGIC SHOCK RESISTANT DOGS. E. Mikat, J. Schaper, D. Hackel, P. Cruz. Path. Dept., Duke Univ., Durham, NC 27’710 The objective of this study was to determine the morphologic changes in the myocardium of dogs resistant to a 2-hour period of hemorrhagic hypotension at 36 mm Hg (Shock). Twelve dogs were given either 1 or ‘2 hours of shock, transfused and allowed to recover. This protocol was repeated at 3-week intervals for up to 6 months. Eight dogs survived (resistant) the final 2 hr. shock episode and were sacrificed The non-resistant dogs which died spontaneously had marked subendocardlal hemorrhage, contraction band necrosis, areas of fibrosis and zonal lesion They showed areas of formation; whereas resistant dogs had few such acute changes. hyperconvoluted intercalated discs, increased amounts of Z-band material, and increased interstitial connective tissue. The hypoxia induced hemorrhage and necrosis was detectable to a slight degree in the resistant dogs 24 hours after the final 2-hour shock period. The increased amounts of Z band material and the increased surface area of hyperconvoluted intercalated discs resemble changes found in developing myocardium of newborn-animals, in myocytes grown in tissue culture and in human myocytes of various forms of congenital and acquired heart disease. An increase in the amount of connective tissue was a consistent finding in shock resistant dogs and has been described as a distinctive feature of ischemia associated myocardial hypertrophy. These morphologic changes indicate that the episodes of shock involved enough myocardial injury to lead to fibrosis as well as to signs of regenerative activity in the myocytes.