With great interest, we read the comprehensive and well-written review article of Drs. Treschan and Peters1
providing a thorough overview of the physiology and therapeutic indications of arginine vasopressin and its synthetic analogs. Nevertheless, we believe that the impact of the long-acting vasopressin analog terlipressin on hepatosplanchnic perfusion in the treatment of sepsis-related arterial hypotension has not been discussed appropriately. The authors conclude that “terlipressin is a potent intestinal vasoconstrictor, and evidence suggests decreased intestinal perfusion with terlipressin infusion.”1
First, we wish to rectify that the cited study of Westphal et al.2
investigated the effects of arginine vasopressin on gut mucosal microcirculation in septic rats, and not of terlipressin (as wrongly cited by Drs. Treschan and Peters1
). Second, the effects of terlipressin on splanchnic perfusion are dependent on two important aspects, which the authors of the current review article did not refer to: (1) the role of aggressive fluid resuscitation and (2) the dose itself. In this context, Asfar et al.3
reported that terlipressin even improved ileal microcirculation in fluid-challenged endotoxic rats. In contrast, in non–fluid-challenged rats, terlipressin infusion contributed to detrimental effects within the intestinal macrocirculation and microcirculation. In addition, the impact of terlipressin on intestinal perfusion seems to be dependent on the drug dosage and application form. Again, Asfar et al.4
demonstrated that a goal-directed continuous low-dose infusion of terlipressin not only reversed the hypotensive–hyperdynamic circulation in porcine endotoxemia but also decreased global systemic oxygen consumption without compromising splanchnic metabolism and organ function. In summary, the current literature, also limited in extent, supports the view that low-dose terlipressin in conjunction with aggressive fluid challenge is a promising adjunct in our therapeutic repertoire for the treatment of systemic arterial hypotension resulting from distributive shock.5
Hugo Van Aken, M.D., Ph.D.
Martin Westphal, M.D., Ph.D.
*University of Muenster, Muenster, Germany. firstname.lastname@example.org