Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats
Autor(a) principal: | |
---|---|
Data de Publicação: | 1997 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1590/S0100-879X1997000900013 http://hdl.handle.net/11449/28051 |
Resumo: | The pathogenesis of fibrosis and the functional features of pressure overload myocardial hypertrophy are still controversial. The objectives of the present study were to evaluate the function and morphology of the hypertrophied myocardium in renovascular hypertensive (RHT) rats. Male Wistar rats were sacrificed at week 4 (RHT4) and 8 (RHT8) after unilateral renal ischemia (Goldblatt II hypertension model). Normotensive rats were used as controls. Myocardial function was analyzed in isolated papillary muscle preparations, morphological features were defined by light microscopy, and myocardial hydroxyproline concentration (HOP) was determined by spectrophotometry. Renal artery clipping resulted in elevated systolic arterial pressure (RHT4: 178 ± 19 mmHg and RHT8: 194 ± 24 mmHg, P<0.05 vs control: 123 ± 7 mmHg). Myocardial hypertrophy was observed in both renovascular hypertensive groups. The myocardial HOP concentration was increased in the RHT8 group (control: 2.93 ± 0.38 µg/mg; RHT4: 3.02 ± 0.40 µg/mg; RHT8: 3.44 ± 0.45 µg/mg of dry tissue, P<0.05 vs control and RHT4 groups). The morphological study demonstrated myocyte necrosis, vascular damage and cellular inflammatory response throughout the experimental period. The increased cellularity was more intense in the adventitia of the arterioles. As a consequence of myocyte necrosis, there was an early, local, conjunctive stroma collapse with disarray and thickening of the argyrophilic interstitial fibers, followed by scarring. The functional data showed an increased passive myocardial stiffness in the RHT4 group. We conclude that renovascular hypertension induces myocyte and arteriole necrosis. Reparative fibrosis occurred as a consequence of the inflammatory response to necrosis. The mechanical behavior of the isolated papillary muscle was normal, except for an early increased myocardial passive stiffness |
id |
UNSP_e738d484bd918e5d8404d68b10d628a7 |
---|---|
oai_identifier_str |
oai:repositorio.unesp.br:11449/28051 |
network_acronym_str |
UNSP |
network_name_str |
Repositório Institucional da UNESP |
repository_id_str |
2946 |
spelling |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive ratscoronary vascular remodelingmyocardial functionpressure overload hypertrophypapillary musclereparative fibThe pathogenesis of fibrosis and the functional features of pressure overload myocardial hypertrophy are still controversial. The objectives of the present study were to evaluate the function and morphology of the hypertrophied myocardium in renovascular hypertensive (RHT) rats. Male Wistar rats were sacrificed at week 4 (RHT4) and 8 (RHT8) after unilateral renal ischemia (Goldblatt II hypertension model). Normotensive rats were used as controls. Myocardial function was analyzed in isolated papillary muscle preparations, morphological features were defined by light microscopy, and myocardial hydroxyproline concentration (HOP) was determined by spectrophotometry. Renal artery clipping resulted in elevated systolic arterial pressure (RHT4: 178 ± 19 mmHg and RHT8: 194 ± 24 mmHg, P<0.05 vs control: 123 ± 7 mmHg). Myocardial hypertrophy was observed in both renovascular hypertensive groups. The myocardial HOP concentration was increased in the RHT8 group (control: 2.93 ± 0.38 µg/mg; RHT4: 3.02 ± 0.40 µg/mg; RHT8: 3.44 ± 0.45 µg/mg of dry tissue, P<0.05 vs control and RHT4 groups). The morphological study demonstrated myocyte necrosis, vascular damage and cellular inflammatory response throughout the experimental period. The increased cellularity was more intense in the adventitia of the arterioles. As a consequence of myocyte necrosis, there was an early, local, conjunctive stroma collapse with disarray and thickening of the argyrophilic interstitial fibers, followed by scarring. The functional data showed an increased passive myocardial stiffness in the RHT4 group. We conclude that renovascular hypertension induces myocyte and arteriole necrosis. Reparative fibrosis occurred as a consequence of the inflammatory response to necrosis. The mechanical behavior of the isolated papillary muscle was normal, except for an early increased myocardial passive stiffnessA01Universidade Estadual PaulistaUniversidade Estadual PaulistaAssociação Brasileira de Divulgação Científica (ABRADIC)Universidade Estadual Paulista (Unesp)Okoshi, M.P.Matsubara, L.S.Franco, M. [UNESP]Cicogna, A.C.Matsubara, B.B.2014-05-20T15:11:29Z2014-05-20T15:11:29Z1997-09-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1135-1144application/pdfhttp://dx.doi.org/10.1590/S0100-879X1997000900013Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 30, n. 9, p. 1135-1144, 1997.0100-879Xhttp://hdl.handle.net/11449/2805110.1590/S0100-879X1997000900013S0100-879X1997000900013S0100-879X1997000900013.pdfSciELOreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengBrazilian Journal of Medical and Biological Research1.492info:eu-repo/semantics/openAccess2023-12-22T06:22:24Zoai:repositorio.unesp.br:11449/28051Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T21:00:34.255815Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats |
