Abstract 175: Vasopressin Maintains Robust Organ Blood Flow During Resuscitation from Hemorrhagic Shock
Background: We have reported beneficial hemodynamic and survival effects of vasopressin (VP) infusion in swine models of hemorrhagic shock (HS), and attributed the effects to increases in peripheral vascular resistance. However, VP may also exert a minor effect on venous return. In the present study we used fluorescent microspheres to measure the effects of VP on blood flow to organs of interest during HS produced by liver laceration (LL).
Methods: Forty male domestic pigs (32.3 to 40.3 kg) had their left lateral liver lobe lacerated with a sharpened steel, X-shaped 5 cm blade clamp. Thirty-two pigs received a second LL in the same lobe 7.5 minutes later and 24 pigs received a third LL in the left medial lobe at 15 minutes from the first LL. Pigs were randomized 1:1 to receive an infusion of VP (0.04 U/kg•min-1) or vehicle intraosseously starting 7 minutes after the first LL until the end of the experiment (240 min). Microspheres were injected into the left ventricle at baseline (BL) and during HS at times shown in the Table.
Results: At 60 minutes of HS, VP infusion was associated with higher aortic blood pressure and lower cardiac index (both NS) along with overall reductions in blood flow to various organs (Table) coincident with a statistically significant reduction in heart rate (157±43 vs 184±29 min-1; p≤0.05). At 120 and 180 minutes of HS, the heart rate was only mildly reduced (NS). The aortic pressures remained high but without a reduction in cardiac index. Organ blood flows were all comparable or higher with VP than in control pigs attaining statistical significance for renal cortical blood flow.
Conclusion: Contrary to the expected hemodynamic effects of VP redistributing blood flow away from “non-vital organs,” we observed a robust hemodynamic effect that adequately perfused vital and “non-vital” organs during HS without deterioration over time. Early and sustained VP infusion could represent a highly effective intervention for hemodynamic stabilization during severe HS.
Author Disclosures: R.J. Gazmuri: Research Grant; Significant; Supported by the Telemedicine and Advanced Technology Research Center (TATRC) at the U.S. Army Medical Research and Materiel Command (USAMRMC) Fort Detrick, MD under contract number: W81XWH-11-2-0019. H.K. Whitehouse: None. A. Baetiong: None. K. Whittinghill: None. J. Radhakrishnan: None.
- © 2014 by American Heart Association, Inc.