TITLE: HYPEROSMOTIC-HYPERONCOTIC SOLUTIONS REDUCE THE RELEASE OF CARDIAC TROPONIN-I AND CEREBRAL S-100 AFTER SUCCESSFUL CARDIOPULMONARY RESUSCITATION IN PIGS

AUTHORS: Heiner Krieter, MD, DEAA¹, Christoph Janke¹, Christof Denz, MD¹, Michaela Weiss, MD¹, Thomas Bertsch, MD², Klaus Ellinger, MD¹
AFFILIATION: ¹Inst. of Anesthesiology, Faculty of Clinical Med. Mannheim, Univ. of Heidelberg, Mannheim, Germany; ²Inst. of Clinical Chemistry, Faculty of Clinical Med. Mannheim, Univ. of Heidelberg, Mannheim, Germany.

INTRODUCTION: Fast response of modern emergency systems as well as advanced drug therapy and electrical defibrillation allow the reversal of cardiac arrest in an increasing number of patients. However, many of those who were resuscitated suffer from severe neurological deficits due to ischemia-reperfusion injury. In this context, the postischemic swelling of endothelial cells may further reduce vascular conductivity and, hence, oxygen supply (1). Hyperosmotic-hyperoncotic solutions (HHS) have been shown to immediately restore hemodynamic and blood flow after severe traumatic (2) and septic shock (3). The main volume effect of those solutions results from a swift shift of fluid from endothelial cells to the intravascular space along a strong osmotic gradient (2). The present study was designed to evaluate the impact of HHS in the setting of ischemia-reperfusion after successful cardiopulmo-nary resuscitation. We measured the release of cardiac troponin-I (TnI) and cerebral protein S100 as specific marker of myocardial and brain damage.
METHODS: 10 domestic pigs (25-30kg) were anesthetized with piritramid and pentobarbital, orotracheally intubated and mechanically ventilated. After placing catheters for blood sampling and hemodynamic measurements, a 30 min equilibration period elapsed before baseline values (basis) were recorded. Cardiac arrest was induced by a 60 V 50 Hz AC-pulse. After 4 min basic life support was begun; after 5 min of cardiac arrest, advanced cardiac life support according to the algorithms of the European Resuscitation Counsel was started. With the first return of spontaneous circulation (ROSC) either 4 mL/kg HHS (10% HES 200.000/0.5 7.2% NaCl) or normal saline (0.9% NaCl) were infused iv over 10 min. Plasma levels of TnI and S100 were measured at baseline, 5, 30, 60, 120, and 180 min after ROSC.
RESULTS: The plasma levels of both TnI (fig. 1) and S100 (fig. 2) increased markedly during the early phase of reperfusion. This increase was significantly blunted in animals that received HHS (filled bars) as compared to pigs receiving normal saline (open bars).
CONCLUSION: As indicated by a significantly reduced release of TnI and S100, infusion of HHS upon successful cardiopulmonary resuscitation appears to reduce reperfusion damage of cardiac and cerebral tissues. Further studies are required to elucidate the exact mechanism of action.
REFERENCES:

1) Kempski et al. J Trauma 1997;42:S38-S40.

2) Kreimeier et al. J Surg Res 1990; 49:493-503.

3) Kreimeier et al. Crit Care Med 1991; 19: 801-809.