Glucose Administration before Cardiac Arrest Worsens Neurologic Outcome in Cats

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Abstract
The effects of glucose on neurologic and neuropathologic outcome following global cerebral ischemia were examined in 20 cats subjected to 14 min of cardiac arrest, followed by closed chest resuscitation and intensive care monitoring. Beginning 30 min prior to cardiac arrest, 15 ml/kg of 5% dextrose in 0.45% saline or the same volume of 0.9% saline was administered in a blinded fashion over 15 min. Ventricular fibrillation was electrically induced and cardiac resuscitation was performed according to a standardized protocol, which included closed chest cardiac compressions, epinephrine, lidocaine, sodium bicarbonate administration, and electrical defibrillation. Animals not resuscitated within 4 min were excluded from further study. Resuscitated animals were managed in an intensive care setting for 24 h postresuscitation. Neurologic deficits were scored at 2, 4, and 7 days postresuscitation. Subsequently, the animals'' brains underwent histologic examinations. Nine cats were excluded from data analysis. Three did not meet protocol criteria and six could not be resuscitated within 4 min. As a result of a technical error, the brain of one glucose-treated cat was not analyzed. Six saline-treated and five glucose-treated animals met all protocol criteria and survived for 7 days postresuscitation. Plasma glucose concentration before cardiac arrest was 118 .+-. 24 mg/dl (mean .+-. SD) in the saline group and 269 .+-. 21 mg/dl in the glucose group (P < 0.01). Neurologic outcome rank at 2, 4, and 7 days postresuscitation was significantly worse in glucose-treated cats (P < 0.01, P < 0.01, and P < 0.01, respectively). The neuropathologic score did not differ between glucose- and saline-treated groups (P = 0.07). Thi sstudy demonstrated that a clinically relevant dose of glucose administered prior to cardiac arrest exacerbates postresuscitation neurologic injury in a feline cardiac arrest model of global cerebral ischemia.