Effects of therapeutic hypothermia on coagulopathy and microcirculation after cardiopulmonary resuscitation in rabbits

Objective: The aim of this study was to investigate the effects of therapeutic hypothermia (TH) on coagulopathy and cerebral microcirculation disorder after cardiopulmonary resuscitation (CPR) in rabbits. Methods: Cardiac ventricular fibrillation was induced by alternating current in 24 New Zealand rabbits, and hypothermia was induced by surface cooling or normothermia (NT) was maintained for 12 hours after the return of spontaneous circulation (ROSC). Several physiologic indexes were measured before CPR and at 4, 8, and 12 hours after ROSC. The microcirculation flow in the cerebral cortex was measured with a PERIMED Multichannel Laser Doppler system (Perimid, Sweden), and glomerular fibrin deposition was determined by microscopy. Results: Compared with the NT group, the prothrombin time, activated partial thromboplastin time, and international normalized ratio in the TH group were increased; there were no differences in anti-thrombin-III, protein C, and D-dimer indexes. The microcirculation flow in the cerebral cortex before CPR and after ROSC at 4, 8, and 12 hours was 401.60 +/- 11.76, 258.86 +/- 34.58, 317.59 +/- 23.36, and 371.98 +/- 5.79 mL/min, respectively, in the NT group, and 398.18 +/- 12.91, 336.19 +/- 19.27, 347.76 +/- 13.80, and 383.78 +/- 3.29 mL/min, respectively, in the TH group. There were apparent disparities at each checkpoint after ROSC in these 2 groups (4 hours: P = .001; 8 hours: P = .011; 12 hours: P = .009). The Pearson correlation test showed that the microcirculation flow in the cerebral cortex was positively correlated with activated partial thromboplastin time after ROSC (4 hours: r = 0.503, P = .033; 8 hours: r = 0.565, P = .035; 12 hours: r = 0.774, P = .009), but not with other coagulation parameters. Conclusions: Therapeutic hypothermia might cause coagulant dysfunction but concomitantly improves the microcirculation flow in the cerebral cortex, which might be an effect of TH that results in cerebral protection. (C) 2011 Elsevier Inc. All rights reserved.