Studies on the alterations of lung endothelial cells and the metabolism of autacoids during lung diseases

肺部疾病过程中肺内皮细胞变化及自体物质代谢的研究

基本信息

批准号：
60480095
负责人：
ITO Katsuaki
金额：
$ 2.05万
依托单位：
Miyazaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1985
资助国家：
日本
起止时间：
1985 至 1986
项目状态：
已结题

项目摘要

To learn how lung vascular injury alters the function to metabolize vaso-active autacoids, lung vascular lesions were produced in rats by a single injection of monocrotaline.Three to five weeks after the injection the degeneration or necrotization of lung endothelial cells was observed. When the metabolism of autacoids in lung was evaluated from the difference of responses to i.v. and i.a. injections of substances, the degradation of prostaglandin (PG) <E_2> was suppressed during the monocrotaline-induced lung injury, while the conversion of angiotensin- (A ) to angiotensin- <II> (A <II> ) and the degradation of bradykinin were unaffected.In the next experiments, the effects of autacoids on the mechanical property of pulmonary artery rings isolated from control and monocrotaline-treated rats were examined. Acetylcholine-induced relaxation of rings precontracted by noradrenaline was suppressed in monocrotaline-injured artery suggesting that the production of endothelium-derived relaxing factor (EDRF) is decreased during lung vascular injury. The contraction induced by <PGF_(2> alpha <)> was enhanced in either monocrotaline-injured artery or de-endothelialized artery by rubbing. This enhancement was considered to be due to decreased degradation of PG by endothelial cells. On the other hand, the conversion of A was not altered by endothelial injury because A was probably converted to A <II> by the enzyme present in other sites than endothelium. Canine and bovine pulmonary artery endothelium showed the characteristics similar to that of rats.It is suggested that lung vascular injury impaires the production of EDRF, which may cause pulmonary hypertension, and that the injury may alter the pulmonary and systemic hemodynamics and fluid-electrolyte balance as a result of decreased metabolism of PGs in pulmonary endothelium.

为了了解肺血管损伤如何改变代谢血管活性自动赛的功能，通过单次注射单蛋白单激素的单脂蛋白在大鼠中产生肺血管病变。注射后五个星期后，观察了肺部内皮细胞的变性或坏死。从对静脉注射的反应差异评估肺中自闭症的代谢。和I.A.物质注射，前列腺素（PG）<e_2>在单激素引起的肺损伤过程中受到抑制，而血管紧张素 - （A ）的转化为血管紧张素 - <ii>（A <ii>）（a <ii>），以及bradykimin decrantiars n of BradySirents。检查了从对照组中分离出的动脉环，检查了单脂素治疗的大鼠。乙酰胆碱诱导的环的松弛在北肾上腺素造成的动脉中被抑制，这表明在肺血管损伤过程中，源自内皮细胞衍生的松弛因子（EDRF）的产生减少。 <pgf_（2> alpha <）>诱导的收缩在损害的动脉或通过摩擦的动脉中增强了。这种增强被认为是由于内皮细胞降低Pg的原因。另一方面，A 的转化并没有因内皮损伤而改变，因为A 可能被其他部位的酶转化为A <ii>。 Canine and bovine pulmonary artery endothelium showed the characteristics similar to that of rats.It is suggested that lung vascular injury impaires the production of EDRF, which may cause pulmonary hypertension, and that the injury may alter the pulmonary and systemic hemodynamics and fluid-electrolyte balance as a result of decreased metabolism of PGs in pulmonary endothelium.