title |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats |
spellingShingle |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats Okoshi, M.P. coronary vascular remodeling myocardial function pressure overload hypertrophy papillary muscle reparative fib |
title_short |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats |
title_full |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats |
title_fullStr |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats |
title_full_unstemmed |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats |
title_sort |
Myocyte necrosis is the basis for fibrosis inrenovascular hypertensive rats |
author |
Okoshi, M.P. |
author_facet |
Okoshi, M.P. Matsubara, L.S. Franco, M. [UNESP] Cicogna, A.C. Matsubara, B.B. |
author_role |
author |
author2 |
Matsubara, L.S. Franco, M. [UNESP] Cicogna, A.C. Matsubara, B.B. |
author2_role |
author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (Unesp) |
dc.contributor.author.fl_str_mv |
Okoshi, M.P. Matsubara, L.S. Franco, M. [UNESP] Cicogna, A.C. Matsubara, B.B. |
dc.subject.por.fl_str_mv |
coronary vascular remodeling myocardial function pressure overload hypertrophy papillary muscle reparative fib |
topic |
coronary vascular remodeling myocardial function pressure overload hypertrophy papillary muscle reparative fib |
description |
The pathogenesis of fibrosis and the functional features of pressure overload myocardial hypertrophy are still controversial. The objectives of the present study were to evaluate the function and morphology of the hypertrophied myocardium in renovascular hypertensive (RHT) rats. Male Wistar rats were sacrificed at week 4 (RHT4) and 8 (RHT8) after unilateral renal ischemia (Goldblatt II hypertension model). Normotensive rats were used as controls. Myocardial function was analyzed in isolated papillary muscle preparations, morphological features were defined by light microscopy, and myocardial hydroxyproline concentration (HOP) was determined by spectrophotometry. Renal artery clipping resulted in elevated systolic arterial pressure (RHT4: 178 ± 19 mmHg and RHT8: 194 ± 24 mmHg, P<0.05 vs control: 123 ± 7 mmHg). Myocardial hypertrophy was observed in both renovascular hypertensive groups. The myocardial HOP concentration was increased in the RHT8 group (control: 2.93 ± 0.38 µg/mg; RHT4: 3.02 ± 0.40 µg/mg; RHT8: 3.44 ± 0.45 µg/mg of dry tissue, P<0.05 vs control and RHT4 groups). The morphological study demonstrated myocyte necrosis, vascular damage and cellular inflammatory response throughout the experimental period. The increased cellularity was more intense in the adventitia of the arterioles. As a consequence of myocyte necrosis, there was an early, local, conjunctive stroma collapse with disarray and thickening of the argyrophilic interstitial fibers, followed by scarring. The functional data showed an increased passive myocardial stiffness in the RHT4 group. We conclude that renovascular hypertension induces myocyte and arteriole necrosis. Reparative fibrosis occurred as a consequence of the inflammatory response to necrosis. The mechanical behavior of the isolated papillary muscle was normal, except for an early increased myocardial passive stiffness |
publishDate |
1997 |
dc.date.none.fl_str_mv |
1997-09-01 2014-05-20T15:11:29Z 2014-05-20T15:11:29Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1590/S0100-879X1997000900013 Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 30, n. 9, p. 1135-1144, 1997. 0100-879X http://hdl.handle.net/11449/28051 10.1590/S0100-879X1997000900013 S0100-879X1997000900013 S0100-879X1997000900013.pdf |
url |
http://dx.doi.org/10.1590/S0100-879X1997000900013 http://hdl.handle.net/11449/28051 |
identifier_str_mv |
Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 30, n. 9, p. 1135-1144, 1997. 0100-879X 10.1590/S0100-879X1997000900013 S0100-879X1997000900013 S0100-879X1997000900013.pdf |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Brazilian Journal of Medical and Biological Research 1.492 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
1135-1144 application/pdf |
dc.publisher.none.fl_str_mv |
Associação Brasileira de Divulgação Científica (ABRADIC) |
publisher.none.fl_str_mv |
Associação Brasileira de Divulgação Científica (ABRADIC) |
dc.source.none.fl_str_mv |
SciELO reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1808129273523863552 |