Koksoy C, Uydes-Dogan B S, Kuzu M A, Aydemir-Koksoy A, Demirpence E, Kesenci M
Department of Surgery, Ankara University Medical School, Turkey.
J Invest Surg. 2000 Jan-Feb;13(1):35-43. doi: 10.1080/089419300272249.
Intestinal ischemia-reperfusion (I-R) is a common and serious clinical condition associated with simultaneous remote organ dysfunction. The purpose of this study was to investigate the effects of intestinal I-R on the vasomotor functions of major conduit arteries. Anesthetized rabbits were randomly assigned to one of three groups: sham-operated controls (Group I), and one-hour intestinal ischemia with two-hour reperfusion (Group II) or four-hour reperfusion (Group III). The following mechanisms of vasomotor functions were studied in abdominal aorta, superior mesenteric, renal, pulmonary, and carotid arterial rings: (1) endothelial-dependent vasodilation response to acetylcholine, (2) endothelial-independent vasodilation response to nitroprusside, (3) beta-adrenergic vasodilation response to isoproterenol, and (4) phenylephrine-induced vasoconstriction. Intestinal injury was quantified using malondialdehyde (MDA) concentration and wet-to-dry intestine weight ratio. Intestinal I-R did not affect the maximal responsiveness or the sensitivity to acetylcholine, nitroprusside, and isoproterenol in all the vessels studied. The maximal contractile response to phenylephrine increased significantly in mesenteric artery in Group II, (227.1+/-15.1% vs. 152.8+/-11.7% in controls) (p<0.05). Intestinal MDA concentration, a marker of oxidant injury, increased from 39.87+/-9.41 nmol/g to 67.8+/-8.8 nmol/g in group II (p<0.01), and to 94.8+/-7.56 nmol/g in Group III (p<0.001). Wet-to-dry intestine weight ratio increased from 3.62+/-0.12 to 4.28+/-0.17 in Group II (p<0.01), to 4.62+/-0.14 in Group III (p<0.001). These data indicate that although the intestines of the animals subjected to intestinal I-R are seriously injured, the smooth muscle relaxation of major conduit arteries was not affected.
肠道缺血再灌注(I-R)是一种常见且严重的临床病症,与同时发生的远隔器官功能障碍相关。本研究的目的是探讨肠道I-R对主要输送动脉血管舒缩功能的影响。将麻醉后的兔子随机分为三组之一:假手术对照组(I组),以及经历1小时肠道缺血和2小时再灌注的组(II组)或4小时再灌注的组(III组)。在腹主动脉、肠系膜上动脉、肾动脉、肺动脉和颈动脉环中研究了以下血管舒缩功能机制:(1)对乙酰胆碱的内皮依赖性血管舒张反应,(2)对硝普钠的非内皮依赖性血管舒张反应,(3)对异丙肾上腺素的β-肾上腺素能血管舒张反应,以及(4)去氧肾上腺素诱导的血管收缩。使用丙二醛(MDA)浓度和肠湿重与干重比来量化肠道损伤。肠道I-R并未影响所研究的所有血管对乙酰胆碱、硝普钠和异丙肾上腺素的最大反应性或敏感性。II组肠系膜动脉对去氧肾上腺素的最大收缩反应显著增加,(227.1±15.1% 对比对照组的152.8±11.7%)(p<0.05)。作为氧化损伤标志物的肠道MDA浓度,II组从39.87±9.41 nmol/g增加至67.8±8.8 nmol/g(p<0.01),III组增加至94.8±7.56 nmol/g(p<0.001)。肠湿重与干重比II组从3.62±0.12增加至4.28±0.17(p<0.01),III组增加至4.62±0.14(p<0.001)。这些数据表明,尽管经历肠道I-R的动物的肠道受到严重损伤,但主要输送动脉的平滑肌舒张并未受到影响。