In vitro and in vivo resuscitation with adenosine retains cardiomyocyte structure and function following hemorrhagic shock in rats

Successful treatment of hemorrhage requires restoration of normal cardiac function following resuscitation. However, many interventions used to attempt to restore cardiac function may cause additional myocardial injury, cardiac dysfunction and failure. The purpose of this study was to examine the ability of therapeutic intervention using adenosine to protect the heart from contractile dysfunction and post-resuscitation injury following hemorrhagic shock. Male Spargue-Dawley rats were divided into 3 groups: 1] In vivo hemorrhagic shock [1hour] followed by in vitro treatment with adenosine and ex vivo resuscitation using the Langendorff apparatus [60 minutes], 2] In vivo hemorrhagic shock [1 hour] followed by in vivo treatment with 20 microM adenosine and resuscitation [30 minutes] then ex vivo perfusion [60 minutes] and 3] In vivo hemorrhagic shock [2 hours] followed by in vivo treatment with 20 microM adenosine and resuscitation [30 minutes] then ex vivo perfusion [60 minutes]. Arterial blood samples were collected for measurements of TNF-alpha. Treatment with adenosine before resuscitation from hemorrhagic shock significantly improved left ventricular contractile function compared to the untreated resuscitated group. Treatment with adenosine also decreased the inflammatory response to shock by lowering the levels of TNF. In conclusion, treatment with adenosine before resuscitation of hemorrhagic shock protected the heart from post-resuscitation myocardial dysfunction and injury in rats

Resuscitation with adenosine retains cardiomyocyte structure following hemorrhagic shock in rats

Despite the improvement in resuscitation strategies, the incidence of post-resuscitation myocardial injury and failure remains high. Hemorrhagic shock activates an inflammatory response that can lead to myocardial cellular injury. Adenosine has been shown to protect the heart against ischemia reperfusion injury. However, the cardioprotective effects of adenosine following hemorrhagic shock may reduce myocardial injury by decreasing the inflammatory response to shock in rats. After 60 min on hemorrhage, 10 rats were randomized in vivo resuscitation with [n=8] microM adenosine for 30 min. heart Biopsies were collected from histological and electron microscopy examination. Light microscopy demonstrated decreased neutrophil infiltration, absence of contraction band necrosis and hydropic degeneration in the adenosine treated group compared to the hemorrhage untreated. Electron microscopy showed relative preservation of myocardial structure with absence of mitochondrial swelling in the hemorrhage treated group. These findings suggest that treatment with adenosine before in vivo resuscitation of hemorrhagic shock protected the heart from post-resuscitation myocardial injury in rats and the mechanism could be mediated by lowering the inflammatory response to shock