Animal models are an important tool for studying ischemic mechanisms of stroke. Among them, the middle cerebral artery occlusion (MCAO) model via the intraluminal suture method in rodents is closest to human ischemic stroke. It is a model of transient occlusion followed by reperfusion, thus representing cerebral ischemia-reperfusion model that simulates patients with vascular occlusion and timely recanalization. Although reperfusion is very beneficial for the possibility of preserving brain functions after ischemia, it also brings a great risk in the form of brain edema, which can cause the development of intracranial hypertension, and increasing morbidity and mortality. In this paper, we present the results of our own transient reperfusion model of MCAO in which we tested the permeability of the blood-brain barrier (BBB) using Evans blue (EB), an intravital dye with a high molecular weight (68,500 Da) that prevents its penetration through the intact BBB. A total of 15 animals were used in the experiment and underwent the following procedures: insertion of the MCA occluder; assessment of ischemia by 2,3,5 -Triphenyltetrazolium chloride (TTC) staining; assessment of the BBB permeability using brain EB distribution. The results are presented and discussed. The test of BBB permeability using EB showed that 120 minutes after induction of ischemia, the BBB is open for the entry of large molecules into the brain. We intend to use this finding to time the application of neuroprotective agents via ICA injection in our next stroke model. Keywords: Cerebral ischemia-reperfusion model, Middle cerebral artery occlusion, Blood-brain barrier, 2,3,5 -Triphenyltetrazolium chloride, Evans blue.

• MeSH
• Blood-Brain Barrier * metabolism   pathology   MeSH
• Infarction, Middle Cerebral Artery * metabolism   pathology   MeSH
• Brain Ischemia * metabolism   pathology   MeSH
• Capillary Permeability * physiology   MeSH
• Rats MeSH
• Disease Models, Animal MeSH
• Permeability MeSH
• Pilot Projects MeSH
• Rats, Sprague-Dawley MeSH
• Rats, Wistar MeSH
• Reperfusion Injury * metabolism   pathology   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

Cerebral perfusion pressure (CPP) is the net pressure gradient that drives oxygen delivery to cerebral tissue. It is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP). As CPP is a calculated value, MAP and ICP must be measured simultaneously. In research models, anesthetized and acute monitoring is incapable of providing a realistic picture of the relationship between ICP and MAP under physiological and/or pathophysiological conditions. For long-term monitoring of both pressures, the principle of telemetry can be used. The aim of this study was to map changes in CPP and spontaneous behavior using continuous pressure monitoring and video recording for 7 days under physiological conditions (group C - 8 intact rats) and under altered brain microenvironment induced by brain edema (group WI - 8 rats after water intoxication) and neuroprotection with methylprednisolone - MP (group WI+MP - 8 rats with MP 100 mg/kg b.w. applicated intraperitoneally during WI). The mean CPP values in all three groups were in the range of 40-60 mm Hg. For each group of rats, the percentage of time that the rats spent during the 7 days in movement pattern A (standard movement stereotype) or B (atypical movement) was defined. Even at very low CPP values, the standard movement stereotype (A) clearly dominated over the atypical movement (B) in all rats. There was no significant difference between control and experimental groups. Chronic CPP values with correlated behavioral type may possibly answer the question of whether there is a specific, universal, optimal CPP at all.

• MeSH
• Intracranial Pressure * physiology   MeSH
• Blood Pressure physiology   MeSH
• Rats MeSH
• Monitoring, Physiologic MeSH
• Brain * MeSH
• Cerebrovascular Circulation physiology   MeSH
• Telemetry MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

Brain edema is a fatal pathological state in which brain volume increases as a result of abnormal accumulation of fluid within the brain parenchyma. A key attribute of experimentally induced brain edema - increased brain water content (BWC) - needs to be verified. Various methods are used for this purpose: specific gravimetric technique, electron microscopic examination, magnetic resonance imaging (MRI) and dry/wet weight measurement. In this study, the cohort of 40 rats was divided into one control group (CG) and four experimental groups with 8 rats in each group. The procedure for determining BWC using dry/wet weight measurement was initiated 24 h after the completion of edema induction by the water intoxication method (WI group); after the intraperitoneal administration of Methylprednisolone (MP) together with distilled water during edema induction (WI+MP group); 30 min after osmotic blood brain barrier disruption (BBBd group); after injection of MP via the internal carotid artery immediately after BBBd (BBBd + MP group). While induction of brain edema (WI, BBBd) resulted in significantly higher BWC, there was no increase in BWC in the MP groups (WI+MP, BBBd+MP), suggesting a neuroprotective effect of MP in the development of brain edema.

• MeSH
• Brain Edema * chemically induced   diagnostic imaging   pathology   MeSH
• Edema pathology   MeSH
• Blood-Brain Barrier MeSH
• Rats MeSH
• Methylprednisolone pharmacology   MeSH
• Brain MeSH
• Water MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Methylprednisolone MeSH
• Water MeSH

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 blood-brain 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.

• MeSH
• Brain Edema drug therapy   metabolism   pathology   MeSH
• Glucocorticoids pharmacology   MeSH
• Blood-Brain Barrier drug effects   metabolism   pathology   MeSH
• Capillary Permeability drug effects   MeSH
• Rats MeSH
• Methylprednisolone pharmacology   MeSH
• Disease Models, Animal MeSH
• Brain drug effects   metabolism   pathology   MeSH
• Neurons drug effects   metabolism   pathology   MeSH
• Neuroprotective Agents pharmacology   MeSH
• Rats, Wistar MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Glucocorticoids MeSH
• Methylprednisolone MeSH
• Neuroprotective Agents MeSH