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The human heart aneurysm
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HI&AN HEART ANEURYSX F. Kblbel, V. Dorazilov4, L.Rmel,J.,Lichtenberg,J.Vaneura Faculty cf Zenera Medicine, Charles University Prague,CSSR Upon combined morphological and biochemical investigations of 33 surgically removed pcstinfarction aneurysms 0~ the left ventricle, the following changes were observed: 1. a thin layer of muscle cells cati be found in every postinfarction aneurysm 2. a combination of signs of hypertrophy of the muscle cells with nonspecific regressive changes of the myocytes in the center of the scar tissue involving nuclei, mitochondria and contractile apparatus of the cells proliferation cf small-size co3. in 3 cases,fibromuscular ronary arteries / O.l- 1.0 mm/ resulting in total obstruction of the inner diameter cf these vessels. In one of them, the fibromJscular proliferation might be the cause of the aneurysm 4. t%e incorporation of 14C- glycine into proteins of the tissue slices was highest with the samples of the scar tissue rich in fibroblasts 5. the myofibrillar proteins of the atrophic muscle cells are reduced to actine and to a fraction resembling myosine light chains. THE
CHANGESIN CYCLIC AMP LEVELS AND IN ACTIVITIES OF PROTEIN KINASE (PK), PHOSPHORYLASEKIN&%?, (PHK), AND PHOSPHORYLASE (PH) IN TKE ISCHE&IC AND NONISCi-fZflTC MYOCARDITJMFOLLOWING CORONARYARTERY LIGATIQN (CAL) Krause, E.-G., S. Bartel, P. Karczewskl, I. Lehmann, P.-K. Lindenau, C. Kensickb, and A. Wollenberger, Berlin, German Democratic Republic Within 2 min after CAL in chloralose-urethane-N20-anesthetized dogs the following sequence of biochemical changes takes place in the ischemic region of the myocardium (IM): Rise in the level of CAMP from 0.60+0.07 to q.O3+O.l2 nmoles /g w.wt., rise in cAMP-dependent-PK-activity rat'io (-CAMP/ +oAMP) from 0.11+0.02 to 0.26+0.01, rise in PHK activity ratio (pH 6.8/pH-8.2) from 0.75+0.02 to O.28+O.O3, rise in PH activity ratio (-AMP/+AMP) f:om 0.12+0.02--M 0.28+0.03, and accumulation of lactate. Increases Th CA&Q and pff, PI& and PH activity ratios after CAL occur to nearly the same extent in nonischemic myocardium (NIM). The rises in CAMP levels and in PK activity ratio are suppressed by propran0101 in IM as well as in NIIVI, atiesting to their B-adrenergic nature. In contrast propranolol was ineffective in suppressing the rise in PH activity 2 min after CAL, pointing to a second, probably Ca++-dependent regulation of glycogenolysis in tbis period.
HI&AN HEART ANEURYSX F. Kblbel, V. Dorazilov4, L.Rmel,J.,Lichtenberg,J.Vaneura Faculty cf Zenera Medicine, Charles University Prague,CSSR Upon combined morphological and biochemical investigations of 33 surgically removed pcstinfarction aneurysms 0~ the left ventricle, the following changes were observed: 1. a thin layer of muscle cells cati be found in every postinfarction aneurysm 2. a combination of signs of hypertrophy of the muscle cells with nonspecific regressive changes of the myocytes in the center of the scar tissue involving nuclei, mitochondria and contractile apparatus of the cells proliferation cf small-size co3. in 3 cases,fibromuscular ronary arteries / O.l- 1.0 mm/ resulting in total obstruction of the inner diameter cf these vessels. In one of them, the fibromJscular proliferation might be the cause of the aneurysm 4. t%e incorporation of 14C- glycine into proteins of the tissue slices was highest with the samples of the scar tissue rich in fibroblasts 5. the myofibrillar proteins of the atrophic muscle cells are reduced to actine and to a fraction resembling myosine light chains. THE
CHANGESIN CYCLIC AMP LEVELS AND IN ACTIVITIES OF PROTEIN KINASE (PK), PHOSPHORYLASEKIN&%?, (PHK), AND PHOSPHORYLASE (PH) IN TKE ISCHE&IC AND NONISCi-fZflTC MYOCARDITJMFOLLOWING CORONARYARTERY LIGATIQN (CAL) Krause, E.-G., S. Bartel, P. Karczewskl, I. Lehmann, P.-K. Lindenau, C. Kensickb, and A. Wollenberger, Berlin, German Democratic Republic Within 2 min after CAL in chloralose-urethane-N20-anesthetized dogs the following sequence of biochemical changes takes place in the ischemic region of the myocardium (IM): Rise in the level of CAMP from 0.60+0.07 to q.O3+O.l2 nmoles /g w.wt., rise in cAMP-dependent-PK-activity rat'io (-CAMP/ +oAMP) from 0.11+0.02 to 0.26+0.01, rise in PHK activity ratio (pH 6.8/pH-8.2) from 0.75+0.02 to O.28+O.O3, rise in PH activity ratio (-AMP/+AMP) f:om 0.12+0.02--M 0.28+0.03, and accumulation of lactate. Increases Th CA&Q and pff, PI& and PH activity ratios after CAL occur to nearly the same extent in nonischemic myocardium (NIM). The rises in CAMP levels and in PK activity ratio are suppressed by propran0101 in IM as well as in NIIVI, atiesting to their B-adrenergic nature. In contrast propranolol was ineffective in suppressing the rise in PH activity 2 min after CAL, pointing to a second, probably Ca++-dependent regulation of glycogenolysis in tbis period.