Vasopressin: the perioperative gift that keeps on giving.

914 November 2014 T HE pulmonary circulation is distinct from the systemic circulation both in structure and in function. Pharmacologic options for selective therapeutic manipulation of pulmonary vascular tone are limited. A major clinical milestone in contemporary perioperative practice has been the advent of selective pulmonary vasodilators that have transformed the management of pulmonary hypertension and right ventricular dysfunction both in the operating room and in the intensive care unit. The pulmonary vasodilators come in intravenous (e.g., prostacyclin), inhalation (e.g., nitric oxide), and oral preparations (e.g., sildenafil). In contrast, clinical vasoconstrictor agents have remained relatively nonselective. Most pharmacologic agents for support of systemic vascular tone increase pulmonary vascular resistance whether desired or not. This therapeutic gap has been studied and it appears that not all intravenous vasoconstrictors lack specificity for the systemic vascular bed. The vasobiology of vasopressin has been studied in this issue of AnEstHEsIology. Currigan et al. have demonstrated that vasopressin, an established systemic vasoconstrictor, has minimal effect on pulmonary vascular tone.1 In their in vitro study utilizing isolated human pulmonary and radial artery ring segments, the investigators demonstrated that phenylephrine, metaraminol, and norepinephrine significantly constricted both the pulmonary and radial arteries – a finding consistent with our current understanding of conventional α-adrenoreceptors. Vasopressin, however, in this laboratory model, was a potent constrictor of the radial artery but exerted no significant effect on the pulmonary artery – this is, to the best of our knowledge, the first time that this selective vasoconstrictor effect of vasopressin has been demonstrated in human tissue at the bench. What are the implications of this seminal observation for the practicing clinician in the perioperative clinical arena? Vasopressin is already established as a systemic pressor in advanced vasoplegic states associated with cardiopulmonary resuscitation, sepsis, anaphylaxis, liver transplantation, cardiopulmonary bypass, and pheochromocytoma resection.2,3 Vasopressin is often the “go-to” drug of choice in the treatment of refractory hypotension due to catecholamine-resistant shock.3 The study by Currigan et al. further supports the use of vasopressin in the setting where increasing pulmonary vascular tone may be deleterious (e.g., acute right ventricular dysfunction). Currigan et al. provide in vitro evidence of yet another gift—that vasopressin is a selective systemic vasoconstrictor in human vascular rings, and therefore, if this effect occurs in vivo, it would spare the right ventricle of the deleterious effects of pulmonary vasoconstriction. In patients with pulmonary hypertension or right ventricular dysfunction, vasopressin is preferred to other vasoconstrictors since it can selectively support systemic vascular tone without increasing pulmonary vascular resistance and right ventricular afterload. Vasopressin provides a dual benefit to the failing right ventricle. Initially, the increased systemic vascular tone increases coronary perfusion pressure to increase myocardial oxygen delivery. Also, the increased oxygen supply due to increased coronary perfusion pressure is not at a cost of increasing right ventricular afterload. Consequently, in Vasopressin