Dexmedetomidine does not produce vasocontraction on human isolated gastroepiploic artery

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.