Der Einfluss von H2S auf Reanimierbarkeit und Hämodynamik nach Herzkreislaufstillstand und kardiopulmonaler Reanimation beim Schwein

Sudden cardiac death is one of the main causes of death in industrialised countries. Therefore, the development and improvement of treatments is one of the main focuses of current research. First attempts of resuscitation date back to Late Antiquity. Cardiopulmonary resuscitation (CPR) as known today is practiced since the 1960s and is complemented by additional therapeutic options such as mild therapeutic hypothermia (TH). TH can cause a reduction in metabolic rate associated with a better outcome for patients post-CPR. In 2005 Blackstone et al. showed that hydrogen sulfide (H2S) can induce similar states of reduced metabolism in mice. Following studies showed cardio protective qualities of this gasotransmitter. Due to their cardiovascular similarity to humans animal experiments with pigs are widely agreed to facilitate the implementation of new findings into clinical practice. The present study investigated the influence of H2S on resuscitability, long term survival post-CPR, hemodynamic parameters, blood gas and troponin T. Ventricular fibrillation was induced at anaesthetised, mechanically ventilated pigs, which were resuscitated via CPR. Depending on the study group either Na2S as a H2S Donor in high or low dose or physiologic salt solution was applied during CPR. A significant influence in resuscitability was not observed. Those animals being treated with a high dose of H2S predeceased those animals which were treated with either low dose of H2S or placebo. Hemodynamic effects of the study medication, including decrease in mean arterial pressure, pulmonary capillary wedge pressure and cardiac output and increase in heart rate, were registered in both H2S groups, though more pronounced in the high dose group. Acidosis and hypercapnia were more distinct and serum levels of troponin T were higher in both H2S groups compared to the placebo group. These results indicate a decrease in end-diastolic filling pressures in the left heart and therefore an aggravation in cardiac capacity. In addition, a more severe ...