Levosimendan increases brain tissue oxygen levels after cardiopulmonary resuscitation independent of cardiac function and cerebral perfusion.

Prompt reperfusion is important to rescue ischemic tissue; however, the process itself presents a key pathomechanism that contributes to a poor outcome following cardiac arrest. Experimental data have suggested the use of levosimendan to limit ischemia-reperfusion injury by improving cerebral microcirculation. However, recent studies have questioned this effect.

Effects of levosimendan on hemodynamics, local cerebral blood flow, neuronal injury, and neuroinflammation after asphyctic cardiac arrest in rats.

Objectives: Despite advances in cardiac arrest treatment, high mortality and morbidity rates after successful cardiopulmonary resuscitation are still a major clinical relevant problem. The post cardiac arrest syndrome subsumes myocardial dysfunction, impaired microcirculation, systemic inflammatory response, and neurological impairment. The calcium-sensitizer levosimendan was able to improve myocardial function and initial resuscitation success after experimental cardiac arrest/cardiopulmonary resuscitation.

Effects of a single-dose hypertonic saline hydroxyethyl starch on cerebral blood flow, long-term outcome, neurogenesis, and neuronal survival after cardiac arrest and cardiopulmonary resuscitation in rats*.

Objective: The beneficial effects of hypertonic saline on neuronal survival and on cerebral blood flow have been shown in several animal models of global and focal brain ischemia. Because of the potential benefits of hypertonic solutions, it is hypothesized that hydroxyethyl starch enhances cerebral blood flow and improves long-term outcome after cardiac arrest and cardiopulmonary resuscitation in an animal model.

Design: Laboratory animal study.

Transpulmonary cardiac output measurement in a rat model of cardiac arrest and CPR: impact of vascular access.

Objective: The present study investigated the impact of the vascular access site for cardiac output (CO) measurement by thermodilution on survival and neurohistopathological injury in a rat model of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Secondary the influence of the vascular access site on cardiac output measurements was examined.

Methods: Rats underwent asphyxial CA and CPR.