Neuroscience Letters, 146 (1992) 121-124 121 © 1992 Elsevier Scientific Publishers Ireland Ltd. All rights reserved 0304-3940/92/$ 05.00 NSL 09028 Post cardiac arrest hyperoxic resuscitation enhances neuronal vulnerability of the respiratory rhythm generator and some brainstem and spinal cord neuronal pools in the dog J. Marsala, M. Marsala, I. Vanicky, J. Galik and J. Orendacova Institute of Neurobiology, Slovak Academy of Sciences, Kosice (Czech and Slovak Federal Republic) (Received 15 May 1992; Revised version received 21 July 1992; Accepted 22 July 1992) Key words: Cardiac arrest; Dog; Hyperoxic resuscitation; Normoxic resuscitation; Selective vulnerability Selective neuronal vulnerability of the motor cortex, basal ganglia, brainstem, medulla, cerebellum, C6 ,md L6 segments of the spinal cord were studied after 15 min of cardiac arrest followed by 1 h of normoxic or hyperoxic resuscitation using the suppressive Nauta method in dogs. Hyperoxic resuscitation causes characteristic somatodendritic argyrophilia of the interneuronal pool in the spinal cord and lower medulla. Cuneate, lateral reticular, supraspinal, and caudal trigeminal nuclei as well as the dorsal and ventral respiratory neuronal groups were heavily involved. Similarly, the Purkinje cells, neurons in the middle and deep portions of the mesencephalic tectum, perirubral, pretectal, posterior commissure, middle-sized striatal and giant pyramidal (Betz's) neurons in the motor cortex became argyrophilic. Hyperoxic resuscitation versus normoxic resuscitation causes statisti- cally significant somatodendritic argyrophilia of the dorsal respiratory group, cuneate, dorsal lateral geniculate and thalamic reticular nuclei. Post cardiac arrest encephalopathy and myelopathy are among the most serious complications occurring after resuscitation. Standardized ischemia-reperfusion models were used aimed at clarifying the pathophysiol- ogical determinants of post cardiac arrest neuronal death [4, 6, 7]. In most of these experiments the hyperoxic re- suscitation (100% oxygen) was used as a crucial compo- nent of the reanimation protocol. Stil~ unanswered are such crucial questions as why some neuronal pools are becoming more vulnerable during the post resuscitation period. Recent studies performed in our laboratory re- vealed that the acute ischemia-induced neuronal damage can be exactly mapped using the suppressive Nauta method [10, 11]. Moreover, it was found that postis- chemic hyperoxia strongly enhanced the neuronal vul- nerability [12] and vice versa the intensity of neuronal and blood-brain barrier damage were significantly de- creased when graded postischemic reoxygenation has been applied [9, 15]. The present study was therefore undertaken to deter- mine whether hyperoxic resuscitation of 1 h duration versus normoxic resuscitation followed after 15 min car- Correspondence: J. Marsala, Institute of Neurobiology, Slovak Acad- emy of Sciences, Srobarova 57, 040 01 Kosice, CSFR. diac arrest is more harmful to the brainstem and spinal cord neuronal pools. Thirteen adult mongrel dogs weighing 12-24 kg were used in this study. The animals were fasted for 24 h be- fore surgery with free access to water. Basically a modi- fied canine model of 15 min cardiac arrest was used [5]. After pentobarbital anaesthesia (30 mg/kg, i.v.) the dogs were intubated and instrumented for monitoring the physiologic variables, i.e., heart rate, mean arterial blood pressure (MABP), EEG, and ECG. Body temperature was measured in the oesophagus at the heart level and maintained at 37.5 + I°C with heating pad and lamp. Prearrest blood glucose and paO2, paCO2, pH and base excess were monitored (AVL 995-Hb). After left thora- cotomy cardiac arrest was induced by intracardial KC1 (0.75 mEq/kg) and the guided ventilation was stopped. Cardiac arrest was maintained for 15 min. Thereafter the dogs were resuscitated reintroducing the guided ventila- tion, internal cardiac massage, epinephrine, bicarbonate and internal defibrillation in the 5th min. MABP > 80 Torr was achieved within the first 2 min of massage and spontaneous heartbeat was restored in all dogs between 5 and 9 min. Then the chest was closed. MABP was maintained during 1 h resuscitation > 100 Torr with low- dose epinephrine infusion, if needed. In group A (n -- 5) the dogs exposed to hyperoxia the