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缺氧对犬和兔基底动脉内皮依赖性舒张的影响。

Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries.

作者信息

Nakagomi T, Kassell N F, Sasaki T, Hongo K, Fujiwara S, Lehman R M, Vollmer D G

机构信息

Department of Neurosurgery, University of Tokyo Hospital, Japan.

出版信息

Acta Neurochir (Wien). 1989;97(1-2):77-82. doi: 10.1007/BF01577744.

Abstract

An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteries in vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in the in vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0 U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10(-6)M prostaglandin F2 alpha. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid.

摘要

内皮依赖性舒张在血管张力的局部调节中所起的重要作用已被提出。在本研究中,采用等长张力记录法,在体外对犬和兔的基底动脉以及兔的颈总动脉进行实验,研究了缺氧对内皮依赖性舒张的影响。通过将体外实验箱中的气体混合物由95%O₂ - 5%CO₂ 改为95%N₂ - 5%CO₂ 来引入缺氧状态。使用凝血酶和乙酰胆碱诱导内皮依赖性舒张。分别为0.1和1.0U/ml的凝血酶,可使由10⁻⁶M前列腺素F₂α预收缩的犬基底动脉产生剂量依赖性舒张。乙酰胆碱也能使由5-羟色胺预收缩的兔基底动脉和颈总动脉产生剂量依赖性舒张。在缺氧条件下,凝血酶或乙酰胆碱的舒张作用在犬和兔的动脉中均降低,尽管在兔基底动脉中不显著。据推测,蛛网膜下腔出血后,蛛网膜下腔血凝块可能会阻碍氧气向大脑主要动脉壁的扩散。这可能导致动脉缺氧,并通过抑制内皮依赖性舒张以及增强大脑动脉对血性脑脊液中血管收缩剂的收缩反应,从而促成血管痉挛。

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