Hypoxemia is the most frequent respiratory abnormality in craniocerebral injuries. we present here the results of a retrospective study of the post-operative changes in arterial oxygenation in 65 cases of craniocerebral injuries. Thirty cases of non-neuro-surgical operations were used as controls.It was found that the PaO2 values in the craniocerebral injury group were significantly lower than those in the controls and often accompanied by obvious hypocapnia and respiratory alkalosis. Seventy-two per cent of the 65 cases had PaO2 values below 80mmHg and 20% below 60mmHg. Obvious hy-poxemia occurred most often in patients with brain stem injuries, extensive cerebral contusions and subdural hematomas. The PaO2 values usually decreased to the lowest level during the period of 24 to 48 hours after operation. There was no mortality in patients whose PaO2 values were above 80mmHg. In contrast, 61% of patients with PaO2 below 60mmHg showed poor prognosis.ICP mornitoring performed in 5 cases of craniocerbral injuries suggested that increased ICP was, in some way, associated with lower PaO2 .Nine dogs, anesthetized with sodium pentobarbital and under controlled ventilation, were studied for changes of arterial blood gases after ICP had been increased by epidu-ral balloon inflation to 50 and 100 mmHg for 30 minutes. All the animals consistently showed a decrease of PaO2 accompanied by a slight increase of PaCO and decrease of pH values after elevaion of ICP.The extent of these changes was greater when ICP was 100mmHg than when it was 50mmHg.Hyperventilation at ICP of 100mmHg could not restore PaO2 to baseline in most animals although their PaCO2 was decreased below baseline. These results indicate that acutely increased ICP has a direct effect on lungs, which is responsible for venous admixture and hypoxemia.The mechanisms,by which hypoxemia is caused after craniocerebral injuries, are discussed, ventilation-perfusion imbalance is considered to be a main factor for hypoxemia.we conclude that instant examination of arterial oxygenation is helpful to the recognition of the status of the patient's respiratory function, to the guidance of medical care and to the assessment of patient's prognois.It is suggested that effective control of increased ICP in head injuries can prevnt further deterioration of the respiratory function.

Objective: : T o study the microanatomy of the facial nerve in the cerebellopontine angle (CPA) a nd the internal auditory meatus (IAM) for the preservation of the facial nerve i n the acoustic neurinomas surgery. Methods: Forty sides of CPA f acial nerve of 20 adult cadaver heads were examined. Results: In the pontomedullary sulcus the facial nerve (1.98? 0.10) mm anterior to the vestibulocochlear nerve,(8.76?1.42) mm lateral to the abducent nerve at the points where the nerves join the brain stem at the lateral end of the sulcu s, (8.15?2.18) mm above the junction of the Ⅸ nerve with the medulla. There were 62 nutritious artery supplying the facial nerve in the CPA, mainly from the anterior inferior cerebellaris artery (AICA) and its branches; and 17 in the IA M were mostly from the internal auditory arteria (IAA). Conclusion: To be familiar with the microanatomy of the facial nerve in CPA and IAM is h elpful for localizing the facial nerve and improve its preservation in acoustic neuroma surgery.

Objective To clarify the role of hypothalamic IL-6 in gastric mucosal blood flow, gastric juice pH value and gastric mucosal injury. Method Model of gastric stress ulcer was established by fluid percussion to make craniocerebral trauma. Twenty male SD rats fed for one week in the experiment room were randomly(random number) divided into control group, one hour group, six hours group and 12 hours group after injury. The levels and distribution of IL-6 in hypothalamus were detected by using immunohistochemistry and Western blot. Simultaneously, gastric pH value, gastric mucosal blood flow and gastric mucosal injury index of rats in each group were measured, and the histology of gastric mucosa was observed. Results IL-6 immunoreactive cells were widely distributed in neuronal cells of hypothalamus of the stressed rats especially in the para-ventricular nucleus (PVN).One hour after injury, the pH value rapidly declined, and the lowest point appeared 6 hours later. One hour after injury, the injury of gastric mucosa was found, and the injury became worse and worse as time got longer and longer. The ulcer index (UI) was increased. One hour after injury, there was a brief increase in blood flow to the peak in gastric mucosa, and then the blood flow declined until 6 hours elapsed and got stable. The experiment prompted the gastric stress ulcer appeared. Conclusions In the SD rats with gastric stress ulcer induced by craniocerebral injury incurred by hydraulic percussion, the hypothalamic IL-6 may activate neuronendocrine metabolism mediated through the activation of PVN, inducing gastric mucosal injury.

The cerebral ischemia was produced by Pulsinellis method in Sparaque-Dawley rats. The brain edema and survival rate of rats with bilateral carotid and vertebral arteries occlusion for 60 min were observed in ip tetradrine at doses of 1 ~ 4 mg/kg groups and control rats.Superoxide dismutase and malondialdehyde in brain tissue were also measured by pyrogallol method and fluorescence spec-trometry. The results suggested that tetradrine have protective effect on cerebral ischemia, which was related to the inhibition of lipoxide and scavenging of oxygen free radical.

