| Project/Area Number |
14571447
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Nagasaki University |
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Principal Investigator |
MAKITA Tetsuji Nagasaki University, Hospital of Medicine and Dentistry, assistant professor, 医学部・歯学部附属病院, 講師 (00229337)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Toshiaki Nagasaki University, Hospital of Medicine and Dentistry, research associate, 医学部・歯学部附属病院, 助手 (00325656)
齋藤 将隆 長崎大学, 医学部附属病院, 助手 (00322305)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | septic shock / splanchnic circulation / vasoconstrictor / tonometry |
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| Research Abstract |
Sepsis continues to be the most common causes of death in intensive care units. However the complex pathophysiology of sepsis remains unknown, especially in regard to vascular tone during sepsis. We hypothesized that the vascular responses to vasoactive substances might be altered during sepsis and there might be different responses between pulmonary and systemic vasculatures. This study was carried out to clarify the responses to vasoactive substances of the thoracic artery(TA) and pulmonary artery(PA) from septicrats.
Wistar rats were treated with cecal ligation and puncture(CLP). Before CLP (control) and 10 or 16 hours after CLP, the PA and TA were dissected from the rats under anesthesia and cut into two or three 2-3 mm rings. The rings were mounted horizontally in organ chambers and stretched progressively to an optimal resting tension. The constriction of the rings was induced by adding norepinephrine (NE;1 microM) or KCl (100 mM) into the chamber.
NE evoked 1.15±0.12g and 1.03±0.15g tensions in control TA and PA, respectively. NE-induced constriction of TA was significantly reduced to 36% at 16hr after CLP. NE-induced constriction of PA was significantly reduced to 64% and 56% at 10hr and 16hr after CLP, respectively. KCl evoked 1.32±0.02g and 1.04±0.19g tensions in control TA and PA, respectively. KCl-induced constriction of TA was significantly reduced to 45% at 16hr after CLP. There was no significant change in KCl-induced constriction of PA either 10hr or 16hr after CLP.
The constrictive responses of TA and PA to NE are markedly reduced in the septic animal model in a time-related manner. KCl-induced constriction is also reduced in TA but not in PA during sepsis. Thus the mechanism involved in the reduced response of TA to NE would be a decreased Ca++ sensitivity of the contractile element but not a reduced activity of alpha-adrenoceptors. The results might account for the characteristic vasodilation during sepsis in clinical settings.
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