Vasopressin increases blood pressure without inducing pulmonary hypertension in a Sus scrofa model of hemorrhage

Abstract

Distinctive roles of vasoactive hormones in severe hemorrhagic shock are unclear. We recently found a blunted vasopressin (VP) response associated with a higher oxygen debt and an increased pulmonary to systemic vascular resistance (PVR/SVR) ratio in non‐survivors of acute hemorrhage compared to survivors. Hence, we tested the hypothesis that in regulating blood pressure after acute hemorrhage, VP may have distinct effects on pulmonary and systemic hemodynamics, unlike norepinephrine (NE) and phenylephrine (PE). Anesthetized Yorkshire pigs (n=18, 32.3±4.5 kg body wt) underwent rapid hemorrhage (1 to 3 ml/kg/min; 35±5 ml/kg shed volume, 44% mean arterial pressure (MAP) decrease), followed by resuscitation with either normal saline (NS), or NS in combination with VP, NE, or PE titrated to baseline MAPs. All groups had an increase in PVR/SVR during hemorrhage. Administration of NS and PE did not change PVR/SVR. NE further increased PVR/SVR, and induced pulmonary hypertension (PHT). In contrast, VP decreased PVR/SVR by 64%. Results suggest a novel role of VP in differential regulation of pulmonary and systemic arterial pressures, which can prevent PHT and eventual hypoxemia following resuscitation.