| Project/Area Number |
07457354
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Mie University |
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Principal Investigator |
MARUYAMA Kazuo Mie University, Faculty of Medicine, Professor, 医学部, 教授 (20181828)
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| Co-Investigator(Kenkyū-buntansha) |
MURASE Sumio Mie University, Hospital, Associate Professor, 医学部・附属病院, 助教授 (70200285)
MARUYAMA Junko Mie University, Faculty of Medicine, Assistant Professor, 医学部, 講師 (50263017)
宗行 万之助 三重県立総合医療センター, 院長(研究者)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥3,800,000 (Direct Cost: ¥3,800,000)
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| Keywords | NO / pulmonary hypertension / calcium / NO吸入 |
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| Research Abstract |
We measured intracellular free calcium ion concentration and vascular tension at the same time in isolated pulmonary artery from rats using CAF-110. Calcium indicator fura-2 was loaded for 3 hours. In isolated pulmonary arteries F340/F380 declined continuously without any agonist, which was different phenomenon in systemic artery. This spontaneous decline in F340/F380 was abolished with indomethacin. We concluded that baseline F340/F380 could not be determined without indomethacin in isolated rat conduit pulmonary artery. Intracellular calcium plays an important role in the control of vascular tension. Recent studies have suggested that the calcium sequestration or distribution is important to determine cell function and that the calcium microdomain regulates specific cell function. In another word, changes in distribution of calcium might regulate cell function without changes in total calcium amount in the cell. In the present study high KCL induced the increase in intracellular calcium in both normal and hypertensive pulmonary arteries in rats. Norepinephrine and prostagrandin F2 alpha also induced the rise in the intracellular calcium concentration, but the magnitude is less than in KCL.Sodium nitroprusside (SNP), an No donor, induced similar relaxation with calcium channel blocker, verapamil, but the reduction of calcium ion concentration in the cell by SNP was much less than by verapamil. This finding might suggest that NO induced relaxation partly by changing calcium distribution in the cell. Another possibility might be that NO alters calcium sensitivity in the contractile protein.
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