Biomedical subjects

A Görgülü

Publications and source records attributed to A Görgülü.

7 recordsLinked to original sources

PubMed2001

Effect of melatonin on cerebral edema in rats.

OBJECTIVE: Melatonin (5-methoxy-N-acetyltrypamine), a chemical naturally produced in the pineal gland, has been suggested to be a free radical scavenger and an antioxidant. In the present study, the effect of melatonin on cold-induced brain edema was evaluated by determination of cerebral water content, blood-brain barrier permeability, and areas of infarct; the effects were also studied histopathologically. METHODS: Brain edema was produced in rats by creating a lesion via cortical freezing. Animals were separated into four groups: sham-operated (craniectomy only); control (cold injury); sham-vehicle (cold injury plus saline); and melatonin treatment (cold injury plus melatonin). Melatonin was administered (50 mg/kg intraperitoneally) 15 minutes after the cold injury was induced. Twenty-four hours later, tissue samples from the core, from the periphery of the cold-injured hemisphere, and from the contralateral hemisphere symmetrical to the cold injury were obtained. RESULTS: Melatonin treatment reduced edema (mean +/- standard deviation; 86.22 +/- 1.54% in the control group versus 80.78 +/- 2.76% in the melatonin treatment group, P < 0.001) and blood-brain barrier permeability (45.34 +/- 2.75% in the control group versus 38.26 +/- 3.40% in the melatonin treatment group, P < 0.001) at the periphery of cold injury. Area of infarct reduced from 5.84 +/- 0.58% in the control group to 3.30 +/- 0.89% in the melatonin treatment group (P < 0.001). The effect of melatonin was also confirmed histopathologically. CONCLUSION: Melatonin was found to be neuroprotective in instances of cold-induced brain edema. Thus, melatonin may be a valuable therapeutic agent in the treatment of cerebral edema.

Animals↗

PubMed2000

Superoxide dismutase activity and the effects of NBQX and CPP on lipid peroxidation in experimental spinal cord injury.

The endogenous activity of the neuroprotective enzyme superoxide dismutase (SOD) and the amount of lipid peroxidation in the early phase of experimental spinal cord injury, together with the effects of N-methyl-D-aspartate (NMDA) antagonist CPP and non-NMDA antagonist NBQX on lipid peroxidation were evaluated. The clip compression model was used for the production of a standardized spinal cord trauma. SOD activity and malondialdehyde (MDA) levels--as an indicator of lipid peroxidation--were determined in the injured segment of the spinal cord 30 and 60 min after injury. SOD activity did not change in this period, whereas MDA levels at 30 and 60 min after trauma were significantly elevated. Intrathecal administration of CPP or NBQX 15 min after injury produced statistically significant reductions in MDA elevation 60 min after injury. NBQX was found to be more effective than CPP. These results demonstrated that intrathecal local application of excitatory amino acid receptor antagonists can protect the spinal cord from secondary damage caused by the generation of lipid peroxides in experimental spinal cord injury.

Animals↗

PubMed2000

Reduction of edema and infarction by Memantine and MK-801 after focal cerebral ischaemia and reperfusion in rat.

N-methyl-D-aspartate (NMDA) receptor antagonists have been found to be protective after cerebral ischemia. However most of these drugs have limited value as neuroprotectives in clinical therapy because of their side effects. Memantine is a noncompetitive NMDA receptor antagonist and it has been used for the treatment of various cerebral disorders with relatively few side effects. We investigated the beneficial effects of Memantine and compared its effect with MK-801 in a temporary focal cerebral ischemia model. As cerebral ischemia model three hours middle cerebral artery occlusion (MCAO) with intraluminal thread and three hours reperfusion was used. 78 male Spraque-Dawley rats were divided into three groups as follows: Control (Saline), treatment 1 (MK-801), and treatment 2 (Memantine) groups. In the treated groups, 15 minutes after MCAO, MK-801 and Memantine were administered in amounts of 1 mg/kg and 10 mg/kg intraperitoneally respectively. After a 3 hour period of reperfusion, the animals were examined for neurological deficits and then killed. The following values were measured; cerebral water content, blood brain barrier (BBB) permeability at the core and periphery of the ischemic hemisphere and contralateral hemisphere and infarct volumes. The severity of neurological deficit (p < 0.001) and infarct volume (p < 0.001) was reduced in both Memantine and MK-801 treated groups compared with saline treated groups. Memantine attenuated brain edema formation and BBB permeability at the periphery (p < 0.01), MK-801 both at the core (p < 0.05) and the periphery (p < 0.01) of the ischemia. These results demonstrated that the NMDA receptor antagonists Memantine and MK-801 were neuroprotective when given 15 min after MCAO in temporary focal cerebral ischemia.

