| Beneficial actions of preconditioning and stretch on postischemic contractile function of isolated working rat heart: effects of staurosporine. | |
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MedLine Citation:
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PMID: 9269946 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Preconditioning is commonly induced by a brief ischemic insult; myocardial stretch can trigger this protection by an unknown mechanism. Myocardial stretch preconditions the in vivo canine heart; however, the existence of a stretch-induced protection in the rat heart remains unknown. The purpose of this study was to test this myocardial protection induced, in isolated working rat heart, by global ischemia and stretch initiated by a transient increase in the left ventricle (LV). Isolated rat hearts underwent 30 min of global ischemia followed by 30 min of reperfusion. Before this, hearts received a 15-min period of either no intervention (control; C), 5 min of global ischemia + 10 min of reperfusion (preconditioning; PC) or 5 min of stretch + 10 min with no intervention (stretch; S). Stretch was induced by a transient increase in LV preload from 5 to 20 cm H2O. LV work started under a afterload of 80 cm H2O. Control, PC, and S hearts received either no drug (untreated) or staurosporine (50 nM), a protein kinase C inhibitor, before the "preconditioning" period. Creatine kinase (CK) release, ventricular fibrillation during reperfusion, and postischemic recovery of contractile function (aortic flow) were the end points of the study. In the S group, the abrupt increase in preload resulted in a significant increase of aortic flow (42 +/- 2 to 47 +/- 2 ml/min; p < 0.05). During the 30-min reperfusion period, control hearts displayed a poor recovery of contractile functions (8 +/- 3 ml/min, 30 min after reflow, versus 40 +/- 2 ml/min at baseline; p < 0.05). Both untreated PC and S groups exhibited a significant reduction in CK release, incidence of ventricular fibrillation (55% of control hearts developed persistent VF vs. 6% in both the PC and S groups), and postischemic dysfunction during reperfusion (p < 0.05 vs. control). Staurosporine prevented these beneficial effects in PC and S groups. Our study suggests that myocardial protection can be induced by stretch in the isolated working rat heart, likely through activation of protein kinase C. In conclusion, our results show that ischemic preconditioning and stretch had comparable favorable effect on functional recovery after a sustained ischemic insult in the isolated rat heart. |
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Authors:
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J F Obadia; M Ovize; V Maupoil; J Terrand; C Abadie; A Ovize; X Andre-Fouët; Y Minaire; L Rochette |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cardiovascular pharmacology Volume: 30 ISSN: 0160-2446 ISO Abbreviation: J. Cardiovasc. Pharmacol. Publication Date: 1997 Aug |
Date Detail:
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Created Date: 1997-10-01 Completed Date: 1997-10-01 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7902492 Medline TA: J Cardiovasc Pharmacol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 191-6 Citation Subset: IM |
Affiliation:
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Hopital Cardiologique Louis Pradel, Lyon, France. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arrhythmias, Cardiac / physiopathology Coronary Circulation / drug effects, physiology Creatine Kinase / metabolism Enzyme Inhibitors / pharmacology* Heart / physiology*, physiopathology* Heart Rate / drug effects, physiology Ischemic Preconditioning, Myocardial* Male Myocardial Contraction / drug effects, physiology Myocardial Ischemia / physiopathology* Myocardium / enzymology Protein Kinase C / antagonists & inhibitors* Rats Rats, Wistar Staurosporine / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 62996-74-1/Staurosporine; EC 2.7.11.13/Protein Kinase C; EC 2.7.3.2/Creatine Kinase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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