中文摘要：

高血压引起的脑卒中、冠心病等严重并发症的发生,均与组织缺血/缺氧导致的动脉血管痉挛有关。为了研究高血压大鼠肠系膜血管缺血/缺氧后的功能学改变,本研究采用三气培养箱模拟缺血/缺氧条件处理自发性高血压大鼠（spontaneously hypertensive rats,SHR）肠系膜动脉血管环,运用敏感的肌张力描记技术测定血管环对不同血管活性物质的反应性。结果显示：与WKY组大鼠相比,SHR组大鼠肠系膜动脉血管对收缩剂KCl和苯肾上腺素（phenylephrine,PE）的反应性明显提高,对内皮依赖的血管舒张剂乙酰胆碱（acetylcholine,ACh）的反应性显著降低;而与SHR组和急性缺血/缺氧对照（WKY＋H）组相比较,高血压合并急性缺血/缺氧（SHR＋H）组对KCl和PE的收缩反应显著性增加,对ACh的舒张反应明显降低。N-硝基-L-精氨酸甲酯（L-NAME）存在时,SHR＋H组和SHR组血管环对ACh的舒张反应没有明显变化,而WKY组血管对ACh的舒张反应显著降低。与SHR组相比,SHR＋H组CaCl2诱导的钙依赖性收缩曲线明显左移。在无钙K-H液中,SHR＋H组PE和咖啡因（caffeine）诱导的血管收缩较WKY＋H组显著增加,SHR组PE和caffeine诱导的血管收缩也显著高于WKY组;与SHR组相比,SHR＋H组PE诱导的血管收缩明显增加,而caffeine诱导的血管收缩无显著性改变。以上结果显示,高血压可使大鼠肠系膜动脉血管功能受损,而合并缺血/缺氧使血管损伤程度更为严重,提示急性缺血/缺氧可加剧高血压大鼠肠系膜收缩/舒张功能紊乱,其机制可能与降低血管内皮细胞NO合成、增加细胞内肌浆网钙离子释放有关。

英文摘要：

Hypertension is a common cardiovascular disease and can induce many complications, such as stroke and coronary heart disease. The purpose of the present study was to investigate the effect of ischemia/hypoxia on mesenteric artery vasomotor function in spontaneously hypertensive rats （SHR）. Rat mesenteric arterial rings were cultured in modified ischemia-mimetic solution in a hypoxia incubator for a certain time period. Isometric tension changes of isolated mesenteric arterial rings were recorded continuously by a myograph system. The results obtained were as follows： In SHR group, the maximum contractions to KC1 and phenylephrine （PE） were increased, and the maximum relaxation to acetylcholine （ACh） was decreased, compared to those in Wistar-Kyoto （WKY） rats group. Compared with SHR group and WKY with acute ischemia/hypoxia （WKY＋H） group, SHR with acute ischemia/hypoxia （SHR＋H） increased the maximum contractions induced by KC1 and PE and inhibited the maximum relaxations by ACh. In SHR＋H and SHR groups, the vasodilation induced by ACh was unaffected by NG-nitro-L-arginine methylester （L-NAME）, whereas in WKY group, the relaxation to ACh was attenuated by L-NAME. CaC12-induced contraction in depolarized rings in SHR＋H group significantly shifted to the left compared with SHR group. In Ca2＋-free K-H solution, the maximum contractions induced by PE and caffeine were increased in SHR＋H group compared to those in WKY＋H group; the PE- and caffeine-induced contractions were also enhanced in SHR group versus WKY group; the maximum contraction induced by PE was significantly increased in SHR＋H group versus SHR group. These findings suggest that acute ischemia/hypoxia aggravates mesenteric artery dysfunction in SHR. The mechanism may be related to the decreased NO generation and increased sarcoplasmic reticulum Ca2＋ release.