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Relation between ischemic preconditioning and the duration of sustained ischemia.

It has been reported that repetitive brief periods of ischemia and reperfusion (ischemic preconditioning, IP) cause a significant reduction in the extent of myocardial necrosis or in the incidence of reperfusion arrhythmias in rat heart. However, recent reports have stated that IP effect is diminish...

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Autores principales: Kim, D. J., Kim, H., Park, J. I., Shim, T. S., Rah, B. J., Kim, H. D.
Formato: Texto
Lenguaje:English
Publicado: Korean Academy of Medical Sciences 1995
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3054136/
https://www.ncbi.nlm.nih.gov/pubmed/7576292
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author Kim, D. J.
Kim, H.
Park, J. I.
Shim, T. S.
Rah, B. J.
Kim, H. D.
author_facet Kim, D. J.
Kim, H.
Park, J. I.
Shim, T. S.
Rah, B. J.
Kim, H. D.
author_sort Kim, D. J.
collection PubMed
description It has been reported that repetitive brief periods of ischemia and reperfusion (ischemic preconditioning, IP) cause a significant reduction in the extent of myocardial necrosis or in the incidence of reperfusion arrhythmias in rat heart. However, recent reports have stated that IP effect is diminished or lost in the canine or bovine heart if ischemia (mostly regional) is sustained for 40 min or longer. The main objective of this study is to assess whether IP provides myocardial protection in prolonged sustained ischemia under the condition of global ischemia in isolated rabbit heart. The hearts were subjected to 10-60 min sustained ischemia (SI) followed by 60 min reperfusion with (IP heart) or without IP (ISCH heart). IP was induced by 4 cycles of 5 min global ischemia and 5 min reperfusion. Left ventricular function (LVF), extent of infarction (EI) and ultrastructural changes were examined. As a whole, the LVF began to recover on reperfusion but there was no significant difference in the functional parameters. However, extracellular Ca2+ concentration was lower in the ISCH hearts (p < 0.05) and the EI was significantly different between the hearts which had received 60 min SI (67% in the ISCH versus 32% in the IP heart, p < 0.01). Ultrastructural changes were homogeneous in the ISCH hearts and became irreversible in accordance with increase of the duration of ischemia, while these changes were heterogeneous and restricted in the IP heart. These results suggest that IP does not attenuate the postischemic dysfunction in prolonged ischemia but it can provide an infarct size-limiting effect and delay ultrastructural changes. This cardioprotective effect may be related to calcium homeostasis.
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spelling pubmed-30541362011-03-15 Relation between ischemic preconditioning and the duration of sustained ischemia. Kim, D. J. Kim, H. Park, J. I. Shim, T. S. Rah, B. J. Kim, H. D. J Korean Med Sci Research Article It has been reported that repetitive brief periods of ischemia and reperfusion (ischemic preconditioning, IP) cause a significant reduction in the extent of myocardial necrosis or in the incidence of reperfusion arrhythmias in rat heart. However, recent reports have stated that IP effect is diminished or lost in the canine or bovine heart if ischemia (mostly regional) is sustained for 40 min or longer. The main objective of this study is to assess whether IP provides myocardial protection in prolonged sustained ischemia under the condition of global ischemia in isolated rabbit heart. The hearts were subjected to 10-60 min sustained ischemia (SI) followed by 60 min reperfusion with (IP heart) or without IP (ISCH heart). IP was induced by 4 cycles of 5 min global ischemia and 5 min reperfusion. Left ventricular function (LVF), extent of infarction (EI) and ultrastructural changes were examined. As a whole, the LVF began to recover on reperfusion but there was no significant difference in the functional parameters. However, extracellular Ca2+ concentration was lower in the ISCH hearts (p < 0.05) and the EI was significantly different between the hearts which had received 60 min SI (67% in the ISCH versus 32% in the IP heart, p < 0.01). Ultrastructural changes were homogeneous in the ISCH hearts and became irreversible in accordance with increase of the duration of ischemia, while these changes were heterogeneous and restricted in the IP heart. These results suggest that IP does not attenuate the postischemic dysfunction in prolonged ischemia but it can provide an infarct size-limiting effect and delay ultrastructural changes. This cardioprotective effect may be related to calcium homeostasis. Korean Academy of Medical Sciences 1995-04 /pmc/articles/PMC3054136/ /pubmed/7576292 Text en
spellingShingle Research Article
Kim, D. J.
Kim, H.
Park, J. I.
Shim, T. S.
Rah, B. J.
Kim, H. D.
Relation between ischemic preconditioning and the duration of sustained ischemia.
title Relation between ischemic preconditioning and the duration of sustained ischemia.
title_full Relation between ischemic preconditioning and the duration of sustained ischemia.
title_fullStr Relation between ischemic preconditioning and the duration of sustained ischemia.
title_full_unstemmed Relation between ischemic preconditioning and the duration of sustained ischemia.
title_short Relation between ischemic preconditioning and the duration of sustained ischemia.
title_sort relation between ischemic preconditioning and the duration of sustained ischemia.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3054136/
https://www.ncbi.nlm.nih.gov/pubmed/7576292
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