Khazaei Majid, Barmaki Babak, Nasimi Ali
Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran.
Int J Prev Med. 2012 Jan;3(1):47-53.
Different vasoactive factors can modulate cardiovascular adaptation to hemorrhagic shock including Nitric Oxide (NO). In this study we investigated the effect of the NO synthase inhibitor for treatment of decompensated hemorrhagic shock in normotensive and hypertensive rats.
Twenty-four male Wistar rats were divided into two groups: The normotensive and hypertensive groups. Hypertension was induced by the DOCA-Salt method for eight weeks. Then, the animals were given hemorrhagic shock by continuously withdrawing blood until the mean arterial pressure (MAP) reached to 40 mmHg. The animals were maintained in the shock state for 120 minutes. Subsequently, they were randomly assigned to L-NAME-treated and non-treated groups and monitored for 60 minutes. The survival time was recorded. Blood samples were taken before and after the shock and 60 minutes after L-NAME administration.
Infusion of L-NAME caused a significant increase in MAP in normotensive animals, however, slightly increased MAP in hypertensive animals. The heart rate did not significantly alter. Hemorrhage caused a marked increase in serum nitrite levels in both groups (P<0.05). L-NAME treatment significantly reduced the serum nitrite concentration in the normotensive group (P<0.05), without any change in the hypertensive group. All animals who received L-NAME treatment survived at the end of experiment. Fifty percent of the hypertensive animals died four hours after the experiment. The 72-hour survival rate was similar in the L-NAME treated groups.
L-NAME infusion during decompensated hemorrhagic shock plays a protective role in the improvement of hemodynamic responses and short-term survival rate in normotensive animals.
不同的血管活性因子可调节心血管系统对失血性休克的适应性，其中包括一氧化氮（NO）。在本研究中，我们调查了一氧化氮合酶抑制剂对正常血压和高血压大鼠失代偿性失血性休克的治疗效果。
将24只雄性Wistar大鼠分为两组：正常血压组和高血压组。通过DOCA-盐法诱导高血压8周。然后，持续放血直至平均动脉压（MAP）达到40 mmHg，使动物发生失血性休克。将动物维持在休克状态120分钟。随后，将它们随机分为L-NAME治疗组和未治疗组，并监测60分钟。记录生存时间。在休克前后以及给予L-NAME后60分钟采集血样。
输注L-NAME可使正常血压动物的MAP显著升高，然而，高血压动物的MAP略有升高。心率无显著变化。出血导致两组血清亚硝酸盐水平显著升高（P<0.05）。L-NAME治疗显著降低了正常血压组的血清亚硝酸盐浓度（P<0.05），而高血压组无任何变化。所有接受L-NAME治疗的动物在实验结束时均存活。50%的高血压动物在实验后4小时死亡。L-NAME治疗组的72小时生存率相似。
在失代偿性失血性休克期间输注L-NAME对改善正常血压动物的血流动力学反应和短期生存率具有保护作用。
