Abstract
Transient global brain ischemia, induced by cardiac arrest and resuscitation, results in reperfusion injury leading to delayed selective neuronal cell loss and post-resuscitation mortality. This study determined the effects of post-resuscitation hypotension and hypothermia on long-term survival following cardiac arrest and resuscitation. The capillary density was also determined. Based on the mean arterial blood pressure (MABP) at 1h of recovery, the normotension group (MABP 80-120mmHg) and hypotension group (MABP <80mmHg) were defined. The overall survival was determined at 4days of recovery. Brain microvascular density was assessed using immunohistochemistry of the glucose transporter, GLUT-1. The pre-arrest MABP was similar in each group; at 1h after resuscitation, the MABP in the normotension groups was about 80% of their pre-arrest values; the hypotension group had a significantly lower MABP compared to the normotension group. The overall survival rate was lower in the hypotension group compared to the normotension group (36%, 4/11 vs. 67%, 14/21) under the normothermic condition. Brain blood flow in the hypotension group was lower (33% decrease) compared to the normotension group at 1-h post-resuscitation. Compared to the pre-arrest baseline, the capillary density was significantly increased at 14days of recovery (355 ± 42 vs. 469 ± 50, number/mm2) in the cortex. The capillary density in hippocampus was also increased at 4-30days following cardiac arrest and resuscitation. Our results suggest that rats able to maintain their post-resuscitation blood pressure at normotension, had higher brain blood flow during the early recovery phase, and improved survival outcome following cardiac arrest and resuscitation. In addition, cardiac arrest and resuscitation induced angiogenesis in brain in the first month of recovery.
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