Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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J. Cereb. Blood Flow Metab. · Mar 1998
Monitoring of cerebral oxygen metabolism in the jugular bulb: reliability of unilateral measurements in severe head injury.
To investigate the reliability of unilateral jugular venous monitoring and to determine the appropriate side, we performed bilateral jugular venous monitoring in 22 head-injured patients. Fiberoptic catheters were placed in both jugular bulbs. Arterial and bilateral jugular venous blood samples were obtained simultaneously for in vitro determination of jugular venous oxygen saturation (SJO2), arterial minus jugular venous lactate content difference (AJDL), and modified lactate-oxygen index (mLOI). ⋯ We conclude that in severe head injury, even calculated unilateral jugular venous monitoring has an unpredictable risk for misleading or missing data. Therefore, the reliability of unilateral jugular venous monitoring appears suspicious. For diagnosing ischemia the CT approach is recommended.
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J. Cereb. Blood Flow Metab. · Mar 1998
Dexamethasone aggravates ischemia-induced neuronal damage by facilitating the onset of anoxic depolarization and the increase in the intracellular Ca2+ concentration in gerbil hippocampus.
The Ca2+ mobilization across the neuronal membrane is regarded as a crucial factor in the development of neuronal damage in ischemia. Because glucocorticoids have been reported to aggravate ischemic neuronal injury, the effects of dexamethasone on ischemia-induced membrane depolarization, histologic outcome, and changes in the intracellular Ca2+ concentration in the gerbil hippocampus were examined in vivo and in vitro. The effects of metyrapone, an inhibitor of glucocorticoid synthesis, were also evaluated. ⋯ The Ca2+-free in vitro hypoxia reduced the elevation compared with that in the Ca2+-containing condition. Treatment with dexamethasone facilitated the increase on both the initiation and the extent in the Ca2+-free condition. Aggravation of ischemic neuronal injury by endogenous or exogenous glucocorticoids is thus thought to be caused by the advanced onset times of both the ischemia-induced direct-current potential shift and the increase in the intracellular Ca2+ concentration.