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Effects of prolonged NO inhalation on calcium concentration in pulmonary arteries.

Effects of prolonged NO inhalation on calcium concentration in pulmonary arteries.
长期吸入一氧化氮对肺动脉钙浓度的影响。
批准号:
07457354
负责人:
MARUYAMA Kazuo
金额:
$3.01万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
1995
资助国家:
日本
项目状态:
已结题
起止时间:
1995 至 1996

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中文摘要
翻译
用CAF-110同时测定大鼠离体肺动脉细胞内游离钙离子浓度和血管张力。钙指示剂Fura-2负载3h。在离体肺动脉中,F340/F380在无任何激动剂的情况下持续下降,而在体循环中则不同。这种自发的F340/F380下降可被消炎痛逆转。我们的结论是,在没有吲哚美辛的情况下,不能测定大鼠离体主动脉的基线F340/F380。细胞内钙离子在血管张力控制中起着重要作用。最近的研究表明,钙的滞留或分布对决定细胞功能是重要的,钙微域调节特定的细胞功能。换句话说,钙分布的改变可能在不改变细胞内总钙含量的情况下调节细胞功能。在本研究中,高钾诱导了正常和高血压大鼠肺动脉细胞内钙离子的增加。去甲肾上腺素和前列腺素F2α也可引起细胞内钙离子浓度升高,但幅度小于KCL。NO供体硝普钠(SNP)的松弛作用与钙通道阻滞剂维拉帕米相似,但SNP对细胞内钙离子浓度的降低幅度远小于维拉帕米。这一发现可能表明,NO诱导的松弛部分是通过改变细胞内的钙分布来实现的。另一种可能性可能是NO改变了收缩蛋白中的钙敏感性。
英文摘要
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.
期刊论文(8)
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会议论文
Yoshida M.et al.: "Combined inhalation of nitric oxide and oxygen in chronic obstructive pulmonary disease" Am.J.Respir.Crit.Care Med.155(in press). (1997)
Yoshida M.等人:“慢性阻塞性肺疾病中一氧化氮和氧气的联合吸入”Am.J.Respir.Crit.Care Med.155(印刷中)。
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Maruyama J. et al.: "Continuous low-dose NO inhalation does not prevent morocrotaline-induced pulmonary hypertension in rats" Am. J. Physiol.272. H517-H527 (1997)
Maruyama J. 等人:“连续吸入低剂量 NO 并不能预防莫罗百他林引起的大鼠肺动脉高压”Am。
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通讯作者:
Yoshida M., Taguchi O., Gabazza EC., Kobayashi T., Yamakami T., Kobayashi H., Maruyama K., Shima T.: "Combined inhalation of nitric oxide and oxygen in chronic obstructive pulmonary disease." Am J Respir Crit Care Med. 155. 526-529 (1997)
Yoshida M.、Taguchi O.、Gabazza EC.、Kobayashi T.、Yamakami T.、Kobayashi H.、Maruyama K.、Shima T.:“一氧化氮和氧气联合吸入治疗慢性阻塞性肺病。”
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通讯作者:
丸山一男: "肺高血圧血管病変とNO" 医学のあゆみ(別冊)NOのすべて. 258-262 (1996)
Kazuo Maruyama:《肺动脉高压血管病变与NO》医学史(分册)全部关于NO.258-262(1996)
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