Department of Pharmacology and Therapeutics, Faculty of Medicine and Health Sciences, United Arab Emirates University, P,O, Box 17666, Al Ain, United Arab Emirates.
BMC Vet Res. 2013 Nov 19;9:232. doi: 10.1186/1746-6148-9-232.
The objective of this study was to provide for the first time data on plasma catecholamines, cortisol, glutathione and malondialdehyde after long term dehydration (20 days) in the presence and absence of angiotensin II (Ang II) AT1 receptor blocker (losartan) versus levels in time-matched, non-dehydrated control camels and to record the responses of glutathione and malondialdehyde activity in liver and kidney homogenates in control, dehydrated-losartan treated and dehydrated camels. Eighteen male camels were studied, six hydrated (control group), six dehydrated and treated with losartan (treated group) and six dehydrated not treated (dehydrated).
Plasma levels of norepinephrine and dopamine were significantly increased (P < 0.01) in both treated and dehydrated groups compared to time matched control, whereas Plasma epinephrine level showed significant decrease (P < 0.05) in both treated and dehydrated groups compared to control. Plasma cortisol also showed significant increase (P < 0.01) in both treated and dehydrated groups compared to control. Glutathione levels in plasma, liver and kidney homogenates for both treated and dehydrated groups reveled significant increase (P < 0.05) Likewise, malondialdehyde levels in plasma, liver and kidney homogenates were substantially and significantly increased in both treated and dehydrated groups.
In conclusion, the results of this study demonstrated that dehydration substantially increased the circulating levels of norepinephrine, dopamine and cortisol but decreased plasma epinephrine. Similarly, losartan showed similar effects to that of dehydration. In addition, this investigation showed dehydration alone or in combination with losartan induced significant increments in glutathione and malondialdehyde activities in plasma, liver and kidney homogenates, presumably in order to counteract the potentially damaging effects of free radicals. Blockade of angiotensin II AT1 receptors did not alter significantly the response of dehydration in any of these indices.
本研究的目的是首次提供在存在和不存在血管紧张素 II(Ang II)AT1 受体阻滞剂(氯沙坦)的情况下,长期脱水(20 天)后血浆儿茶酚胺、皮质醇、谷胱甘肽和丙二醛的数据,并记录在对照、脱水-氯沙坦治疗和脱水骆驼中,肝和肾匀浆中谷胱甘肽和丙二醛活性的反应。研究了 18 头雄性骆驼,6 头水合(对照组),6 头脱水并用氯沙坦治疗(治疗组)和 6 头脱水未治疗(脱水组)。
与时间匹配的对照组相比,治疗组和脱水组的血浆去甲肾上腺素和多巴胺水平均显著升高(P <0.01),而血浆肾上腺素水平在治疗组和脱水组均显著降低(P <0.05)与对照组相比。治疗组和脱水组的血浆皮质醇水平也显著高于对照组(P <0.01)。与对照组相比,治疗组和脱水组的血浆、肝和肾匀浆中的谷胱甘肽水平均显著升高(P <0.05)。同样,治疗组和脱水组的血浆、肝和肾匀浆中的丙二醛水平均显著升高。
总之,本研究结果表明,脱水显著增加了循环中的去甲肾上腺素、多巴胺和皮质醇水平,但降低了血浆肾上腺素水平。同样,氯沙坦表现出与脱水相似的作用。此外,这项研究表明,单独脱水或与氯沙坦联合使用会导致血浆、肝和肾匀浆中谷胱甘肽和丙二醛活性显著增加,可能是为了抵消自由基的潜在破坏性影响。血管紧张素 II AT1 受体阻滞剂的阻断并未显著改变这些指标中任何一个对脱水的反应。