FUNCTIONAL ACTIVATION OF CEREBRAL BLOOD-FLOW AFTER CARDIAC-ARREST IN RAT

After a period of global cerebral ischemia, CO2 reactivity and the hem odynamic-metabolic activation to functional stimulation are transientl y suppressed. This raises the question of whether the impaired functio nal coupling reflects disturbances of functional integrity of the brai n or an impaired cerebrovascular reactivity. We, therefore, compared t he recovery of CO2 reactivity with that of somatosensory evoked potent ials, functional flow activation and neurologic deficits in a rodent m odel of cardiac arrest-induced cerebral ischemia, followed by up to 7 days of reperfusion. Cardiac arrest of 10 minutes' duration was produc ed in 24 animals by electrical fibrillation of the heart. Five animals were sham-operated controls. Resuscitation was performed by external cardiac massage, using standard resuscitation procedures. Functional a ctivation was carried out under chloralose anesthesia by electrical st imulation of forepaws. CO2 reactivity was tested by ventilation of ani mals with 6% CO2. During functional and hypercapnic stimulation CBF wa s measured in the somatosensory cortex using laser-Doppler flowmetry, and at the end of the experiment by C-14-iodoantipyrine autoradiograph y. Neurologic deficits were scored by evaluating consciousness and var ious sensory and motor functions. Tn control animals 6% CO2 increased CBF measured by laser-Doppler flowmetry by 28.8% +/- 8.7%. Forepaw sti mulation generated somatosensory evoked potentials with an amplitude o f 750 +/- 217 mu V and increased CBF measured by laser-Doppler flowmet ry by 86.0% +/- 18.1%. After return of spontaneous circulation, CO2 re activity was transiently reduced to about 30% of control at 1 hour of reperfusion (P < 0.05) but returned to near control at 5 hours. Somato sensory evoked potential amplitudes were reduced to 15% of control at 45 minutes of reperfusion and returned to only 50% to 60% at 3 and 7 d ays after return of spontaneous circulation (P < 0.05). Functional act ivation of blood flow was completely suppressed during the first hour after return of spontaneous circulation but also recovered to 50% to 6 0% of control at 3 days after return of spontaneous circulation (P < 0 .05). Linear regression analysis revealed a significant correlation be tween recovery of functional activation of blood flow and both recover y of the amplitude of somatosensory evoked potentials (P = 0.03) and t he neurologic deficit score (P = 0.02), but not between neurologic def icit score and recovery of CO2 reactivity or somatosensory evoked pote ntial amplitudes. These data demonstrate that the suppression of funct ional activation of blood flow after 10 minutes cardiac arrest is not related to impairment of coupling mechanisms but reflects ongoing dist urbances of the functional integrity of the brain. Assessment of funct ional flow coupling is a reliable way to study postischemic recovery o f the brain.