pilocarpine/edema

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Increased calcineurin expression after pilocarpine-induced status epilepticus is associated with brain focal edema and astrogliosis.

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Calcineurin plays an important role in the development of neuronal excitability, modulation of receptor's function and induction of apoptosis in neurons. It has been established in kindling models that status epilepticus induces brain focal edema and astrocyte activation. However, the role of

4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid attenuates spontaneous recurrent seizures and vasogenic edema following lithium-pilocarpine induced status epilepticus.

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Vasogenic edema induced by blood brain barrier disruption and neuronal loss play an important role in the epileptogenic process. 4,4'- diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) is a commonly used anion channel inhibitor that has been reported to exert an anticonvulsant effect in rat

Dexamethasone exacerbates cerebral edema and brain injury following lithium-pilocarpine induced status epilepticus.

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Anti-inflammatory therapies are the current most plausible drug candidates for anti-epileptogenesis and neuroprotection following prolonged seizures. Given that vasogenic edema is widely considered to be detrimental for outcome following status epilepticus, the anti-inflammatory agent dexamethasone

Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus.

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In the present study we analyzed aquaporin-4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine-induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non-SE-induced animals, AQP4 immunoreactivity was

Reduced hippocampal manganese-enhanced MRI (MEMRI) signal during pilocarpine-induced status epilepticus: edema or apoptosis?

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Manganese-enhanced MRI (MEMRI) has been considered a surrogate marker of Ca(+2) influx into activated cells and tracer of neuronal active circuits. However, the induction of status epilepticus (SE) by kainic acid does not result in hippocampal MEMRI hypersignal, in spite of its high cell activity.

[The course of experimental pulmonary edema as a function of the dose and time of administration of adrenaline, pilocarpine and caffeine].

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[Proceedings: Preliminary animal experiments on the usability of pilocarpine and a pilocarpine-alupent combination as therapeutic agents in dropsy].

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Two-year safety study of dorzolamide as monotherapy and with timolol and pilocarpine. Dorzolamide Safety Study Group.

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OBJECTIVE To evaluate the safety of open-label 2.0% dorzolamide as monotherapy and when used with timolol and/or pilocarpine for as long as 2 years. METHODS The safety of dorzolamide was evaluated in patients with open-angle glaucoma or ocular hypertension over a 2-year period. The incidence of the

Edema due to altered sweating function.

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We report a case with idiopathic edema accompanied with excessive sweating on bathing. The subject is a 26 year-old male. He was admitted to our hospital because of pretibial edema. He complained of excessive sweating only after daily bathing. Sweating on daily bathing reduced pretibial edema after

Heparin ameliorates cerebral edema and improves outcomes following status epilepticus by protecting endothelial glycocalyx in mice.

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Blood brain barrier (BBB) hyperpermeability and brain edema contribute to increased seizure susceptibility and brain injury in status epilepticus (SE). The endothelial glycocalyx is the coating on luminal side of the endothelium and can be considered as the first barrier of BBB. Currently, little is

Damage of substantia nigra pars reticulata during pilocarpine-induced status epilepticus in the rat: immunohistochemical study of neurons, astrocytes and serum-protein extravasation.

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The substantia nigra has a gating function controlling the spread of epileptic seizure activity. Additionally, in models of prolonged status epilepticus the pars reticulata of substantia nigra (SNR) suffers from a massive lesion which may arise from a massive metabolic derangement and

Tumor necrosis factor-α-mediated threonine 435 phosphorylation of p65 nuclear factor-κB subunit in endothelial cells induces vasogenic edema and neutrophil infiltration in the rat piriform cortex following status epilepticus.

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BACKGROUND Status epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption

Effect of LiCl pretreatment on cholinomimetic-induced seizures and seizure-induced brain edema in rats.

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Male Sprague-Dawley rats received LiCl (5 mEq/kg; sc) or saline 24 h prior to injection of cholinomimetics. Physostigmine (PHY, 0.54-0.80 mg/kg), diisopropylfluorophosphate (DFP, 1.3-2.5 mg/kg), pilocarpine (PIL, 23-30 mg/kg), or saline was injected subcutaneously at time 0. Rats were observed for

ADENOSINE A1 RECEPTOR AGONIST PROTECTS AGAINST HIPPOCAMPAL NEURONAL INJURY AFTER LITHIUM CHLORIDE-PILOCARPINE-INDUCED EPILEPSY.

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Adenosine A1 receptor (AA1R) is widely present in the central nervous system, exerting brain protective antiepileptic effects, mainly by binding corresponding G proteins. We evaluated the neuroprotective effects of AA1R on hippocampal neuronal injury after lithium

The toxic effects of pilocarpine gel and drops on rabbit cornea.

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Pilocarpine drops and gel were applied daily for 3 months to rabbit cornea to determine their cytotoxic effects. The corneas were examined clinically with slit lamp biomicroscopy and histologically with scanning and transmission electron microscopy. The gel-treated corneas developed edema and

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