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Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents
BACKGROUND: Although clinical diabetes mellitus is obviously a high risk factor for myocardial infarction (MI), in experimental studies disagreement exists about the sensitivity to ischemic injury of an infarcted myocardium. Recently, our group demonstrated that diabetic animals presented better car...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084163/ https://www.ncbi.nlm.nih.gov/pubmed/21470409 http://dx.doi.org/10.1186/1475-2840-10-26 |
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author | Rodrigues, Bruno Rosa, Kaleizu T Medeiros, Alessandra Schaan, Beatriz D Brum, Patricia C De Angelis, Kátia Irigoyen, Maria Cláudia |
author_facet | Rodrigues, Bruno Rosa, Kaleizu T Medeiros, Alessandra Schaan, Beatriz D Brum, Patricia C De Angelis, Kátia Irigoyen, Maria Cláudia |
author_sort | Rodrigues, Bruno |
collection | PubMed |
description | BACKGROUND: Although clinical diabetes mellitus is obviously a high risk factor for myocardial infarction (MI), in experimental studies disagreement exists about the sensitivity to ischemic injury of an infarcted myocardium. Recently, our group demonstrated that diabetic animals presented better cardiac function recovery and cellular resistance to ischemic injury than nondiabetics. In the present study, we evaluated the chronic effects of MI on left ventricular (LV) and autonomic functions in streptozotocin (STZ) diabetic rats. METHODS: Male Wistar rats were divided into 4 groups: control (C, n = 15), diabetes (D, n = 16), MI (I, n = 21), and diabetes + MI (DI, n = 30). MI was induced 15 days after diabetes (STZ) induction. Ninety days after MI, LV and autonomic functions were evaluated (8 animals each group). Left ventricular homogenates were analyzed by Western blotting to evaluate the expression of calcium handling proteins. RESULTS: MI area was similar in infarcted groups (~43%). Ejection fraction and +dP/dt were reduced in I compared with DI. End-diastolic pressure was additionally increased in I compared with DI. Compared with DI, I had increased Na(+)-Ca(2+ )exchange and phospholamban expression (164%) and decreased phosphorylated phospholamban at serine(16 )(65%) and threonine(17 )(70%) expression. Nevertheless, diabetic groups had greater autonomic dysfunction, observed by baroreflex sensitivity and pulse interval variability reductions. Consequently, the mortality rate was increased in DI compared with I, D, and C groups. CONCLUSIONS: LV dysfunction in diabetic animals was attenuated after 90 days of myocardial infarction and was associated with a better profile of calcium handling proteins. However, this positive adaptation was not able to reduce the mortality rate of DI animals, suggesting that autonomic dysfunction is associated with increased mortality in this group. Therefore, it is possible that the better cardiac function has been transitory, and the autonomic dysfunction, more prominent in diabetic group, may lead, in the future, to the cardiovascular damage. |
format | Text |
id | pubmed-3084163 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30841632011-04-29 Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents Rodrigues, Bruno Rosa, Kaleizu T Medeiros, Alessandra Schaan, Beatriz D Brum, Patricia C De Angelis, Kátia Irigoyen, Maria Cláudia Cardiovasc Diabetol Original Investigation BACKGROUND: Although clinical diabetes mellitus is obviously a high risk factor for myocardial infarction (MI), in experimental studies disagreement exists about the sensitivity to ischemic injury of an infarcted myocardium. Recently, our group demonstrated that diabetic animals presented better cardiac function recovery and cellular resistance to ischemic injury than nondiabetics. In the present study, we evaluated the chronic effects of MI on left ventricular (LV) and autonomic functions in streptozotocin (STZ) diabetic rats. METHODS: Male Wistar rats were divided into 4 groups: control (C, n = 15), diabetes (D, n = 16), MI (I, n = 21), and diabetes + MI (DI, n = 30). MI was induced 15 days after diabetes (STZ) induction. Ninety days after MI, LV and autonomic functions were evaluated (8 animals each group). Left ventricular homogenates were analyzed by Western blotting to evaluate the expression of calcium handling proteins. RESULTS: MI area was similar in infarcted groups (~43%). Ejection fraction and +dP/dt were reduced in I compared with DI. End-diastolic pressure was additionally increased in I compared with DI. Compared with DI, I had increased Na(+)-Ca(2+ )exchange and phospholamban expression (164%) and decreased phosphorylated phospholamban at serine(16 )(65%) and threonine(17 )(70%) expression. Nevertheless, diabetic groups had greater autonomic dysfunction, observed by baroreflex sensitivity and pulse interval variability reductions. Consequently, the mortality rate was increased in DI compared with I, D, and C groups. CONCLUSIONS: LV dysfunction in diabetic animals was attenuated after 90 days of myocardial infarction and was associated with a better profile of calcium handling proteins. However, this positive adaptation was not able to reduce the mortality rate of DI animals, suggesting that autonomic dysfunction is associated with increased mortality in this group. Therefore, it is possible that the better cardiac function has been transitory, and the autonomic dysfunction, more prominent in diabetic group, may lead, in the future, to the cardiovascular damage. BioMed Central 2011-04-06 /pmc/articles/PMC3084163/ /pubmed/21470409 http://dx.doi.org/10.1186/1475-2840-10-26 Text en Copyright ©2011 Rodrigues et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Investigation Rodrigues, Bruno Rosa, Kaleizu T Medeiros, Alessandra Schaan, Beatriz D Brum, Patricia C De Angelis, Kátia Irigoyen, Maria Cláudia Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents |
title | Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents |
title_full | Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents |
title_fullStr | Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents |
title_full_unstemmed | Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents |
title_short | Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents |
title_sort | hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084163/ https://www.ncbi.nlm.nih.gov/pubmed/21470409 http://dx.doi.org/10.1186/1475-2840-10-26 |
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