Changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To explore changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats, and to investigate the relationship between cytosolic free calcium concentration ([Ca(2+)](i)) in the synaptosome and Ca(2+)-ATPase activities of mitochondria.</p><p><b>METHODS</b>The level of [Ca(2+)](i) in the synaptosome and Ca(2+)-ATPase activities of mitochondria in the acute brain damage induced by injection of pertussis bacilli (PB) in rat was determined and nimodipine was administrated to show its effects on [Ca(2+)](i) in the synaptosome and on alteration of Ca(2+)-ATPase activity in the mitochondria. Seventy-three rats were randomly divided into four groups, ie, normal control group (Group A), sham-operation control group (Group B), PB group (Group C) and nimodipine treatment group (Group D).</p><p><b>RESULTS</b>The level of [Ca(2+)](i) was significantly increased in the PB-injected cerebral hemisphere in the Group C as compared with that in the Group A and the Group B at 30 minutes after injection of PB. The level of [Ca(2+)](i) was kept higher in the 4 hours and 24 hours subgroups after the injection in the Group C (P<0.05). In contrast, the Ca(2+)-ATPase activities were decreased remarkably among all of the subgroups in the Group C. Nimodipine, which was administered after injection of PB, could significantly decrease the [Ca(2+)](i) and increase the activity of Ca(2+)-ATPase (P<0.05).</p><p><b>CONCLUSIONS</b>The neuronal calcium channel is opened after injection of PB. There is a negative correlation between activities of Ca(2+)-ATPase and [Ca(2+)](i). Nimodipine can reduce brain damage through stimulating the activities of Ca(2+)-ATPase in the mitochondria, and decrease the level of [Ca(2+)](i) in the synaptosome. Treatment with nimodipine dramatically reduces the effects of brain damage induced by injection of PB.</p>

A new model of decelerating head injury in rabbits / 中华创伤杂志

Objective　To set up an experimental animal model of head injury of deceleration. 　Methods　The decelerating head injury was produced in r abbits by utilizing an impactor consisting of a rotor, elastic strips, a platfor m and a revolving board. Sixty-nine rabbits were used in this experiment: 33 ra bbits were for pre-experiment to establish the correlation of impact force and brain damage, 36 rabbits were divided into a control group (n=12), a mild injur y group (n=12) and a severe injury group (n=12) to elucidate the pathophysiologi cal changes after head injury at different injury levels. 　Results　The physiological responses after impact were observe d in all traumatic animals, which showed a sudden rise or reduction of blood pre ssure, deep and fast breath and apnea, and pain reflects inhibition, etc. The re s ponses were more obvious in the severe injury group than in the mild injury grou p. The water content of the brain increased 6 h after injury and the intracrania l pressure went up 1- 6 h after injury in the severe injury group. The patholog ical lesions were noted at or above the impact force level of (800±50) N. At th e severe injury level of (1 100±100) N,there were almost all kinds of lesions, such as skull fracture, brain contusion ( coup injury and contre-coup injury),b rain stem injury and subdural hematoma. When the impact force rose to or over (1 400±150) N,the animals died of persistent apnea mostly. 　Conclusions　A new practical and simple model of head injury of deceleration in rabbits has been developed with several features similar to t he experience in the clinical setting. This model with the same biomechanical me chanism as the clinical head injury of deceleration is quite useful for further study of the pathophysiological mechanisms of head injury, safe measure of abati ng head injury and investigating the effective therapeutic method for severe hea d injuries.