Objective: : To investigate whether development of the sph e noid sinus affect the surgical approach via saddle area. Methods: The pneumatization of sphenoid sinus of 50 cadaver heads was studied through t hinner CT scanning of coronal, sagittal and axial position. The sphenoid sinus w as classified according to the degree of pneumatization of sphenoid sinus toward s sphenoid bone, small wing of sphenoid bone and epippium. Results: There were 4% conchal, 18% pre-sellar, 18% semi-sellar, 14% sellar, 46% sellar -occipital in 100 sphenoid sinus cases. The transversal diameter of left and ri ght was 18.48 mm and 17.58 mm; The sagittal diameter of left and right was 2 2.20 mm and 20.82 mm, The vertical diameter of left and right was 21.02 mm and 2 0.38 mm. The distance between centre track and the later wall of sphenoid sinus was 14.78 mm in left side and 15.18 mm in right side. Conclusion: Thinner CT scanning with coronal and sagittal position can clearly show pneum atization of sphenoid sinus on both sides. Different pneumatization of sphenoid sinus provide anatomical basis for choosing operation approach.

Objective To review the features of diagnosis and treatment of craniocerebral firearm wounds in peacetime. Methods A total of 86 cases with various kinds of firearm wounds were retrospectively analyzed for discussing the characteristics of diagnoses and treatment of firearm wounds so as to provide the best treatment methods for firearm wounds of the brain. Results Of all, 80 cases (93%) won full recovery and four (5%) partial recovery but two (2%) were died of massive vascular damage and severe cerebral injuries within 24 hours after operation. Conclusions Craniocerebral firearm wounds are among the most devastating causes for morbidity and mortality in the civilian population. It is important to remove all foreign bodies, especially broken bones and necrotic tissues, and turn the open injury to the close injury. Stereotactic technique, localization of foreign bodies, culture of foreign body bacteria, drug allergy test and correct use of antibiotic and antiepileptic drugs are also critical for eliminating mortality and complications of craniocerebral firearm wounds.

Objective To investigate the effect of acute high intracranial pressure on the static pressure-volume curve of dogs' total respiratory system in order to evaluate the relationship between brain injury and respiratory insufficiency.Methods Fourteen dogs were divided into two groups.Animals were anesthetized,paralyzed and mechanical ventilated.The intracranial hypertension in experimental group(n=8)was induced by injecting blood-clots into the right frontal lobe.The other six dogs served as control.The intracranial pressure was monitored by an optical fiber transmitter inserted into the left cerebral hemisphere.The pressure-volume curves of the respiratory system were measured before and after induction of high intracranial pressure by a self-made apparatus consisting of two sealed bottles and a U shaped glass tube.The curves were also measured correspondingly in control group.The static compliance was calculated by equation C=?V/?P.The volume of intracerebral hematoma was calculated.The histopathology of lung was studied under microscope.Results The intracerebral hematoma was located in the right frontal lobe with volume from 4.8-11.5ml(average 8.48ml).The intracranial pressure was elevated from 18.13?5.96mmHg to 46.88?16.42mmHg,which induced a shift of pressure-volume curve to the right in experimental group,while no obvious change was found in control group.Compared to pre-injection,the static compliance of total respiratory system decreased significantly(P

To investigate the effects of antisense oligonucleotides directed at TNF-? on the intracranial pressure following craniocerebral explosive injury. Eighteen dogs were randomly divided into artificial cerebrospinal fluid (ACSF) group, sense group and antisense group. Using the model of craniocerebral explosive injury, ACSF, the sense oligonucleotides to TNF-? and the antisense oligonucleotides to TNF-? were administered into cerebellomedullar cisterna before injury respectively in three groups, and then the intracranial pressure and contents of brain H 2 O in the bilateral hemispheres in three groups were compared. As compared with the ACSF groups and the sense groups, the contents of brain H 2 O in the antisense groups were significantly reduced( P

Objective: To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis follow ing traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPBI) of moderate severity. bax and bcl-xL mRNA and protein expression was detected by RT-PCR an d immunohistochemistry. In addition to morphological evidence of apoptosis, TUNE L histochemistry was used to identify DNA fragmentation in situ under both l ight and electron microscope, whereas characteristic internucleosomal DN A fragm entation of apoptosis was demonstrated by DNA gel electrophoresis. Resul ts: bcl-xL mRNA and protein decreased in the ipsilateral hemisphere t o the impact site as early as 6 h post-injury［(67.42±7.54)% and (85.85±5.72)% r espectively］. The decrease in bcl-xL mRNA and protein preceded apoptosis was observed 12 h post-injury. And this was the main cause of up-regulation of the ratio of bax to bcl-xL in the acute period(minutes-hours) followin g FPBI. bax mRNA and protein were observed to rise slowly, doubled 3 d post- injury, returned to sham level slowly. The delayed cell death (days-weeks) migh t associated with the up-regulation of pro-apoptotic gene bax. Conclusio n: The expression of bcl-xL and bax coincide with apoptosis following TBI. The reg ulation of bax and bcl-xL by TBI occur before transcription. The balance of bax/bcl-xL ratio determines the neurocytes to survive or die following FPBI.

Objective: To investigate the alteration of bcl- 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague -Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of mo derate severity. Bcl-2, Bcl-x and Bax protein expression was detected by immun ohistochemistry. Results: (1) The immunoreactivity of Bcl-2 and Bcl-x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post-injury, and this was the main cause of down-regulation of the ratio of Bcl-2+Bcl-x to Bax. (2) During 1-3 d after injury, the Bax protein express i on increased significantly, while the Bcl-2 and Bcl-x protein expression decre ased relatively slow. The decreased ratio of Bcl-2+Bcl-x to Bax was mainly due to the Bax up-regulation. Conclusion: The bcl-2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.