Vasopressin Decreases Pulmonary–to–Systemic Vascular Resistance Ratio in a Porcine Model of Severe Hemorrhagic Shock

Abstract

Vasopressors are gaining renewed interest as treatment adjuncts in hemorrhagic shock. The ideal vasoconstrictor will increase systemic blood pressure without increasing pulmonary vascular resistance (PVR), which hinders pulmonary perfusion and exacerbates hypoxemia. However, the selectivity of pressors for pulmonary versus systemic vasoconstriction during hemorrhage has not been characterized. The purpose of this study was to test the hypothesis that vasopressin (VP) has distinct effects on pulmonary versus systemic hemodynamics, unlike the catecholamine vasopressors norepinephrine (NE) and phenylephrine (PE). Anesthetized and ventilated pigs were assigned to resuscitation with saline only (n = 7) or saline with VP (n = 6), NE (n = 6), or PE (n = 6). Animals were hemorrhaged to a target volume of 30 mL/kg and a mean arterial pressure of 35 mmHg. One hour after the start of hemorrhage, animals were resuscitated with saline up to one shed blood volume, followed by either additional saline or a vasopressor. Hemodynamics and oxygenation were measured hourly for 4 h after the start of hemorrhage. Vasopressin increased systemic vascular resistance (SVR) while sparing the pulmonary vasculature, leading to a 45% decrease in the PVR/SVR ratio compared with treatment with PE. Conversely, NE induced pulmonary hypertension and led to an increased PVR/SVR ratio associated with decreased oxygen saturation. Phenylephrine and crystalloid had no significant effect on the PVR/SVR ratio. Sparing of pulmonary vasoconstriction occurs only with VP, not with administration of crystalloid or catecholamine pressors. The ability of VP to maintain blood oxygenation indicates that VP may prevent hypoxemia in the management of hemorrhagic shock.

Effect of vasopressin on a porcine model of persistent pulmonary hypertension of the newborn

“…However, the addition of vasopressin had no effect on this parameter in either group, during either normoxic or hypoxic ventilation. These data are in accord with recent studies of vasopressin in pulmonary hypertension that, while noting a vasopressin‐induced decrease in the pulmonary‐to‐systemic pressure ratio, ascribe this improvement to a rise in aortic pressure rather to pulmonary vasodilation . Vasopressin may be unique among pressors in having no pulmonary constrictor effect, but we concur that it has no apparent pulmonary vasodilator effect .…”

“…However, we cannot provide evidence for any increase in with recent studies of vasopressin in pulmonary hypertension that, while noting a vasopressin-induced decrease in the pulmonary-tosystemic pressure ratio, ascribe this improvement to a rise in aortic pressure rather to pulmonary vasodilation. 42,43 Vasopressin may be unique among pressors in having no pulmonary constrictor effect, 44 but we concur that it has no apparent pulmonary vasodilator effect. 45 Indirect vasodilation has been postulated, for example, through vasopressin-induced release of atrial natriuretic peptide 39 ; but these effects would fall outside of the timeframe of the present study.…”

ECMO with vasopressor use during early endotoxic shock: Can it improve circulatory support and regional microcirculatory blood flow?

“…Persistent pulmonary hypertension contributes to worsening hypoxemia in endotoxic shock. We previously showed that vasopressin spares the pulmonary vasculature of its potent vasoconstrictive action [21], thus it was not surprising to see that when vasopressin and dopamine were used in conjunction with ECMO that the elevated pulmonary to systemic vascular resistance ratio (PVR/SVR) caused by ET returned to baseline. Because oxygen delivery was already increased with ECMO alone, the relative vasoconstrictive sparing of the pulmonary bed did not contribute additional systemic oxygen delivery gains.…”

Effect of arginine vasopressin on systemic and pulmonary arterial pressure in a patient with pulmonary hypertension secondary to pulmonary emphysema: a case report

“…AVP is a nonsympathomimetic vasopressor, which causes vasoconstriction via activation of the V 1 vasopressin receptor [ 11 ]. In vitro and in vivo studies have demonstrated that AVP produces systemic vasoconstriction with relatively fewer effects on the pulmonary circulation; such combined effects produce a desirable decrease in the pulmonary vascular resistance/systemic vascular resistance ratio [ 12 – 14 ]. This AVP-mediated selective vasoconstriction of the systemic vessels has also been shown in several clinical studies in patients undergoing cardiac surgery [ 4 – 6 ].…”