Impact of age on cardiovascular function, inflammation, and oxidative stress in experimental asphyxial cardiac arrest

BackgroundAdvanced age is an independent predictor of poor outcome after cardiac arrest (CA). From experimental studies of regional ischemia-reperfusion injury, advanced age is associated with larger infarct size, reduced organ function, and augmented oxidative stress. The objective of this study was to investigate the effect of age on cardiovascular function, oxidative stress, inflammation, and endothelial activation after CA representing global ischemia-reperfusion. MethodsAged (26months) and young (5months) rats were subjected to 8min of asphyxia induced CA, resuscitated and observed for 360min. Left ventricular pressure-derived cardiac function was measured at baseline and 360min after CA. Blood samples obtained at baseline, 120min, and 360min after CA were analyzed for IL-1, IL-6, IL-10, TNF-, elastase, sE-selectin, sL-selectin, sI-CAM1, hemeoxygenase-1 (HO-1) and protein carbonyl. Tissue samples of brain, heart, kidney, and lung were analyzed for HO-1. ResultsCardiac function, evaluated by dP/dt(max) and dP/dt(min), was decreased after CA in both young and aged rats, with no group differences. Mean arterial pressure increased after CA in young, but not old rats. Aged rats showed significantly higher plasma levels of elastase and sE-selectin after CA, and there was a significant different development over time between groups for IL-6 and IL-10. Young rats showed higher levels of HO-1 in plasma and renal tissue after CA. ConclusionIn a rat model of asphyxial CA, advanced age is associated with an attenuated hyperdynamic blood pressure response and increased endothelial activation.