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首页> 外文期刊>Life sciences >Modulation of diaspirin crosslinked hemoglobin induced systemic and regional hemodynamic response by ethanol in normal rats.
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Modulation of diaspirin crosslinked hemoglobin induced systemic and regional hemodynamic response by ethanol in normal rats.

机译：在正常大鼠中，乙醇调节diaspirin交联的血红蛋白诱导的全身和区域血流动力学反应。

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DCLHb, a hemoglobin based oxygen carrier, has been extensively studied for the treatment of hemorrhagic shock in both animal models and humans. Numerous accidents resulting in trauma are due to ethanol intoxication, in particular cases of car accidents. Therefore, trauma patients might be intoxicated with drugs of abuse like ethanol. Ethanol has significant effects on the cardiovascular system including peripheral vasodilation and decreased myocardial contractility. Such effects are likely to alter the cardiovascular actions of DCLHb, a resuscitative agent. Hence, this study investigated the effect of ethanol on the cardiovascular actions of DCLHb. Urethane anesthetized male Sprague-Dawley rats were divided into following groups (i) Saline + DCLHb (400 mg/kg) (n = 9), (ii) Ethanol (1 g/kg) + DCLHb (400 mg/kg) (n = 9), and (iii) Ethanol (4 g/kg) + DCLHb (400 mg/kg) (n = 8). Cardiovascular parameters were determined using a radioactive microsphere technique. DCLHb when administered to saline treated rats produced an increase in MAP, TPR, decreased renal and hepatic blood flow and increased blood flow to the skin and mesentery & pancreas. A high dose of ethanol (4 g/kg) significantly attenuated the DCLHb induced pressor response (p < 0.05) and increase in TPR (p < 0.05). Cardiac output was severely reduced by DCLHb in rats treated with high dose ethanol as compared to saline. No changes in TPR and cardiac output were observed in the low dose ethanol (1 g/kg) group. DCLHb reduced blood flow to the heart and mesentery & pancreas in rats treated with high dose ethanol. DCLHb caused a decrease in musculo-skeletal vascular resistance in rats treated with high dose ethanol. This decrease in vascular resistance in the musculo-skeletal system appears to be contributing to a decrease in TPR. It is concluded that ethanol in higher doses significantly alters the hemodynamic effects of DCLHb and may interfere with the resuscitative effects of DCLHb.
机译：DCLHb，一种基于血红蛋白的氧气载体，已经在动物模型和人类中进行了广泛的研究，用于治疗失血性休克。大量导致伤害的事故是由于乙醇中毒引起的，特别是在车祸中。因此，创伤患者可能会被滥用药物如乙醇所陶醉。乙醇对心血管系统具有重大影响，包括外周血管舒张和心肌收缩力降低。此类作用可能会改变DCLHb（一种复苏剂）的心血管作用。因此，本研究调查了乙醇对DCLHb心血管作用的影响。氨基甲酸乙酯麻醉的雄性Sprague-Dawley大鼠分为以下几组（i）盐水+ DCLHb（400 mg / kg）（n = 9），（ii）乙醇（1 g / kg）+ DCLHb（400 mg / kg）（n = 9），和（iii）乙醇（4 g / kg）+ DCLHb（400 mg / kg）（n = 8）。使用放射性微球技术确定心血管参数。当将DCLHb给予生理盐水处理的大鼠时，其MAP，TPR升高，肾和肝血流量降低，皮肤，肠系膜和胰腺的血流量增加。高剂量的乙醇（4 g / kg）显着减弱了DCLHb诱导的升压反应（p <0.05）和TPR升高（p <0.05）。与盐水相比，用高剂量乙醇治疗的大鼠的DCLHb严重降低了心脏的输出。在低剂量乙醇（1 g / kg）组中未观察到TPR和心输出量的变化。 DCLHb减少了用高剂量乙醇治疗的大鼠的心脏，肠系膜和胰腺的血流。 DCLHb导致用高剂量乙醇治疗的大鼠的骨骼肌血管阻力降低。肌肉骨骼系统中血管阻力的这种降低似乎有助于TPR的降低。结论是较高剂量的乙醇会明显改变DCLHb的血液动力学作用，并可能干扰DCLHb的复苏作用。

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