SELECTIVE MOTOR-NEURON DEATH AND HEAT-SHOCK PROTEIN INDUCTION AFTER SPINAL-CORD ISCHEMIA IN RABBITS

Paraplegia is a serious complication that sometimes results from opera tion on the thoracic aorta, The mechanism of spinal cord injury has be en thought to involve tissue ischemia, and spinal motor neurons are su ggested to be vulnerable to ischemia, The exact mechanism, however, is not fully understood, To evaluate the mechanism of such vulnerability of motor neurons, we attempted to make a reproducible model for spina l cord ischemia and statistically analyzed cell damage, With this mode l, induction of heat shock protein 70 (HSP70) and heat shock cognate p rotein (HSC70) messenger ribonucleic acid molecules were investigated with Northern blot analysis for up to 7 days of reperfusion after 5 or 15 minutes of ischemia, Immunohistochemical studies of their proteins were also done, (heat shock proteins are a set of markers of neuronal injury after ischemia.) After 5 minutes of ischemia, there was no ind uction of HSP70 and HSC70 messenger ribonucleic acid molecules or thei r proteins, and all cells remained intact, In contrast, after 15 minut es of ischemia, HSP70 messenger ribonucleic acid was induced at 8 hour s of reperfusion, and HSC70 messenger ribonucleic acid was expressed c ontinuously at the control level, Immunoreactivity of HSP70 protein wa s slightly induced at 8 hours of reperfusion selectively in motor neur ons, and about 70% of motor neuron cells showed selective cell death a fter 7 days of reperfusion, This study demonstrated induction of HSP70 messenger ribonucleic acid and its protein in motor neuron cells afte r transient ischemia in the spinal cord, This phenomenon was not accom panied by HSC70 induction.