Vascular reactivity following thermal injury

Abstract

Major thermal injury is associated with alterations in both pulmonary and systemic vascular resistance. Pulmonary artery hypertension may lead to right heart dysfunction and pulmonary insufficiency. The effect of thermal injury on vascular reactivity is unknown. Increases in circulating vasoactive substances, as well as alterations in vascular smooth muscle receptor activity, have been hypothesized to occur following thermal injury. We have studied aorta and pulmonary artery vascular sensitivity to five agonists in a 35% full-thickness thermal injury rat model. Vascular reactivity was normal to agonists that constrict vascular smooth muscle via receptor-mediated calcium influx. Unresuscitated and resuscitated burn injury resulted in a decrease in peak tension development to prostaglandin F2 alpha (PGF2 alpha) and potassium, agonists whose effects are mediated via membrane depolarization. Fluid resuscitation synchronous with burning did not alter peak tension development in agonists whose actions were mediated via receptor mechanisms. Peak tension development in resuscitated animals to agonists that affect contraction by depolarization remained deficient. To rule out simple blood loss as the etiology for these changes, the experiment was repeated in rats sustaining an acute 25% blood volume loss. Simple hypovolemia induced no changes in aortic or pulmonary vascular sensitivity. We hypothesize that thermal injury may result in a depolarization of vascular smooth muscle membranes altering voltage-dependent calcium channels.