The hemodynamic aspects of pharmacological manipulation of cardiac contractility and vascular resistance in rewarming from hypothermia

Abstract

<p><i>Paper I</i> <br>To describe hemodynamic response and phosphorylation of cardiac troponin I during rewarming from deep, stable hypothermia with use of the calcium sensitizer and PDE3 inhibitor levosimendan, compared to animals given placebo. <p> <p><i>Paper II</i> <br>To describe hemodynamic response to lowered systemic vascular resistance by nitroprusside administration during rewarming from hypothermia, compared to animals given placebo.<p> <p><i>Paper III</i> <br>To describe and compare the effects of levosimendan and nitroprusside on vital organ perfusion during rewarming from hypothermia, compared to animals given placebo.<p>

<i>Main results and conclusions</i> <br>Hypothermia and rewarming depressed hemodynamic function in all control groups. Levosimendan improved cardiac output more than nitroprusside, while nitroprusside reduced vascular resistance. Nitroprusside demonstrated to superiorly improve organ blood flow. The hemodynamic state after rewarming seems to be a combination of reduced cardiac function and unwanted systemic vasoconstriction. Organ perfusion is not only limited by available CO, but also altered autoregulation and vascular pathology.<p>