Our previous experiments revealed that water intoxication and osmotic BBB disruption in the rat allow penetration of high- molecular substances into the brain and that resulting changes in the internal environment of th e CNS lead to pathological development, such as the loss of integrity of myelin. The aim of the present study was to determine whether the previously described phenomena are associated with increased water content in the brain. To answer the question following methods were used: a) water intoxication : intraperitoneal administration of distilled water, b) osmotic BBB disruption: application of mannitol (20 %) selectively into the internal carotid artery, c) brain wet weight was measured after decapitation, and subsequently (after six days in thermostat set at 86 °C) the dry weight were estimated d) in animals with 20 % and 30 % hyperhydration the degree of myelin deterioration was estimated e) animal locomotor activity was tested by continuous behavior tracking and analysis. Brai n water content after water intoxication and following the administration of mannitol was higher than in the control group. Different degrees of hyperhydration led to different levels of brain water content and to different degrees of myelin impairment. Hyperhydration corresponding to 20 % of the body weight brought about lower locomotor activity. Increased water content in the brain after the BBB osmotic disruption is surprising because this method is frequently used in the clinical practice., P. Kozler, V. Riljak, J. Pokorný., and Obsahuje bibliografii a bibliografické odkazy
Magnetic resonance imaging has been used for evaluating of a brain edema in experimental animals to assess cytotoxic and vasogenic edema by the apparent diffusion coefficient (ADC) and T2 imaging. This paper brings information about the effectiveness of methylprednisolone (MP) on experimental brain edema. A total of 24 rats were divided into three groups of 8 animals each. Rats with cytotoxic/intracellular brain edema induced by water intoxication were assigned to the group WI. These rats also served as the additional control group CG when measured before the induction of edema. A third group (WIMP) was intraperitoneally administered with methylprednisolone 100 mg/kg during water intoxication treatment. The group WI+MP was injected with methylprednisolone 50 mg/kg into the carotid artery within two hours after the water intoxication treatment. We evaluated the results in four groups. Two control groups (CG, WI) and two experimental groups (WIMP, WI+MP). Rats were subjected to MR scanning 24 h after edema induction. We observed significantly increased ADC values in group WI in both evaluated areas - cortex and hippocampus, which proved the occurrence of experimental vasogenic edema, while ADC values in groups WIMP and WI+MP were not increased, indicating that the experimental edema was not developed and thus confirming the protective effect of MP., Petr Kozler, Vít Herynek, Dana Marešová, Pablo D. Perez, Luděk Šefc, Jaroslav Pokorný., and Obsahuje bibliografii
Brain edema – a frequently fatal pathological state in which brain volume increases resulting in intracranial pressure elevation – can result from almost any insult to the brain, including traumatic brain injury. For many years, the objective of experimental studies was to find a method to prevent the development of brain edema at the onset. From this perspective, the use of methylprednisolone (MP) appears promising. High molecular MP (MW>50 kDa) can be incorporated into the brain – in the conditions of the experimental model – either by osmotic bloodbrain barrier disruption (BBBd) or during the induction of cellular edema by water intoxication (WI) – a condition that increases the BBB permeability. The time window for administration of the MP should be at the earliest stages of edema. The neuroprotective effect of MP on the permeability of cytoplasmatic membranes of neuronal populations was proved. MP was administrated in three alternative ways: intraperitoneally during the induction of cytotoxic edema or immediately after finishing cytotoxic edema induction in a dose of 100 mg/kg b.w.; into the internal carotid artery within 2 h after finishing cytotoxic edema induction in a dose of 50 mg/kg b.w.; into internal carotid artery 10 min after edema induction by BBBd in a dose of 50 mg/kg b.w.
Continuous monitoring of the intracranial pressure (ICP) detects impending intracranial hypertension resulting from the impaired intracranial volume homeostasis, when expanding volume generates pressure increase. In this study, cellular brain edema (CE) was induced in rats by water intoxication (WI). Methylprednisolone (MP) was administered intraperitoneally (i.p.) before the start of CE induction, during the induction and after the induction. ICP was monitored for 60 min within 20 h after the completion of the CE induction by fibreoptic pressure transmitter. In rats with induced CE, ICP was increased (Mean±SEM: 14.25±2.12) as well as in rats with MP administration before the start of CE induction (10.55±1.27). In control rats without CE induction (4.62±0.24) as well as in rats with MP applied during CE induction (5.52±1.32) and in rats with MP applied after the end of CE induction (6.23±0.73) ICP was normal. In the last two groups of rats, though the CE was induced, intracranial
volume homeostasis was not impaired, intracranial volume as well as ICP were not increased. It is possible to conclude that methylprednisolone significantly influenced intracranial homeostasis and thus also the ICP values in the model of cellular brain edema.