Neuroprotective effects of bloodletting at Jing points combined with mild induced hypothermia in acute severe traumatic brain injury

Bloodletting at Jing points has been used to treat coma in traditional Chinese medicine. Mild induced hypothermia has also been shown to have neuroprotective effects. However, the therapeutic effects of bloodletting at Jing points and mild induced hypothermia alone are limited. Therefore, we investigated whether combined treatment might have clinical effectiveness for the treatment of acute severe traumatic brain injury. Using a rat model of traumatic brain injury, combined treatment substantially alleviated cerebral edema and bloodbrain barrier dysfunction. Furthermore, neurological function was ameliorated, and cellular necrosis and the inflammatory response were lessened. These findings suggest that the combined effects of bloodletting at Jing points（20 μL, twice a day, for 2 days） and mild induced hypothermia（6 hours） are better than their individual effects alone. Their combined application may have marked neuroprotective effects in the clinical treatment of acute severe traumatic brain injury.

Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury

The adipocytokine,apelin-13,is an abundantly expressed peptide in the nervous system.Apelin-13 protects the brain against ischemia/reperfusion injury and attenuates traumatic brain injury by suppressing autophagy.However,secondary apelin-13 effects on traumatic brain injury-induced neural cell death and blood-brain barrier integrity are still not clear.Here,we found that apelin-13 significantly decreases cerebral water content,mitigates blood-brain barrier destruction,reduces aquaporin-4 expression,diminishes caspase-3 and Bax expression in the cerebral cortex and hippocampus,and reduces apoptosis.These results show that apelin-13 attenuates secondary injury after traumatic brain injury and exerts a neuroprotective effect.

RELATIONS OF INTRACRANIAL PRESSURE, CREATINE KINASE AND BRAINSTEM AUDITORY EVOKED POTENTIAL IN PATIENTS WITH TRAUMATIC BRAIN EDEMA

We studied the relations of intracranial pressure (ICP),creatine kinase (CK) and bralnstem auditory evoked potential (BAEP) in 44 patients with traumatic brain edema who were admitted to our hospital from June 1990 to February 1991. There were 30 males and 14 females, with age range from 9 to 67 years. The results showed that the abnormal BAEP could reflect the severity of cerebral edema in acute head injury and was related to ICP and serum CK levels. When ICP>30 mmHg (4kPa), the abnormality of BAEP was more obvious than that of the control group (P<0.05); the serum CK levels were also elevated markedly. In patients with ICP over and below 4kPa, the rate of abnormal BAEP was 38.46% and 77.78% respectively (P<0.05). The serum CK level in the normal group or in the group with moderate abnormality of BAEP was significantly different from that in the group with severe abnormality or lack of BAEP (274.8± 98.24 U/L vs 705.3± 364.27 U/L; P<0.001). After treatment, the ICP returned to normal, and the BAEP norm