Effect of pregabalin in preventing secondary damage in traumatic brain injury: an experimental study.

BACKGROUND: In this study we aimed to explore the effects of pregabalin on a traumatic brain injury model in rats. MATERIAL AND METHODS: This study included 40 adult male Sprague-Dawley rats randomized into 4 groups, each of which contained equal numbers of animals. The control group had no head trauma and thus was not treated. The trauma group had head trauma but was not treated. The pregabalin group had no head trauma but was treated by pregabalin. The trauma + pregabalin group had head trauma treated with pregabalin. The biopsy samples taken from the study animals were histopathologically examined for the presence of edema, inflammation, and neuronal damage. RESULTS: All animals in the trauma group had edema, inflammation, and neuronal damage. Four subjects in the control group, 6 in the pregabalin group, and 4 in the trauma + pregabalin group had edema; inflammation was present in 1 subject in the control group, 3 subjects in the pregabalin group, and 3 subjects in the trauma + pregabalin group; neuronal damage existed in 1 subject in the control group, 1 subject in the pregabalin group, and 6 subjects in the trauma+pregabalin group. The trauma group had significantly higher edema and neuronal damage scores than the other groups. Similarly, inflammation was significantly more prevalent in the trauma group than the control and trauma+pregabalin groups. CONCLUSIONS: The results of the present study indicated anti-edema, anti-inflammatory, and neuroprotective effects of pregabalin in an experimental head trauma model in rats. Pregabalin may thus be beneficial in humans with acute TBI by relieving concomitant edema and inflammation.

Effects of decompressive craniectomy, hypertonic saline solution and mannitol on an experimental model of cerebral ischemia.

BACKGROUND: Cerebral ischemia is a cause of serious morbidity and mortality. Strategies that would protect cerebral tissue against ischemic injury are important. The present study aimed to evaluate effects of surgical and medical treatments, either alone or in combination, on infarction area in an experimental rat model of cerebral ischemia. METHODS: Adult male Sprague-Dawley rats (n=30) were divided into 6 groups, each including 5 experimental animals. Cerebral ischemia was created by right common carotid artery occlusion (CCAO) under anesthesia. Decompressive craniectomy (DC) was performed in the relevant groups at the 12th hour following CCAO, whereas medical treatments were performed in the relevant groups at the 1st, 12th, and 24th hours following CCAO. After CCAO, the control group received 1 mL/kg physiological saline, hypertonic saline (HS) group received 3% hypertonic saline (1 mL/kg), and mannitol (MAN) group received 20% mannitol (1 g/kg). While only DC was performed following CCAO in the DC group, DC+HS group underwent DC together with hypertonic saline treatment and DC+MAN group underwent DC together with mannitol treatment. The rats were decapitated at the end of the 24th hour following ischemia. Cerebral sections were stained with 2% 2,3,5-triphenyltetrazolium chloride (TTC). The ratio of infarction area to the total area of section was calculated as percentage. RESULTS: Mean infarction areas were 27.9% in the control group, 13.7% in the HS group, 15.1% in the MAN group, 10.6% in the DC group, 8.1% in the DC+HS group, and 9.7% in the DC+MAN group. Mean infarction areas were significantly lower in all groups than in the control group. While the mean infarction area did not differ between the HS and MAN groups, it was lower in the groups undergoing DC as compared to these two groups. The best outcome was observed in the DC+HS group. CONCLUSION: Both medical and surgical treatments were effective in decreasing cerebral ischemic infarction. There was no difference between medical treatments groups in terms of efficacy, whereas DC led to a substantial decrease in ischemic infarction volume as compared with the medical treatment groups. Combined treatment approaches performed to decrease infarction volume also resulted in favorable outcomes.

[Effects of anti-edema drugs on diffuse cerebral edema in rats: experimental study]. / Siçanlarda, antiödem olarak kullanilan ilaçlarin diffüz beyin ödemine etkileri: Deneysel çalisma.

BACKGROUND: Traumatic brain edema is one of the most common problems encountered in neurosurgical practice and it leads to morbidity and mortality via increased intracranial pressure. The aim of this study was to examine the effect of hypertonic saline on traumatic brain edema in comparison to mannitol. METHODS: Eighty adult male Sprauge-Dawley rats weighting 300-350 g were used in this experimental study. Rats were randomly divided into control (C); trauma (T); mannitol only trauma+mannitol; NaCl 3% only; Trauma+NaCl 3%; NaCl 7.5% only; trauma+NaCl 7.5%; NaCl 23.4% only and trauma+NaCl 23.4% groups. All medications were given intraperitoneally. Rats were sacrificed and decapitated 24 hours after trauma with or without medications and the brains were examined histopatologically. RESULTS: Although no difference was observed with regard to hemorrhage between trauma only and trauma+NaCl 23.4% groups, there was a statistically significant difference in brain edema within these two groups (p=0.003). There were no statistically significant differences within groups with respect to plasma osmolarity and serum sodium levels. CONCLUSION: This study demonstrates that 23.4% NaCl is more effective than other concentrations of hypertonic saline or mannitol in the prevention of posttraumatic brain edema. Further clinical studies with different dosages and concentrations of hypertonic saline are required.