Effect of hyperventilation on brain tissue oxygen pressure, carbon dioxide pressure, pH value and intracranial pressure during intracranial hypertension in pigs / 中华创伤杂志(英文版)

OBJECTIVE: To study the effect of hyperventilat ion on brain tissue oxygen pressure (P(ti)O(2)), brain tissue carbon dio xide pressure (P(ti)O(2)), pH value and intracranial pressure (ICP) dur ing intracranial hypertension in pigs. METHODS: Autologous arterial blood (5.5 mlplus minus0.5 ml) was injected into the left frontal lobe by micropump to establish the model of intr acerebral hematoma in pigs. After blood injection, the animals were hyperventila ted for 15 minutes to decrease the pressure of carbon dioxide in arterial blood (P(a)CO(2)) to 27.35 mm Hgplus minus11.97 mm Hg (1 mm Hg=0.133 kPa). The mean arterial pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), P(ti)O(2), (P(ti)CO(2)), pH value and [HCO(3)(-)] were continuously monitored and the blood gas was analyzed. RESULTS: After hyperventilation, the ICP significantly decr eased (P<0.01), the CPP significantly increased (P<0.05), while the P(ti)O(2) greatly decreased to t he ischemic level (8.20 mm Hgplus minus2.50 mm Hg) (P<0.01), the P(ti)CO(2) decreased (P<0.01) and the pH value increased (P<0.01). At the same time, bl ood gas analysis showed that the P(a)CO(2) greatly decreased and the pH valu e increased. CONCLUSIONS: Hyperventilation can decrease the ICP and the P(ti)O(2) significantly. Therefore, hyperventilation should be avoided earl y after brain injury. The P(ti)O(2) monitoring will be helpful for detec ting cerebral ischemia early.

Alterations of bcl-2, bcl-x and bax protein expressions in area CA-3 of rat hippocampus following fluid percussion brain injury / 中华创伤杂志(英文版)

OBJECTIVE: To investigate the alterations of bcl-2 gene family in the area of CA-3 in rats and the molecular mechanism of neuronal apoptosis following traumatic brain injury. METHODS: To investigate the alterations of bcl-2 gene family in the area of CA-3 in rats and the molecular mechanism of neuronal apoptosis following traumatic brain injury. RESULTS: The immunoreactivity of bcl-2 and bcl-x proteins decreased in the hippocampus ipsilateral impact site at 6 hours after injury, and this was the main cause of down-regulation of the value of (bcl-2+bcl-x)/ bax. During the period of 1-3 days after injury, bax protein expression increased significantly, while bcl-2 and bcl-x protein expressions decreased relatively slowly. The decreased value of (bcl-2+bcl-x)/ bax was mainly due to the bax up-regulation. CONCLUSIONS: The bcl-2 gene family is involved in neuronal apoptosis after traumatic brain injury, and the protein-expression alterations of the bcl-2 gene family members lead to apoptosis of the neuronal cells.