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首页> 外文期刊>Life sciences >Normalization of aortic function during arousal episodes in the hibernating ground squirrel
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Normalization of aortic function during arousal episodes in the hibernating ground squirrel

机译：冬眠的松鼠在唤醒事件中主动脉功能正常化

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Hypothermia is commonly used to restrict organ damage during preservation of tissue, but does not offer complete protection. Organ damage after reperfusion/rewarming is amongst others caused by an impairment of vascular properties, particularly endothelium-dependent vasodilatation. We hypothesized that hibernating small animals, which frequently cycle through periods of deep cooling (torpor) and full rewarming (arousal), employ specific mechanisms to preserve vascular function after cooling and reperfusion. Therefore we measured contraction of aortic tissue of hibernating European ground squirrels after 24 h and 7 days of torpor, arousal (1.5 h) and in non-hibernating animals. To assess the role of nitric oxide (NO), experiments were performed in the absence and presence of the NO-synthesis inhibitor, L-NMMA (10(-4) M). Maximum contraction to phenylephrine and angiotensin 11 was doubled in 7-days torpid animals without a shift in EC50, compared to the other 3 groups. Maximum contraction to KCl was doubled in 7-days torpid animals compared to the arousal group and non-hibernating animals. Relaxation to acetylcholine (ACh) and sodium nitrite in phenylephrine precontracted rings did not differ between groups. In the presence of L-NMMA, the maximum of concentration-response curves for all three vasoconstrictors was increased by about 30% in the arousal group, but unaffected in other groups. L-NNMA completely inhibited ACh-induced relaxation in 24-h torpid animals and non-hibernating animals, but only partially in 7-days torpid animals and in the arousal group. From this we conclude that vascular adaptation proceeds during torpor. Further, increased contractility of aortic tissue during long torpor returns to normal within 1.5 hours of arousal, which is associated with an increased basal NO synthesis. In addition, involvement of NO in agonist-mediated relaxation differs between the various stages of hibernation. Thus, hibernating animals have effectively developed mechanisms to preserve vascular function after cooling and rewarming. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 34]
机译：体温过低通常用于限制组织保存过程中的器官损伤，但不能提供完全的保护。再灌注/再武装后的器官损伤尤其是由于血管特性受损，尤其是内皮依赖性血管舒张引起的。我们假设冬眠的小动物经常在深冷（torpor）和完全变暖（肛门）期间循环，采用特定的机制在冷却和再灌注后保持血管功能。因此，我们测量了冬眠的欧洲松鼠的主动脉组织收缩后的24小时和7天的折腾，唤醒（1.5 h）和非冬眠动物。为了评估一氧化氮（NO）的作用，在没有和存在NO合成抑制剂L-NMMA（10（-4）M）的情况下进行了实验。与其他3组相比，在7天的动物中，对苯肾上腺素和血管紧张素11的最大收缩增加了一倍，而EC50却没有变化。与唤醒组和非冬眠动物相比，在7天的to性动物中对KCl的最大收缩增加了一倍。组间苯肾上腺素预缩环中对乙酰胆碱（ACh）和亚硝酸钠的弛豫没有差异。在存在L-NMMA的情况下，唤醒组中所有三个血管收缩剂的最大浓度反应曲线均增加了约30％，但在其他组中未受影响。 L-NNMA完全抑制ACh诱导的24 h过敏性动物和非冬眠动物的放松，但仅在7天的过敏性动物和唤醒组中部分抑制。据此我们得出结论，在适应过程中，血管的适应过程不断进行。此外，在长时间的煎熬过程中，主动脉组织收缩力的增加在唤醒后的1.5小时内恢复正常，这与基础NO合成的增加有关。另外，在冬眠的各个阶段之间，NO参与激动剂介导的舒张作用也不同。因此，冬眠动物有效地发展了在冷却和变暖后保持血管功能的机制。 （C）2002 Elsevier Science Inc.保留所有权利。 [参考：34]

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