Drugs online research references
Biotech Histochem. 1994 Mar;69(2):102-11.
Phagocytosis of intravenously administered particles by leukocytes adhered to the aortic endothelium of the rat.
Gabaldon M, Capdevila C, Zuniga A.
Research Center, Hospital La Fe, Valencia, Spain.
Phagocytosis has been used to characterize on a functional basis leukocytes adhered to the aortic endothelium of the rat. After intravenous administration of particles, phagocytosis was observed microscopically in esterase-positive leukocytes adhered to the endothelium in whole mounts of aorta. Polybead blue and red, 0.5 and 1 microns particle size, were inadequate because they were insufficiently colored to be identified individually at 400 x. Fluoresbrite YG 0.25 and 0.50 micron at doses of 0.2 and 2 x 0.3 ml/100 g, respectively, produced endothelial lesions. The same occurred with Monastral blue B (MbB) at 0.3 ml/100 g, red iron at 2 x 16 mg/100 g and India ink at different concentrations depending on the supplier. At lower particle doses, lesions were not found. Deferoxamine mesylate 1.5 mg/100 g intravenous and allopurinol 5 mg/100 g intraperitoneal administered before the particles diminished the number and intensity of lesions. In none of the cases studied was the percentage of phagocytic cells greater than 50%. Clearance curves of MbB and Fluoresbrite indicated rapid disappearance of particles from the blood. Results indicate that administration of particulate suspensions is not a good method for characterizing the phagocytic leukocytes adhering to the aortic endothelium because low doses produce rapid clearance of particles, thus impeding sufficient leukocyte loading, and higher doses produce endothelial lesions that often impair reliable counting of the adhering leukocytes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7515698&dopt=Abstract
Neurochem Res. 1994 Dec;19(12):1557-64.
Oxidative mechanisms involved in kainate-induced cytotoxicity in cortical neurons.
Cheng Y, Sun AY.
Department of Pharmacology, University of Missouri-Columbia School of Medicine 65212.
In our previous experiments, evidence of free radical formation has been demonstrated in gerbil brain after kainic acid (KA) administration. In the present study, the mechanisms involved in KA-induced free radical formation and subsequent cell degeneration were investigated using high density cortical neuron cultures. A free radical trapping agent, alpha-phenyl-N-tert- butyl-nitrone (PBN), as well as the combined action of superoxide dismutase and catalase attenuated KA neurotoxic effect. Calpain-induced xanthine oxidase (XO) activation may play an important role in KA excitotoxicity since calpain inhibitor I as well as allopurinol, a selective XO inhibitor, significantly protected the cortical neurons from KA-induced cell death. However, XO activation may not be the only source producing free radicals, other free radical generating systems such as nitric oxide synthase may also play a role in KA insult.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7877729&dopt=Abstract
Circ Shock. 1984;12(4):229-39.
Superoxide radical involvement in the pathogenesis of burn shock.
Saez JC, Ward PH, Gunther B, Vivaldi E.
The pathogenesis of burn shock syndrome involves the production of superoxide radicals which are first generated in the burned skin. They are responsible for an increase in vascular permeability with loss of plasma, which results in hemoconcentration and hypovolemia. The resulting systemic hypoperfusion leads to a generalized production of superoxide radicals and subsequent cellular damage. Prior administration of allopurinol or superoxide dismutase increases the survival rates of mice subjected to burn shock.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6327114&dopt=Abstract
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