1996 Fiscal Year Final Research Report Summary
脳血管攣縮の平滑筋細胞障害におけるアポトーシスの関与とサイトカインの効果の研究
| Project/Area Number |
07671501
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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 |
Cerebral neurosurgery
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| Research Institution | Dokkyo University School of Medicine (1996)
The University of Tokyo (1995) |
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Principal Investigator |
KIM Phyo Dokkyo University School of Medicine, Associate Professor, 医学部, 助教授 (90231290)
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| Co-Investigator(Kenkyū-buntansha) |
ASAI Akio University of Tokyo Hospital, Lecture, 医学部, 講師 (50231858)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Intracellular calcium / Basilar artery / Dog / Cerebral arterial spasm / Viability / Smooth muscle / Subarachnoid hemorrhage / Fura-2 |
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| Research Abstract |
The intracellular calcium level was determined in the canine basilar artery in order to investigate whether Ca2+ regulation of its smooth muscle is altered during chronic vasospasm following subarachnoid hemorrhage. A double hemorrhage model was used. The occurrence of vasospasm was confirmed angiographically seven days after initial hemorrhage. The intracellular calcium concentration ( [Ca2+] i) of smooth muscle was measured using Fura-2. Fluorescence to excitation at 340 and 356 nm was monitored and the ratio R340/356 was used as the indicator of [Ca2+] i. When the extracellular calcium concentration ( [Ca2+] e) was increased from pCa 8 to 2, [Ca2+] i also increased. In the spastic arteries, the [Ca2+] e- [Ca2+] i curve was elevated as compared to the normal rteries. Treatment with ionomycin elevated the curve in the normal group, but it had little effect in the spastic arteries. Values of [Ca2+] i, calculated in multiples of Kd, were greater in the spastic arteries. Diltiazem (10-5 mol/l) partially suppressed the augmented [Ca2+] i signal in the spastic arteries, whereas it did not affect the curve in the control group. These results indicate that calcium regulation of smooth muscle impaired after subarachnoid hemorrhage, which may contribute to the pathogenesis of chronic vasospasm.
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