Expression of antiapoptotic survivin and aven genes in rat heart tissue after traumatic brain injury.

We have recently shown that experimental traumatic brain injury (TBI) results in ultrastructural damage in heart tissue. The aim of this study was to determine the two antiapoptotic signals "survivin" and "aven" in rat heart tissue following TBI, and comparing the effects of erythropoietin (EPO) and methylprednisolone (MPS). Thirty-six Wistar-Albino female rats weighing 190 to 230 g were randomly allocated into six groups: group 1 underwent head trauma with no treatment; group 2 and group 3, head trauma and intraperitoneally delivered EPO (1000 IU/kg) and MPS (30 mg/kg), respectively; group 4 (vehicle), head trauma and intraperitoneal albumin (0.4 mL/rat); groups 5 and 6, control and sham-operated groups, respectively. Three-hundred g-cm impact trauma was produced by the method of weight-drop. Real-time quantitative polymerase chain reactions were used to estimate survivin and aven gene expression at the total RNA level. Both survivin and aven were higher among the treatment than the trauma group (P = .0006, .0001 and P = .0038, .0033, respectively). Comparing survivin and aven between EPO and MPS treatment groups showed no significance (P = .3027, .2171, respectively). Also, both survivin and aven were significantly higher among the treatment than the vehicle, the control, or the sham-operated groups. These findings suggested that both EPO and MPS may play important roles in the expression of antiapoptotic survivin and aven genes in heart tissue after TBI.

Effect of erythropoietin on bcl-2 gene expression in rat cardiac myocytes after traumatic brain injury.

The purpose of this study was to investigate whether erythropoietin (EPO) has an effect on the expression of bcl-2 in rat cardiac myocytes following experimental isolated traumatic brain injury (TBI). Forty-eight Wistar-Albino female rats were randomly allocated into eight groups. Groups AC and BC were controls; groups AS and BS were sham-operated animals. Groups A1 and B1 underwent head trauma without treatment. Groups A2 and B2, head traumas plus EPO intraperitoneally (1000 IU/kg); groups A3 and B3, the vehicle groups, head traumas and intraperitoneal albumin (0.4 ml/rat). The method of weight drop was used to produce impact trauma at 24 hours after injury. Samples obtained from the left ventricle were assayed for lipid peroxidation and bcl-2 gene expression using real-time quantitative polymerase chain reactions. Lipid peroxidation in the heart tissue was determined by the concentration of thiobarbituric acid reactive substances (TBARs). The results showed that administration of EPO significantly reduced the increase in lipid peroxidation by-products after moderate or severe trauma. The bcl-2 expression was significantly higher in EPO (A2 and B2) compared to trauma groups (A1 and B1) suggesting a protective effect. These findings suggest that EPO may play an important role in the expression of bcl-2 and decrease in TBARs-the end product of lipid peroxidation in myocytes-after moderate or severe TBI.

Prolonged cerebral salt wasting syndrome associated with the intraventricular dissemination of brain tumors. Report of two cases and review of the literature.

Hyponatremia is a frequent event in neurosurgery practice and is usually associated with subarachnoid hemorrhage, head trauma, infections and neoplasms. The two common clinical manifestations are the inappropriate secretion of antidiuretic hormone (SIADH) and the cerebral salt wasting syndrome (CSWS), which were usually attributed to each other due to identical clinical presentation. In contrast to the better-recognized SIADH, there has not been a uniform consensus over the humoral and neural mechanisms of CSWS and functional aspects of renal response. In this article, we report on 2 cases of a primitive neuroectodermal tumor with prolonged CSWS manifested during the intraventricular dissemination of primary disease and the high catabolic stage.