Intracranial hypertension remains the key biomarker of severe traumatic brain injury for neurosurgery doctors. The monitoring of intracranial pressure (ICP) provides the technical support of precision and effective treatment strategy. In this article, the authors analyze the methodology, timing, function and development trend of ICP monitoring. The developing process of ICP monitoring contains the efforts of exploring a safe and precise technique to reflect the pressure in an injured brain. The modern ICP monitoring technology provides sufficient information flow for the management of craniocerebral trauma. Neurosurgeons could follow the information in the value and trends of ICP monitoring and implement it into decision making throughout the whole process of patient management. With the advanced data collecting and analyzing system the clinician can look into the waveform and parameter generalized by ICP value, and can interpret to the pathophysiological profiling in brain. ICP monitoring could exert efficacy not only in reflecting the mechanism of brain injury but also in the directing the clinical practice.

To evaluate the protective effect of MgSO_4 during cerebral ischemia reperfusion,twentyfour SD rats were divided randomly into control group (n=7),ischemic reperfusion group (n=9)and MgSO_4 treatment group (n=8)with Pnlsinelli and Brierley's animal ischemic reperfusion model. Compared with the control and ischemic reperfusion group,cerebral tissue contents of water and malondialdehyde reduced markedly (P

Objective To determine the effect of hypothermia on gene transcription and protein expression of calpain after traumatic brain injury (TBI). Methods Twenty-seven rats were randomly divided into three groups, ie, normal control group, normothermia TBI group and hypothermia TBI group. All rats with TBI were suffered from a lateral fluid percussion injury (FPI) at the right parietal lobe. Hy-pothermia intervention [rectal temperature for (32 ± 0.5) ℃] was performed for four hours immediately after TBI in hypothermia TBI group. Fluorescence PCR and Western blot were utilized to semi-quantify gene transcription and protein expression of ealpain and immunofluorescence used to observe protein dis-tribution of Calpain. Results Compared with normothermia TBi group and normal control group, hypo-thermia TBI group showed increased calpain gene transcription at 12 and 24 hours respectively after FPI (P <0.05). However, the increase of ealpain protein expression in hypothermia TBI group was inhibited more significantly by hypothermia at 6,12,24 and 72 hours after TBI, compared with normothermia TBI group (P < 0.05). Conclusion Neuroproteetion of hypothermia after TBI may somewhat be related to the decrease of calpain protein expression after its gene transcription.

Objecfive To explore pathological mechanism and treatment of central hyponatrem-ia. Methods Synchronous assay was made to detect changes of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP),endogenous digitalis-like substance(EDLS),antideuretic hormone (ADH),Na+ concentrations in blood and urine as well as osmotic pressure of plasma and urine in 68 pa-tients with traumatic brain injury(TBI). Results Of all,there were 27 patients with hyponatremia,mostly in patients with severe or critical TBI.There found syndrome of inappropriate secretion of antidi-uretic hormone(SIADH)in 7 patients and cerebral salt wasting syndrome(CSWS)in 20. Conclu-sions The central hyponatremia in patients with TBI may be related to the increased secretion of EDLS and ADH.The decrease of ANP and BNP in blood has no direct effect on Na+ concentration in blood.In-travenous injection of extrinsic thyrotropin releasing hormone(TRH)may inhibit dilutional hyponatremia resulted from increased secretion of ADH in TBI patients.

Objective To investigate the therapeutic effect of NSR siRNA on nerve regeneration following spinal cord hemi-transsection injury in rats. Methods Rats with T8 spinal cord hemi-trans-section were didded into 3 groups, ie, siRNA group, NS group and control group. SiRNA or NS was in-jected into lateral cerebral ventricle just after spinal cord injury. The therapeutic effect of NgR siRNA was evaluated by using BBB locomotor rating scale, retrograde horseradish peroxidase(HRP)tracing and HE staining. Results BBB locomotor rating scale showed that the recovery of the locomotor function of siRNA group seemed to be better than that of the other two groups from the 4th week, but there was no statistical difference. Retrograde HRP tracing showed a large number of positive cells in the anterior horn of spinal cord, with statistical difference compared with NS group and control group(P<0. 05). Eight weeks after spinal injury, HE staining showed disorderly distribution of the fibres in NS group and control group but serial fibres in the injury region in siRNA group. Conclusion NSR siRNA may promote the nerve regeneration following spinal cord injury.

Progressive brain injury after traumatic brain injury,including intracranial hemorrhage,cerebral ischemia and edema,is an important factor affecting the prognosis of patients with traumatic brain injury.On basis of reviewing literatures,the research progress on incidence,mechanism,methods for early diagnosis,treatment and prognosis of progressive brain injury after traumatic brain injury was reviewed.

Objective To evaluate the changes in water, electrolyte and acid-base balance after seawater immersion in cases of open abdominal trauma associated with intestinal rupture, and to obtain a theoretical basis for the early treatment of open abdominal injury with intestinal rupture in naval combat. Methods A canine model of open abdominal trauma with intestinal rupture was established in 26 healthy adult dogs, and they were divided randomly into three groups. All animals were subjected to abdominal wall incision and intestinal rupture. Seawater immersion group(n=10) was immersed into artificial seawater after trauma; normal saline solution group(n=6) was immersed into normal saline solution after trauma; control group (n=10) had no immersion. The 3 groups were observed for changes in water, electrolyte and acid-base balance, and the results were analysed and compared. Results Signficant disturbance of water, electrolyte and acid-base imbalance were observed in the seawater immersion groups, but no significant changes of these parameters were seen in the control group and normal saline group. Conclusion Seawater immersion is the main factor leading to the disturbance of body metabolism after open abdominal trauma with intestinal rupture.

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 moderate severity. Bcl 2, Bcl x and Bax protein expression was detected by immunohistochemistry. 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 expression increased significantly, while the Bcl 2 and Bcl x protein expression decreased 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.

Objective: To investigate the effects of adenosine A 1 receptor agonist N 6 cyclohexyladenosine(CHA) on neurofunction after fluid percussion injury in rats. Methods: The effects of CHA intra cerebroventricular injection 10 min before brain trauma on rats neurofunction and neuropathological changes were evaluated. Results: Compared with the control group, CHA could ameliorate the behavior deficits and improve pathological change. Conclusion: Adenosine A 1 receptor plays an important neuroprotective role in rat secondary injuries following brain trauma.

Objective To study the causes, significance of alteration of PtiO 2, PtiCO 2 and pHti in liver tissue during liver ischemia reperfusion (I R). Methods After rabbits were anesthetized, liver ischemia was induced by complete occlusion of the hepatoduodenal ligment for 45 min, then the portal and arterial flow were released, and observed for 120 min for measuring the PtiO 2, PtiCO 2 and pHti in liver tissue and the pathology of the liver during ischemia reperfusion. Results After 15 min of hepatic vascular occlusion, PtiO 2 decreased to 4 mmHg, PtiCO 2 increased fast to (149.63?9.80) mmHg (P