| Project/Area Number |
06454410
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | University of Tokyo |
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Principal Investigator |
SASAKI Tomio University of Tokyo, Dept.of Neurosurgery, Associate professor, 医学部(病), 助教授 (10134561)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMOTO Yuhei University of Tokyo, Dept.of Neurosurgery, Research Associate, 医学部(病), 助手 (50242061)
SAITO Nobuto University of Tokyo, Dept.of Neurosurgery, Research Associate, 医学部(病), 助手 (60262002)
KIM Phyo University of Tokyo, Dept.of Neurosurgery, Research Associate, 医学部(病), 助手 (90231290)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥5,700,000 (Direct Cost: ¥5,700,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1994: ¥4,600,000 (Direct Cost: ¥4,600,000)
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| Keywords | Cerebral Vasospasm / Calcium / Oxyhemoglobin / Subarachnoid Hemorrhage / オキシヘモグロビン / 平滑筋収縮 / カルシウムイオン |
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| Research Abstract |
The present study was undertaken to determine whether oxyhemoglobin (OxyHb) is responsible for the functional alterations in the cerebral arteries observed during chronic vasospasm after subarachnoid hemorrhage. Vascular strips of canine basilar arteries were kept in organ culture for 3 days with or without repetitive exposure to OxyHb (OxyHb-treated and control strips). Contractions elicited by high levels of potassium (80mM) and uridine 5'-triphosphate (310^<-4>M) were reduced in the OxyHb-treated group in a concentration-dependent manner. The relaxations evoked by nitric oxide and 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP) were not affected. Relaxations elicited by the calcium channel blocker, diltiazem, were attenuated in the OxyHb-treated rings, When the extracellular calcium concentration ([Ca^<++>] _e) was changed from a concentration in the external solution of 10^<-8> M to 10^<-3> M,myogenic tension developed. Myogenic tension, expressed as a percentage of the maximum contraction in each segment, was augmented in the OxyHb-treated group at [Ca^<++>] _e of 10^<-5> M and 10^<-4> M.There were no significant differences in passive compliance of the arterial wall between the two groups. These results demonstrated that prolonged exposure to OxyHb in vitro results in a decrease in contractile capacity and an increase in sensitivity to [Ca^<++>] _6, in agreement with previous findings in spastic arteries. By contrast, impairment of the 8-bromo-cGMP-mediated relaxation pathway and increased stiffnes of the arterial wall, which have been reported to occur in spastic arteries, were not induced by prolonged exposure to OxyHb in vitro.
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