Animals↗

PubMed2000

Bilateral epidural hematoma.

Bilateral epidural hematomas are very rare and are associated with high mortality. The purpose of this study is to identify the clinical features, mechanisms, and outcomes of bilateral epidural hematomas. This report considers 19 cases of bilateral epidural hematoma hospitalized between 1987 and 1997. All of the cases, with the exception of three, were diagnosed within the first 6 h. The neurologic evaluations on admission and during hospital stay were based on the Glasgow Coma Scale. Hematomas were determined by CT scans in all cases. The patients were evaluated using the Glasgow Outcome Scale after 6 months. In 13 patients, the bilateral epidural hematoma was in the midline. In six patients, hematomas were at different locations on either side. Surgical approach was chosen as the primary treatment modality in 18 patients. One was treated conservatively. The mortality rate was 15.7% in this series. With the widespread use of CT scan, diagnosis before deterioration of the neurological status affects the results of surgery and prognosis or even presents the possibility of a conservative treatment.

Adolescent↗

PubMed1999

Superoxide dismutase activity and the effect of N-methyl-D-aspartate antagonists on lipid peroxidation in the early phase of cold injury.

Free radicals, lipid peroxidation and excitatory amino acids have been implicated in the secondary mechanisms of traumatic brain injury. We used the cold injury model in rats to assess the endogenous activity of the protective enzyme superoxide dismutase (SOD) and the lipid peroxidation level in the contused tissue at an early phase of injury. Furthermore, we treated the rats with two different N-methyl-D-aspartate receptor antagonists, namely MK-801 and CPP, and evaluated their effect on lipid peroxidation in the contused tissue. Rats were divided into four groups: sham, control, treatment 1 and treatment 2 groups (n= 16 for each group). Thirty and 60 min after craniectomy or injury, tissue samples were removed. SOD activity didn't change in this period. However, lipid peroxidation in terms of malondialdehyde (MDA) amount showed a significant increase at 60 min. Fifteen minutes after injury, MK-801 (1 mg/kg), CPP (10 mg/kg) or saline (1 ml) were applied intraperitoneally in treatment 1, treatment 2 and the control groups. Treatment with MK-801 attenuated MDA levels, whereas treatment with CPP did not. The protective effect of MK-801 achieved statistical significance. These results demonstrate that SOD activity does not change in the early period of cold injury. Moreover, these results show that lipid peroxidation increases after 60 min of cold injury, and treatment with MK-801 15 min after injury can prevent this elevation.

Animals↗

PubMed1999

Protective effect of the N-methyl-D-aspartate receptor antagonists, MK-801 and CPP on cold-induced brain oedema.

Cold injury model in rat was used to determine the effect of treatment with the competitive NMDA antagonists CPP and the non-competitive NMDA antagonist MK-801 in cerebral oedema. MK-801 was applied in doses of 1 mg/kg and CPP of 10 mg/kg, 15 min. after injury. Control animals received 1 ml saline at the same time interval after injury. Tissue samples from the core and periphery of the lesion of the injured hemisphere and from the symmetrical location of the undamaged contralateral hemisphere were removed 24 hours after injury. Blood brain barrier permeability, brain water content and tissue specific gravity values were determined. MK-801 was found beneficial for reducing the oedema and restore the blood brain barrier permeability at the penumbral zone of the lesion, whereas both MK-801 and CPP were found ineffective for prevention of oedema accumulation at the core of the lesion.

Analysis of Variance↗

PubMed1998

The effect of aprotinin on extraneural scarring in peripheral nerve surgery: an experimental study.

Extraneural scarring is one of the factors negatively influencing the result of peripheral nerve surgery. Many organic materials have been used to prevent fibrosis. The effect of aprotinin on peripheral nerve scarring in rats was investigated in this study. Three types of surgical intervention were carried out; namely external neurolysis (I), abrasive injury (II), and anastomosis (III). The coded samples which consisted of pure collagen fibers soaked with aprotinin or phosphate-buffered saline were applied around the left sciatic nerves of rats whereas only sham operations were performed on the right sciatic nerves. Animals were sacrificed after 4 or 6 weeks. Neurological examination, gross evaluation of extraneural fibrosis, and histological study were undertaken. The results have demonstrated that aprotinin is a promising agent in the prevention of extraneural scarring.

Animals↗