Cho Jun Woo, Lee Chul Ho, Jang Jae Seok, Kwon Oh Choon, Roh Woon Seok, Kim Jung Eun
Department of Cardiovascular and Thoracic Surgery, Catholic University of Daegu School of Medicine, Korea.
Department of Anesthesiology, Catholic University of Daegu School of Medicine, Korea.
Korean J Thorac Cardiovasc Surg. 2013 Dec;46(6):402-12. doi: 10.5090/kjtcs.2013.46.6.402. Epub 2013 Dec 6.
Moderate and severe hypothermia with cardiopulmonary bypass during aortic surgery can cause some complications such as endothelial cell dysfunction or coagulation disorders. This study found out the difference of vascular reactivity by phenylephrine in moderate and severe hypothermia.
Preserved aortic endothelium by excised rat thoracic aorta was sectioned, and then down the temperature rapidly to 25℃ by 15 minutes at 38℃ and then the vascular tension was measured. The vascular tension was also measured in rewarming at 25℃ for temperatures up to 38℃. To investigate the mechanism of the changes in vascular tension on hypothermia, NG-nitro-L-arginine methyl esther (L-NAME) and indomethacin administered 30 minutes before the phenylephrine administration. And to find out the hypothermic effect can persist after rewarming, endothelium intact vessel and endothelium denuded vessel exposed to hypothermia. The bradykinin dose-response curve was obtained for ascertainment whether endothelium-dependent hyperpolarization factor involves decreasing the phenylnephrine vascular reactivity on hypothermia.
Fifteen minutes of the moderate hypothermia blocked the maximum contractile response of phenylephrine about 95%. The vasorelaxation induced by hypothermia was significantly reduced with L-NAME and indomethacin administration together. There was a significant decreasing in phenylephrine susceptibility and maximum contractility after 2 hours rewarming from moderate and severe hypothermia in the endothelium intact vessel compared with contrast group.
The vasoplegic syndrome after cardiac surgery might be caused by hypothermia when considering the vascular reactivity to phenylephrine was decreased in the endothelium-dependent mechanism.
主动脉手术期间的中度和重度低温伴体外循环可导致一些并发症,如内皮细胞功能障碍或凝血紊乱。本研究旨在找出中度和重度低温下苯肾上腺素引起的血管反应性差异。
将切除的大鼠胸主动脉制成保留主动脉内皮的切片,先在38℃下15分钟内迅速降温至25℃,然后测量血管张力。在从25℃复温至38℃的过程中也测量血管张力。为研究低温时血管张力变化的机制,在给予苯肾上腺素前30分钟给予N-硝基-L-精氨酸甲酯(L-NAME)和吲哚美辛。为了解复温后低温效应是否持续,将完整内皮血管和去内皮血管暴露于低温环境。获取缓激肽剂量-反应曲线,以确定内皮依赖性超极化因子是否参与降低低温时苯肾上腺素的血管反应性。
15分钟的中度低温可使苯肾上腺素的最大收缩反应阻断约95%。联合给予L-NAME和吲哚美辛可显著降低低温诱导的血管舒张。与对照组相比,中度和重度低温复温2小时后,完整内皮血管中苯肾上腺素的敏感性和最大收缩性显著降低。
考虑到在内皮依赖性机制中对苯肾上腺素的血管反应性降低,心脏手术后的血管麻痹综合征可能由低温引起。