Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock

Abstract

OBJECTIVES:The anesthetic gas xenon is reported to preserve hemodynamic stability during general anesthesia. However, the effects of the gas during shock are unclear. The objective of this study was to evaluate the effect of Xe on hemodynamic stability and tissue perfusion in a canine model of hemorrhagic shock.METHOD:Twenty-six dogs, mechanically ventilated with a fraction of inspired oxygen of 21% and anesthetized with etomidate and vecuronium, were randomized into Xenon (Xe; n = 13) or Control (C; n = 13) groups. Following hemodynamic monitoring, a pressure-driven shock was induced to reach an arterial pressure of 40 mmHg. Hemodynamic data and blood samples were collected prior to bleeding, immediately after bleeding and 5, 20 and 40 minutes following shock. The Xe group was treated with 79% Xe diluted in ambient air, inhaled for 20 minutes after shock.RESULT:The mean bleeding volume was 44 mL.kg−1 in the C group and 40 mL.kg−1 in the Xe group. Hemorrhage promoted a decrease in both the cardiac index (p<0.001) and mean arterial pressure (p<0.001). These changes were associated with an increase in lactate levels and worsening of oxygen transport variables in both groups (p<0.05). Inhalation of xenon did not cause further worsening of hemodynamics or tissue perfusion markers.CONCLUSIONS:Xenon did not alter hemodynamic stability or tissue perfusion in an experimentally controlled hemorrhagic shock model. However, further studies are necessary to validate this drug in other contexts.

Pulmonary Hemodynamics

“…This is a much lower driving pressure for the blood flow than the systemic circulation, where the arterial-venous pressure gradient is approximately 90 mmHg in humans. Table 1 summarizes the pulmonary hemodynamic parameters for other species from different studies (Barer and Nusser, 1957a;Drougas et al, 1996;Holm et al, 1998;Morris et al, 2000;Grant and Canty, 1989;Baxter et al, 1952;Duke and Stedeford, 1960;Chen et al, 2005;Yuan et al, 2011;Liu et al, 2005;Emery et al, 2001;Fesler et al, 2006;Chick et al, 1988;Franceschi et al, 2013;Chaliki et al, 2002;Romand et al, 1994;Takeda et al, 1987;Johnson et al, 1992;Ravikumar et al, 2011;Reddy et al, 1995;Polglase et al, 2006;Newman et al, 1993;Nachar et al, 2001;Krebs et al, 2007;Hinder et al, 1998;Pennington et al, 1992;Patschova et al, 2010;Stickland et al, 2007;Li et al, 2013;Goetz et al, 1999;Tournoux et al, 2011;Ortiz et al, 2002;Ullrich et al, 1999). Although the blood flow through the pulmonary circulation is essentially the same as the blood flow through the systemic circulation, the pulmonary vascular resistance is 10-to 15-fold lower than the systemic vascular resistance.…”

“…These vessels compress and distort during lung inflation, and the degree to which these forces and blood pressures interact determines blood flow through that region of the lung (Franceschi et al, 2013;Keilholz et al, 2001;Milic-Emili et al, 1966). However, as the lung inflates, the inflation or pleural pressures have additional effects on other segments of the pulmonary vasculature.…”

Establishment of a canine model of acute pulmonary embolism with definite right ventricular dysfunction through introduced autologous blood clots

“…The heart rate (HR) was measured using a surface electrocardiogram (Philips, Eindhoven, Netherlands). Cardiac shock was defined as a mean arterial pressure (MAP) b 40 mmHg [16].…”