contraction mechanisms of blood vessels in the liver to cause anaphylactic shock
Project/Area Number |
25462827
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Emergency medicine
|
Research Institution | Nagoya City University |
Principal Investigator |
Takano Hiromichi 名古屋市立大学, 医学(系)研究科(研究院), 助教 (70410313)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
Keywords | アナフィラキシー / 肝臓 / 循環 / 肝静脈 / ショック / 収縮 |
Outline of Final Research Achievements |
The hepatic vein was isolated from the liver in guinea pig and was measured the vasoconstriction and the intracellular Ca2+ concentration. By the transmural nerve stimulation (TNS) transiently increased the tension of the vein. Phenylephrine increased the tension. These responses were not inhibited by nifedipne. Cyclopiazonic acid (CPA) and Y-27632 inhibited the responses. TNS also elicited a transient increase of the cytosolic Ca2+ concentrationx The response was inhibited in presence of tetrodotoxin or phentolamin. Phenylephrine also increased the cytosolic Ca2+. These cytosolic Ca2+ responses were inhibited in presence of CPA. These results suggest that, in the guinea pig hepatic vein, adrenergic nerves stimulate α receptor, which induce the increase of the cytosolic Ca2+ mainly through the intracellular Ca2+ stores or ROK signal, and evoked vasoconstriction to increase the vascular resistance.
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Report
(4 results)
Research Products
(6 results)