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Histopathological study on myocardial hypertrophy associated with ischemic heart disease
J MO]
Cell
Cardioi
21 (Supplement
IV) (1989)
P46
DLTBASTBUCTUBAL CHANGES ADD DAMAGE OF THg CYTOSKELgTON IN DILATED CARDIOMYOPATHY. Jutta Schaper, 8. Froede. S. Hein, W. Konertz. N. Bleese. Plan-Planck-Institute, Dept. Cardiology; Kerckhoff-Clinic, Dept. Thoracic and Cardiovascular Surgery, &P. Bad Nauheim, PR Germany. In viable human myocardial tissue obtained from 8 explanted hearts at the time of transplantation surgery the cytoskeleton was investigated by inraunofluroescence microscopy using monoclonel antibodies against either desmin CD), alpha and beta-tubulin (T), vinculin (V). or vimentin (Vi). Results were compared with ultrastructural data from the same tissue. In ultrastructurally normal cells D was localized at the Z-bands, T showed diffuse staining of the cytoplasm and localized staining of microtubules. V was localized at the sarcolemma. Vi was present only in vascular endothefial cells and in fibroblasts. In rnyocytas shoving aubcellular degeneration loss of contractile material was accompanied by either lose of D or by accumulation of irregularly arranged D. T was present in increased amounts. V was significantly increased at the sarcoleasaa and was also observed within myocytes. Vi positive elements were more numerous corresponding to the increased amount of fibrosis. Conclusion: Loss of contractile material and degenerative changea of nuclei. mitochondria and T- and S&system are accompanied by accumulation of D, V as wsll as of T. Both, alterations of the ultrastructure as well as of the cytoskeleton , may be the morphological correlate of contractile failure in dilated cardiomyopathy.
P47
HISTOPATHOLOGICAL M.Ishijima, S.Kawai,
cular
Pathology,
STUDY ON MYOCAROIAL R.Okada, Y.Fukuda*,
Dept.
of
Pathology*,
HYPERiROPHY H.Simada**.
&tend0
ASSOCIATED Research
University
WITH ISCHEMIC Laboratorv
and
Dept.
HEART DISEASE for Cardiovas-
of bathology,
Tokyo
Metropolitan Geriatric Hospital**, Tokyo, Japan. To clarify mode of myocardial hypertrophy in cases with ischemic heart disease, 15 cases with subendocardial infarction (SE), 27 with transmural infarction (TM), 20 with non-infarcted 3 vessel disease (3VD), and 17 of control were histopathologically examined. The average heart weight was 4629 in SE, 3949 in TM, 3189 in 3VD, and 3149 in control. The average luminal size of the left ventricle was 30.4mm in diameter in SE, 28.6 mm in TM, 18.2nnn in 3VD, and 17.3mm in control. The average size of myocytes was 24.7~ in diameter without difference by locations in SE cases. It was 22.9u at the proximal area to the infarct and 20.7~ at the distal area in TM cases. It was 18.4~ in 3VD cases compared with 12.5~ in control. The gross infarcted area was 26.7% in SE and 22.3% in TM. The myocardial non-infarcted area was 12.4% in SE, 10.1% in TM,17.8% in 3VDand 4.2% in control. The number of myocyte layer in stratum compactum counted along the ventrical line to the luminal surface was 203 in SE, 383 in TM, 324 in 3VD and 329 in control. Because the grade of hypertrophy was more prominent in SE than TM, according to more extensive infarcted area, fibrosis area, and larger luminal size and heart weight though less number of myocyte layers, it concluded that myocardial ischemia promotes hypertrophy through compensatory mechanism for loss of contracting capacity due to fibrosis replacing myocyte loss and increased mechanical load resulted by luminal dilatation.
