To investigate the relationship between development of traumatic brain edema and changes in posterior hypothalamus excitability, different nuclei of the hypothalamus were excited with electrical stimulation. According to the stimulation method, forty rabbits were randomly divided into the following groups. Group A animals( n =8) were not stimulated and used as the sham control. Group B animals( n =8) underwent stimulation of the posterior nucleus of hypothalamus (PH), Group C ( n =8) stimulation of the dorsal medial nucleus of the hypothalamus (DMH), and Group D ( n =8) stimulation of the ventral medial nucleus of the hypothalamus (VMH). In group E animals( n =8), ? receptor antagonist Regitine was injected intravenously before stimulating PH. During the course of stimulation, intracranial pressure (ICP) was monitored continuously. 3h later, the animals were sacrificed and their cerebral tissue was examined for content of water, K + and Na + . Changes in blood brain barrier (BBB) were traced by a colloidal gold technique. The results showed that stimulation of the three nuclei caused an acute elevation of ICP,which was significantly higher than that before stimulations ( P

OBJECTIVE: Exploring the intra-axonal overloading of calcium ion (Ca(2+)) in brain diffuse axonal injury (DAI) and the therapeutic effect of calcium antagonist(Nimotop) on DAI. METHODS: Fourteen SD rats were divided into injury group, treatment group and control group. The DAI model of rats was produced by using a head-instant-axial-rotation device. Tissues from the medulla oblongata of rats were taken 2-24 h post-injury and processed for electron microscopic observation by a cytochemical technique for calcium ion. RESULTS: In the injured rats there was evidence of local disruption of myelin sheath,lucent spaces between myelin sheath lamellae, separation of axolemma from the inner layer of myelin sheath, peripheral accumulation of organellae, intra-axonal formation of vacuoles and reduction of mitochondria. A large number of fine calcium deposits were seen on the affected myelin sheath. The severity of the myelin sheath lesion was related positively to the number of calcium deposits on it. In the later post-injury period the coarse calcium particles appeared within the damaged axon. Neuronal somas and microvascular endotheliums showed a lot of vacuoles and some fine calcium deposits. Many microvilli formed on the luminal aspect of endothelium. In the treatment group myelin sheath tended to be injured locally, and axoplasmic mitochondria were nearly normal in number, structure, and distribution. Few calcium deposits were found in axons. Vacuolization was obviously reduced in neuronal soma and endothelium. CONCLUSIONS: In DAI there exists an intra-axonal overloading of calcium ion, which is a key factor to the occurrence and development of DAI. Early use of Nimotop can alleviate DAI.

OBJECTIVE: To explore the content change of neurofilament (NF) protein subunits in the experimental brain diffuse axonal injury (DAI) by lateral head rotation. METHODS: Twenty-four Sprague Dawley (SD) rats were equally divided into three injury groups (2 h, 12 h, and 24 h post injury) and one control group. The models of DAI were made in the injury groups by lateral head rotation. Western blotting technique was used to measure the content of NF68 (a kind of NF protein subunit) in the brainstem tissues among all the injured and control rats. The NF68 immunohistochemical staining was used in another six SD rats in order to observe the morphological changes in DAI. RESULTS: The NF68 content in the brainstem tended to decrease at 2 h post injury, decreased significantly at 12 h and continued its decrease at 24 h. NF56 and NF52, as the breakdown products of NF68, had a tendency to increase at 2-12 h after the injury, and amounted to a significantly higher level at 24 h. Microscopically, there were a lot of swelling neuronal axons in the ventral part of the medullar oblongata at 2 h after the injury. Some axons were disconnected, and axonal retraction balls formed on their proximal end. CONCLUSIONS: There is an occurrence of phosphorolysis within the brainstem in DAI by lateral head rotation. These reactions cause the breakdown of NF68, which results in the decrease of NF68 in content. It suggests that the breakdown of neurofilament protein subunits is an important reason for structur al destroy of neurofilaments in DAI.