Department of Anesthesia and Pain Medicine, Pusan National University School of Medicine, Yangsan, Korea.
Korean J Anesthesiol. 2011 Jun;60(6):428-33. doi: 10.4097/kjae.2011.60.6.428. Epub 2011 Jun 17.
Recently, the addition of dexmedetomidine to sedation regimens after cardiac surgery had been reported and there is a possibility that dexmedetomidine can cause vasoconstriction. Vasopressin has been used as a prophylactic treatment for refractory vasodilatory shock during coronary artery bypass graft (CABG). Also, vasopressin may play an important role in initiating spasms at the graft artery. Here we evaluate the direct effect of dexmedetomidine on isolated human gastroepiploic arteries and the synergistic effect of dexmedetomidine and vasopressin.
Discarded gastroepiploic arteries from elective subtotal gastrectomy (n = 10) were used in this study. We measured the level of contraction in isolated human gastroepiploic arteries induced by increasing concentrations of dexmedetomidine (10(-10) to 10(-6) M) with or without vasopressin (10(-10), 10(-9) M). Arterial contractions caused by increasing concentrations of vasopressin (10(-10) to 10(-7.5) M) with or without dexmedetomidine (10(-9), 10(-7) M) were also measured in the tissue samples.
Supraclinical concentrations of dexmedetomidine elicited contractions at concentrations of 10(-7) M and 10(-6) M (P < 0.05 versus resting tension). The same concentrations of dexmedetomidine (10(-7), 10(-6) M) significantly enhanced vasopressin-induced contractions (P < 0.05 versus vasopressin-induced contraction). Vasopressin produced concentration-dependent contractions and vasopressin (10(-10), 10(-9.5), 10(-9) M) also increased the intensity of dexmedetomidine (10(-7) M) induced contractions.
There was a synergistic effect between supraclinical doses of dexmedetomidine and vasopressin on the degree of contraction in isolated human gastroepiploic arteries. However, a sedative dose of dexmedetomidine (clinical dose: 0.2-0.7 µg/kg/hr, plasma concentration: 0.36-1.25 ng/ml) did not enhance vasopressin induced-contraction in isolated human gastroepiploic arteries.
最近有报道称，心脏手术后在镇静方案中加入右美托咪定，并且右美托咪定有可能引起血管收缩。血管加压素已被用作冠状动脉旁路移植术（CABG）期间难治性血管扩张性休克的预防性治疗。此外，血管加压素可能在吻合动脉痉挛的发生中发挥重要作用。在此，我们评估了右美托咪定对离体人胃网膜动脉的直接作用以及右美托咪定和血管加压素的协同作用。
本研究使用了来自择期胃大部切除术的废弃胃网膜动脉（n=10）。我们测量了在有或没有血管加压素（10（-10），10（-9）M）的情况下，浓度递增的右美托咪定（10（-10）至 10（-6）M）引起的离体人胃网膜动脉的收缩程度。还在组织样本中测量了在有或没有右美托咪定（10（-9），10（-7）M）的情况下，浓度递增的血管加压素（10（-10）至 10（-7.5）M）引起的动脉收缩。
超临床浓度的右美托咪定在 10（-7）M 和 10（-6）M 浓度时引起收缩（与静息张力相比，P<0.05）。相同浓度的右美托咪定（10（-7），10（-6）M）显著增强了血管加压素引起的收缩（与血管加压素引起的收缩相比，P<0.05）。血管加压素产生浓度依赖性收缩，并且血管加压素（10（-10），10（-9.5），10（-9）M）还增加了右美托咪定（10（-7）M）诱导的收缩强度。
超临床剂量的右美托咪定和血管加压素对离体人胃网膜动脉收缩程度有协同作用。然而，右美托咪定的镇静剂量（临床剂量：0.2-0.7μg/kg/hr，血浆浓度：0.36-1.25ng/ml）不会增强离体人胃网膜动脉中血管加压素诱导的收缩。
