热应激对大鼠肠系膜动脉内皮依赖性NO-、EDHF-介导舒张途径的损伤

摘要

目的 探讨热应激对大鼠肠系膜动脉内皮依赖性舒张功能降低的机制.方法 使用微血管张力描记系统,观察热应激大鼠肠系膜动脉环5-羟色胺预收缩后加入乙酰胆碱的舒张性改变,考察一氧化氮(NO)途径、内皮源性超极化因子(EDHF)途径以及前列环素(PGI2)途径在热应激后肠系膜动脉舒张功能的改变,反应特征表述为最大松弛百分率(Rmax)和产生一半最大松弛百分率时所需要乙酰胆碱浓度的负对数(pIC50).结果 热应激大鼠肠系膜动脉Rmax和pIC50较正常大鼠肠系膜动脉降低,分别为(97±6)%、(52±8)%和8.67±0.59、7.66±1.33(P<0.01,P<0.05).正常大鼠肠系膜动脉NO介导的舒张Rmax和pIC50分别为(53±6)%和6.89±0.93,在热应激后分别为(21±8)%(P<0.01)和4.91±0.31(P<0.01);正常大鼠肠系膜动脉EDHF介导的舒张Rmax和pIC50分别为(35±14)%和6.30±0.56,在热应激后分别为(13±3)%(P<0.01)和5.23±1.07(P<0.01);正常大鼠肠系膜动脉PGI2介导的舒张Rmax和pIC50分别为(8±3)%和5.69±0.37,在热应激后分别为(10±6)%(P>0.05)和5.74±0.79(P>0.05).结论 热应激引起的动脉血管内皮依赖性舒张功能降低主要是损伤了NO-和EDHF-途径.%Objective To investigate the mechanisms of reduced endothelium-dependent relaxation in mesenteric artery in rats after heat stress. Methods With the myograph system, we examined the vessel dilatory responses by cumulative addition of acetylcholine (ACh) and pre-contraction with 5-hydroxytryptamine in heat stress rats and control rats. We studied the effects of nitric oxide (NO)-, prostacyclin I2 (PGI2)- and endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in mesenteric artery after heat stress. The responses were characterized in terms of maximum relaxant effect (Rmax) and negative logarithm of the molar concentration that produced half maximum relaxation (pIC50). Results The Rmax and pIC50 were decreased from (97 ±6)％ and (52 ±8)％ in control rats to 8.67±0.59(P＜0.01) and 7.66±1.33(P＜0.05), respectively, in heat stress rats. In NOmediated relaxation, the Rmax and pIC50 were (53±6)％ and 6.89±0.93 in control rats, and (21±8)％(P＜0.01)and 4.91± 0.31 (P＜0.01) in heat stress rats. In EDHF-mediated relaxation, the Rmax and pIC50 were (35 ± 14)％and 6.30±0.56 in control rats, and (13±3)％(P＜0.01) and 5.23± 1.07(P＜0.01) in heat stress rats. In PGI2mediated relaxation, the Rmax and pIC50 were (8±3)％ and 5.69±0.37 in control rats, and (10±6)％ (P＞0.05)and 5.74 ± 0.79 ( P＞ 0.05) in heat stress rats. Conclusion The decreased endothelium-dependent relaxation in mesenteric artery induced by heat stress damages NO- and EDHF-pathways.