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The possible effects of the polyamine interconversion pathway on tissue polyamine levels, brain edema formation, and ischemic injury volume were studied by using a selective irreversible inhibitor, MDL 72527, of the interconversion pathway enzyme, polyamine oxidase. In an intraluminal suture
We studied the role of reactive oxygen intermediates (ROI) in lipopolysaccharide (LPS)-induced pulmonary edema. LPS treatment (600 micrograms/mouse, IP) was associated with a marked induction of the superoxide-generating enzyme xanthine oxidase (XO) in serum and lung. Pretreatment with the
1. Nilvadipine (FK 235, FR 34235) suppressed ischemia (20 min)-reflow (20 min)-induced paw edema of mice (ED30:0.4 mg/kg i.v. and 2 mg/kg p.o.). Other calcium entry blockers of dihydropyridine-type also suppressed the edema, but 30-fold higher doses were required. 2. Oral dosing of nilvadipine
Despite numerous investigations, the mechanisms underlying the neurological deficits observed in association with interstitial edema remain unclear. A recent study has demonstrated that the cerebral blood flow (CBF) in edematous white matter is unchanged if the blood flow values are corrected for
Pulmonary hypoperfusion/ischemia-reperfusion (I/R) may initiate ARDS (nonhydrostatic pulmonary edema). Endothelial damage via xanthine oxidase (XO)-derived oxygen radicals (O2*) may mediate I/R injury. We previously documented Factor VIII antigen (F8) as a marker for endothelial injury. The purpose
OBJECTIVE
To observe the therapeutic effect of monoamine oxidase (MAO) monoclonal antibody (mAb) for vasogenic brain edema (VBE) in rats.
METHODS
A total of 75 Wistar rats were randomized into non-edema, non-treated edema, saline-treated edema, mannitol-treated edema and MAO mAb-treated groups. Rat
Cochlear dysfunction may indicate inadequate generation of intracellular metabolic energy which is necessary for the regulation of the transport of ions and fluid as well as production of electro-energy in the cochlea. Changes in cochlear function in the early stages of endolymphatic hydrops
The relationship between the pulmonary toxicity of 3- methylindole (3MI, skatole) and the mixed-function oxidase (MFO) system was investigated. Nine goats assigned to three groups were given a jugular infusion of [14C]3MI (0.02 to 0.03 g of 3MI/kg of body weight containing 0.5 muCi/kg of body
In order to elucidate the role of arachidonic acid in the pathogenesis of ozone-induced pulmonary edema, isolated rat lungs were exposed to 14C-arachidonic acid in the presence or absence of ozone and the incorporation of radiolabelled arachidonate into pulmonary cell lipids was studied. The
The contribution of toxic O2 metabolites to cerebral ischemia reperfusion injury has not been determined. We found that gerbils subjected to temporary unilateral carotid artery occlusion (ischemia) consistently developed neurologic deficits during ischemia with severities that correlated with
Diffuse brain injury (DBI) is a leading cause of mortality and disability among young individuals and adults worldwide. In specific cases, DBI is associated with permanent spatial learning dysfunction and motor deficits due to primary and secondary brain damage. Nicotinamide adenine dinucleotide
This study examined the effects of lung collapse, a condition that causes relative hypoxia in lung tissues, on superoxide dismutase (SOD), cytochrome oxidase (cyt ox), and pyruvate kinase (py ki) activities in rabbits. Cyanide-insensitive respiration measurements were done in collapsed and