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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。
Hypertension caused by stroke, coronary heart disease and other serious complications, are associated with tissue ischemia / hypoxia-induced arterial vasospasm. In order to study the functional changes of mesenteric vessels after ischemia / hypoxia in hypertensive rats, we investigated the effects of ischemia / hypoxia on the mesenteric arterial vessels in spontaneously hypertensive rats (SHR) Circumference, using sensitive muscle tension mapping technique to measure the reactivity of vascular rings to different vasoactive substances. The results showed that compared with rats in WKY group, the reactivity of mesenteric artery of rats in SHR group with KCl and phenylephrine (PE) as contractile agents was significantly increased, and the activity of endothelium-dependent vasodilator acetylcholine (ACh) (P <0.05). Compared with SHR group and acute ischemia / hypoxia control group (WKY + H), the contractile responses to KCl and PE in hypertension with acute ischemia / hypoxia (SHR + H) Sex increased, diastolic response to ACh significantly reduced. In the presence of N-nitro-L-arginine methyl ester (L-NAME), there was no significant change in the vasodilatory response to ACh in the SHR + H and SHR groups, whereas the vasodilatation response to ACh in the WKY group was significantly reduced. Compared with SHR group, CaCl2-induced calcium-dependent contraction curve of SHR + H group shifted significantly to the left. In calcium-free KH solution, PE and caffeine-induced vasoconstriction in SHR + H group was significantly increased compared with WKY + H group, while PE and caffeine-induced vasoconstriction in SHR group was also significantly higher than WKY group. Compared with SHR group Compared with SHR + H group, the vasoconstriction induced by PE significantly increased, while the caffeine induced vasoconstriction showed no significant change. The above results show that hypertension can cause impaired mesenteric artery function in rats, and the combined ischemia / hypoxia makes the degree of vascular injury more serious, suggesting that acute ischemia / hypoxia can aggravate mesenteric systolic / diastolic function in hypertensive rats The mechanism may be related to the reduction of NO synthesis in vascular endothelial cells and the increase of intracellular sarcoplasmic reticulum calcium release.