P48INVESTIGATION OF THE LEUCYL-tRNA SYNTHETASE FROM PIG HEART DURING MYOCARDIAL ISCHEMIA. R. Stapulionis, I. Daukantaite. Kaunas Medical Institute, Central Research Laboratory, Kaunas. Lithuanian SSR. USSR. Some properties of free and aggregated-forms of 1eucylltRNA synthetase from normal pig myocardium and after 15 and 30 min of total myocardial ischemia have been compared. Free enzyme both from normal tid ischemic myocardium possesses-one polypeptidic chain with Mr IjO kDa and sedimentation constant 8 S. High-molecular weight camplex is composed at least from six aminoacyl-tRNA synthetases and has M, 840 kDa. No significant differences in Km and V,,& values for free and aggregated leucyl-tRNA svnthetase durina ischemla were observed. Free enzyme appears to be more thermolabile in comparison with the complexed. Free enzyme from normal myocardium is more resistant to thermoinactivation than that from ischemic mvocardium. After 15 min of total ischemia the leucyl-tRNA synthetase activity translocates partly into the complex, whereas 30 min ischemia exhibits this activity in the fraction of free enzyme, what may be one of the possibilities for changes in intensity and rate of protein biosynthesis during myocardial ischemia. S.25
Cell
Cardioi
21 (Supplement
IV) (1989)
P46
DLTBASTBUCTUBAL CHANGES ADD DAMAGE OF THg CYTOSKELgTON IN DILATED CARDIOMYOPATHY. Jutta Schaper, 8. Froede. S. Hein, W. Konertz. N. Bleese. Plan-Planck-Institute, Dept. Cardiology; Kerckhoff-Clinic, Dept. Thoracic and Cardiovascular Surgery, &P. Bad Nauheim, PR Germany. In viable human myocardial tissue obtained from 8 explanted hearts at the time of transplantation surgery the cytoskeleton was investigated by inraunofluroescence microscopy using monoclonel antibodies against either desmin CD), alpha and beta-tubulin (T), vinculin (V). or vimentin (Vi). Results were compared with ultrastructural data from the same tissue. In ultrastructurally normal cells D was localized at the Z-bands, T showed diffuse staining of the cytoplasm and localized staining of microtubules. V was localized at the sarcolemma. Vi was present only in vascular endothefial cells and in fibroblasts. In rnyocytas shoving aubcellular degeneration loss of contractile material was accompanied by either lose of D or by accumulation of irregularly arranged D. T was present in increased amounts. V was significantly increased at the sarcoleasaa and was also observed within myocytes. Vi positive elements were more numerous corresponding to the increased amount of fibrosis. Conclusion: Loss of contractile material and degenerative changea of nuclei. mitochondria and T- and S&system are accompanied by accumulation of D, V as wsll as of T. Both, alterations of the ultrastructure as well as of the cytoskeleton , may be the morphological correlate of contractile failure in dilated cardiomyopathy.
P47
HISTOPATHOLOGICAL M.Ishijima, S.Kawai,
cular
Pathology,
STUDY ON MYOCAROIAL R.Okada, Y.Fukuda*,
Dept.
of
Pathology*,
HYPERiROPHY H.Simada**.
&tend0
ASSOCIATED Research
University
WITH ISCHEMIC Laboratorv
and
Dept.
HEART DISEASE for Cardiovas-
of bathology,
Tokyo
Metropolitan Geriatric Hospital**, Tokyo, Japan. To clarify mode of myocardial hypertrophy in cases with ischemic heart disease, 15 cases with subendocardial infarction (SE), 27 with transmural infarction (TM), 20 with non-infarcted 3 vessel disease (3VD), and 17 of control were histopathologically examined. The average heart weight was 4629 in SE, 3949 in TM, 3189 in 3VD, and 3149 in control. The average luminal size of the left ventricle was 30.4mm in diameter in SE, 28.6 mm in TM, 18.2nnn in 3VD, and 17.3mm in control. The average size of myocytes was 24.7~ in diameter without difference by locations in SE cases. It was 22.9u at the proximal area to the infarct and 20.7~ at the distal area in TM cases. It was 18.4~ in 3VD cases compared with 12.5~ in control. The gross infarcted area was 26.7% in SE and 22.3% in TM. The myocardial non-infarcted area was 12.4% in SE, 10.1% in TM,17.8% in 3VDand 4.2% in control. The number of myocyte layer in stratum compactum counted along the ventrical line to the luminal surface was 203 in SE, 383 in TM, 324 in 3VD and 329 in control. Because the grade of hypertrophy was more prominent in SE than TM, according to more extensive infarcted area, fibrosis area, and larger luminal size and heart weight though less number of myocyte layers, it concluded that myocardial ischemia promotes hypertrophy through compensatory mechanism for loss of contracting capacity due to fibrosis replacing myocyte loss and increased mechanical load resulted by luminal dilatation.
P48INVESTIGATION OF THE LEUCYL-tRNA SYNTHETASE FROM PIG HEART DURING MYOCARDIAL ISCHEMIA. R. Stapulionis, I. Daukantaite. Kaunas Medical Institute, Central Research Laboratory, Kaunas. Lithuanian SSR. USSR. Some properties of free and aggregated-forms of 1eucylltRNA synthetase from normal pig myocardium and after 15 and 30 min of total myocardial ischemia have been compared. Free enzyme both from normal tid ischemic myocardium possesses-one polypeptidic chain with Mr IjO kDa and sedimentation constant 8 S. High-molecular weight camplex is composed at least from six aminoacyl-tRNA synthetases and has M, 840 kDa. No significant differences in Km and V,,& values for free and aggregated leucyl-tRNA svnthetase durina ischemla were observed. Free enzyme appears to be more thermolabile in comparison with the complexed. Free enzyme from normal myocardium is more resistant to thermoinactivation than that from ischemic mvocardium. After 15 min of total ischemia the leucyl-tRNA synthetase activity translocates partly into the complex, whereas 30 min ischemia exhibits this activity in the fraction of free enzyme, what may be one of the possibilities for changes in intensity and rate of protein biosynthesis during myocardial ischemia. S.25