| Project/Area Number |
19592087
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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 |
Emergency medicine
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| Research Institution | Gunma University |
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Principal Investigator |
HINOHARA Hiroshi Gunma University, 医学部, 助教 (70361376)
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| Co-Investigator(Kenkyū-buntansha) |
KADOI Yuji 群馬大学, 医学部, 准教授 (10292591)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 敗血症 / Vasopressin / 糖尿病 / 循環動態 / NO / 腸間脈動脈 / 血管反応性 / Nitric oxide / 免疫抑制 / 鎮静薬 / 集中治療 |
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| Research Abstract |
Purpose : The purpose of this study was to compare the effects of norepinephrine (NE) and vasopressin on systemic hemodynamics, renal and mesenteric artery blood flow, inflammatory response and inducible nitric oxide synthase (iNOS) activity during endotoxin shock in streptozotocin-induced diabetic rats.
Methods : The study was designed to include 3 sets of experiments : 1) measurement of changes in systemic hemodynamics and mesenteric and renal artery blood flow ; 2) measurement of biochemical variables ; and 3) measurement of iNOS activity in the mesenteric artery. Systemic hemodynamics, regional artery blood flow changes and biochemical variables were assessed before treatment and 1, 2 and 3 h after treatment.
Results : Vasopressin, but not NE, prevented the decreases in aortic blood flow, but did not restore mesenteric artery blood flow. In addition, vasopressin partially restored renal artery blood flow in diabetic rats. Plasma nitrite levels and iNOS activity in the mesenteric artery were elevated after intravenous LPS in diabetic rats. Endotoxin-induced decreases in mesenteric arterial blood flow were partially restored by vasopressin with non-selective NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), in diabetic rats. Moreover, L-NAME prevented increases in plasma nitrite levels and iNOS activity in the mesenteric artery. In contrast, endotoxin-induced decreases in renal arterial blood flow were partially restored by vasopressin with L-NAME, but not by NE in diabetic rats.
Conclusions : Nitric oxide may be one possible contributor to reduced sensitivity of the mesenteric and renal arteries to vasopressin during septic shock in streptozotocin-induced diabetic rats.
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