Introduction: Global ischemia associated with cardiac arrest stimulates nitric oxide (NO) production by NO synthase and formation of free oxygen radicals. Methylene blue (MB) can inhibit formation of NO and oxygen radicals by serving as an electron ca...
Introduction: Global ischemia associated with cardiac arrest stimulates nitric oxide (NO) production by NO synthase and formation of free oxygen radicals. Methylene blue (MB) can inhibit formation of NO and oxygen radicals by serving as an electron carrier. This study aimed to evaluate the effect of MB in asphyixal cardiac arrest in rat model according to arrest time. Material & Methods: Forty-three anesthesized male Sprague-Dawley rats were subjected to asphyxial arrest and allocated to arrest time (7.5, 9, and 12-minute arrest). Rats received cardiopulmonary resuscitation (CPR) with either MB or saline administration of same volume, and were observed for 6 hous after return of spontaneous circulation (ROSC. Neurological deficit scores (NDS) were measured every 24 hours for 3 days and 7-day mortality were recorded. Results: Hemodynamic data such as mean arterial pressure and heart rate were not significantly different between the experimental groups. 7-day mortality have a tendency to increase as arrest time prolonged. In addition, mortality was lower in rats received MB infusion than in rats received saline infusion, and this tenency was more prominent as arrest was prolonged. NDSs were not significantly difference among the groups. Conclusion: MB has a beneficial effect in improving survival rates in asphyxial cardiac arrest of rats, and is more efficient in prolonged arrest.