Vasopressin maintains tissue oxygenation in a piglet model of septic shock

Vasopressin (VP) can acutely reverse hypotension in catecholamine‐resistant septic shock, yet there is concern that its potent vasoconstriction may increase tissue ischemia. Thus, we compared the effects of VP (100 ng/kg/min; n=10) on O 2 utilization and tissue perfusion in endotoxin (ETX; 10–30 μg/kg iv)‐induced shock, to that of no treatment (UNTX; n=9) or first line drugs dopamine (DA; 50 μg/kg/min; n=7) or norepinephrine (NE; 1 μg/kg/min; n=8). ETX caused a 45% decrease in mean arterial pressure (MAP), 30% drop in cardiac output, 40% decrease in O 2 delivery, and 3‐fold increase in the pulmonary to systemic vascular resistance ratio (PVR/SVR). VP restored MAP whereas NE and DA did not. VP reversed the PVR/SVR increase which helped maintain PaO 2 and prevented escalating pulmonary hypertension. Whole body O 2 consumption was maintained in UNTX, VP‐ and NE‐treated groups via reduced shunt fraction Q S /Q T and more efficient % O 2 extracted whereas O 2 consumption decreased with DA. VP preserved flow to the brain, heart, and kidneys, which revealed no pathologic tissue changes suggestive of ischemia. In comparison, NE and DA preserved flow to the heart, but not to the brain, and DA further decreased flow to the kidneys. Although DA increased flow to the small bowel, VP and NE shunted flow away from the gastrointestinal tract in favor of vital organs, with no further small bowel ischemic damage. Results indicate that VP promotes better whole body O 2 utilization in hypotensive conditions of septic shock by sparing pulmonary vasoconstriction, and causing preferential vital organ perfusion. ( Supported by USAMRAA grant DAMD 170310072)