Nitric oxide prevents cardiovascular collapse during shock

Abstract

This study investigated the systemic and microvascular hemodynamic changes after severe hemorrhage. Nitric oxide (NO) availability was increased by administration of NO releasing nanoparticles (NO‐nps). Hemodynamic responses to hemorrhagic shock were studied in the hamster window chamber. Acute hemorrhage was induced by arterial controlled bleeding of 50% of blood volume, and the resulting hemodynamic parameters were followed over 90 min. Exogenous NO was administered in the form of NO‐nps (5 mg/kg suspended in 50 μl saline) 10 min following induced hemorrhage. Control groups received equal dose of NO free nanoparticles (Control‐nps) and Vehicle solution (50 μl saline). Animals treated with NO‐nps partially maintained systemic and microvascular function during hypovolemic shock compared to animals treated with Control‐nps or the Vehicle. The continuous NO released by the NO‐nps reverted arteriolar vasoconstriction, partially recovered both functional capillary density and microvascular blood flows. Additionally, NO supplementation prevented cardiac decompensation. Paradoxically, peripheral vasodilation induced by the NO‐nps did not decrease blood pressure or vascular resistance. NO‐nps promoted intravascular pressure redistribution, increased blood flow and prevented ischemia. Therefore, NO released from NO‐nps can ultimately increase survivability and reduce shock sequelae.