Browsing by Subject "Brain Edema"

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    Effect of difluoromethylornithine on reperfusion injury after temporary middle cerebral artery occlusion
    (2005) Temiz C.; Dogan A.; Baskaya M.K.; Dempsey R.J.
    Polyamines have been shown to play an important role in the disturbance of the blood-brain barrier (BBB) in a number of pathological states including ischemia. BBB disturbances may be almost completely prevented by treating animals with the ornithine decarboxylase (ODC) inhibitor, α- difluoromethylornithine (DFMO). DFMO has been also shown to prevent N-Methyl-d-aspartate (NMDA) toxicity in tissue cultures. It has been suggested that the pathological disturbances in polyamine metabolism observed following cerebral ischemia, particularly the post-ischemic increase in putrescine, may contribute to the ischemic injury that is most evident in the CA1 subfield of the hippocampus. In this study, effects of DFMO in cerebral ischemia and reperfusion were examined. The results showed that inhibition of the polyamine system by DFMO decreased ischemic injury volume and brain tissue water content in a dose-dependent manner, without change in vital signs, including systemic arterial blood pressure, arterial partial oxygen pressure, regional cerebral blood flow and body temperature. © 2005 Published by Elsevier Ltd.
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    The blood-brain barrier is continuously open for several weeks following transient focal cerebral ischemia
    (2008) Strbian D.; Durukan A.; Pitkonen M.; Marinkovic I.; Tatlisumak E.; Pedrono E.; Abo-Ramadan U.; Tatlisumak T.
    The blood-brain barrier (BBB) is the principal regulator of blood-borne substance entry into the brain parenchyma. Therefore, BBB leakage, which leads to cerebral edema and influx of toxic substances, is common in pathological conditions such as cerebral ischemia, inflammation, trauma, and tumors. The leakage of BBB after ischemia-reperfusion injury has long been considered to be biphasic, although a considerable amount of discrepancies as for the timing of the second opening does exist among the studies. This led us to evaluate systematically and quantitatively the dynamics of BBB leakage in a rat model of 90-min ischemia-reperfusion, using gadolinium-enhanced (small molecule) magnetic resonance imaging and fluorescent dye Evans Blue (large molecule). BBB leakage was assessed at the following time points after reperfusion: 25 min, 2, 4, 6, 12, 18, 24, 36, 48, and 72 h, and 1, 2, 3, 4, and 5 weeks. We observed BBB leakage for both gadolinium and Evans Blue as early as 25 min after reperfusion. Thereafter, BBB remained open for up to 3 weeks for Evans Blue and up to 5 weeks for gadolinium. Our results show that BBB leakage after ischemia-reperfusion injury in the rat is continuous and long-lasting, without any closure up to several weeks. This is the first systematic and extensive study fully demonstrating BBB leakage dynamics following transient brain ischemia and the findings are of major clinical and experimental interest. © 2008 IBRO.
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    Post-ischemic leakiness of the blood-brain barrier: A quantitative and systematic assessment by Patlak plots
    (2009) Abo-Ramadan U.; Durukan A.; Pitkonen M.; Marinkovic I.; Tatlisumak E.; Pedrono E.; Soinne L.; Strbian D.; Tatlisumak T.
    The Patlak plot analysis of dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) allows estimation of blood-brain barrier (BBB) leakage following temporary focal cerebral ischemia. Thus far, a systematic and quantitative in vivo evaluation of post-ischemic BBB leakage is lacking. Here, using DCE-MRI and the Patlak plot method, we quantitatively assessed BBB leakage in rats at the following time-points after reperfusion: 25 min, 2, 4, 6, 12, 18, 24, 36, 48, and 72 h, and 1, 2, 3, 4, and 5 weeks. Sham-operated animals served as controls. Data collected for each time-point were: the blood-to-brain transfer rate constant (Ki) of the contrast agent gadolinium, distribution volume (Vp), ischemic lesion volume, and apparent diffusion coefficient (ADC) values. Compared to controls, Ki, measured at all time-points, except for 5 weeks, appeared significantly different (p < 0.001). At several time-points (25 min, 48 and 72 h, 4 and 5 weeks), Vp was similar compared to that of controls, but for the remaining groups the difference was significant (p < 0.001). Analyzing the relationship of Ki values to time-points, we observed a trend towards a decrease over time (r = - 0.61, p = 0.014). Both ADC values (r = - 0.58, p = 0.02) and ischemic lesion volumes (r = 0.75, p = 0.0015) correlated with Ki values. These results suggest that after ischemia-reperfusion in rats, BBB leakage is continuous during a 4-week period. Its magnitude diminishes over time and correlates with severity and extent of ischemic injury. © 2009 Elsevier Inc. All rights reserved.
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    The effects of lornoxicam on brain edema and blood brain barrier following diffuse traumatic brain injury in rats; [Lornoksikamin siçanlarda diffüz travmatik beyin hasarinda beyin ödemi ve kan beyin bariyeri üzerine etkileri]
    (Turkish Association of Trauma and Emergency Surgery, 2013) Topçu I.; Gümüşer G.; Bayram E.; Aras F.; Çetin I.; Temiz C.; Çivi M.
    BACKGROUND In this experiment, the effects of lornoxicam on brain edema and the blood brain barrier (BBB) following diffuse traumatic brain injury (TBI) were studied. METHODS Twenty adult male Wistar albino rats were anesthetized, and experimental closed head trauma was induced by the Marmarou method. After head injury, the rats were randomly divided into two groups: Group I was the control group, to which 2 ml saline was administered intraperitoneally, and Group II was the lornoxicam group, to which 2 ml 1.3 mg kg-1 lornoxicam was administered intraperitoneally. Twenty-four hours after head trauma, 99 mTc pentetate (DTPA) was injected at a dose of 37 MBq, and posterior planar images of each rat were obtained using an Infinia gamma camera. After imaging of BBB permeability, brain tissues were dissected from the cranium. The brain water content (BWC) of each sample was calculated using the wet-dry method. RESULTS The lesion/background (L/b) ratio of Group I was 3.76±0.46 and 3.02±0.66 for early (5th min) and late (60th min) imaging, respectively. In Group II, the L/b ratios were 3.52±0.96 and 2.63±0.63 for early and late imaging, respectively (p>0.05). BWC was 79.6±2.5% and 77.5±1.1% for Groups I and II, respectively (p<0.05). CONCLUSION In this rat model of TBI, lornoxicam reduced brain edema but did not affect BBB permeability.