2003 Fiscal Year Final Research Report Summary
Sympathetic innervation in rat cultured cardiac myocytes increases the effect of ischemic precondtioning
| Project/Area Number |
14570781
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Nippon Medical School |
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Principal Investigator |
OGAWA Shunichi Nippon Medical School, Pediatrics, Associate Professor, 医学部, 助教授 (50194436)
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| Co-Investigator(Kenkyū-buntansha) |
FUKAZAWA Ryuji Nippon Medical School, Pediatrics, Assistant Professor, 医学部, 講師 (80277566)
TATSUBE Yoshihiro Nippon Medical School, Pediatrics, Assistant Professor, 医学部, 講師 (20246523)
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| Project Period (FY) |
2002 – 2003
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| Keywords | cardiac myocyte / sympathetic nerve / co-culture / myocardial ischemia / ischemic precondition / K-ATP channel / current density / patch-clump |
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| Research Abstract |
To clarify whether sympathetic innervation protects myocardial disturbance caused by myocardial ischemeia in rat cardiac myocyte, we evaluated sarcolemmal or mitochondorial K_<ATP> channel currents induced by Pinacidil which is sarcolemmal channel opener, Cyanide which is metabolic inhibitor, and Diazoxide which is mitochondrial K_<ATP> channel opener in next cultured or co-cultured myocytes ; cultured myocytes using 1day old neonatal rat cardiac myocytes which was not sympathetic innervation until 1day old, co-cultured cardiac myocytes with sympathetic ganglion, and denervaed cardiac myocytes. Outward current of K_<ATP> channel was significantly increased after application of Pinacidil in sympathetic innervated myocytes (56.8±5.2^*) compared to those in myocytes (10.8±3.4) and denervated myocytes (9.8±3.1) (p<0.05). Almost same results were obtained by application of Cyanide and Diazoxide. These show that sarcolemmal and mitochondorial K_<ATP> channel currents were increased by sympatheic innervation. Increased K_<ATP> current leads shortening of ventricular myocardial action potential duration and may protect Ca^<2+> overloading in ischemic ventricular myocytes. Thus, sympathetic innervation could be protected myocardial disturbance in ischemic myocardium by activation of sarcolemmal and mitochondrial K_<ATP> channels.
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