Drugs online research references
Eur J Surg. 1994 Feb;160(2):77-86.
Effects of a combined drug regimen on tumour necrosis factor and plasma kallikrein activity in experimental endotoxaemia.
Naess F, Waage A, Roeise O, Stadaas JO, Aasen AO.
Department of Surgery, Ulleval Hospital, University of Oslo, Norway.
OBJECTIVE: To clarify the relationship between changes in haemodynamics, liberation of tumour necrosis factor and generation of plasma kallikrein, and to see if treatment with a combination of drugs was successful in preventing activation of tumour necrosis factor and plasma kallikrein in experimental endotoxic shock. DESIGN: Controlled study. MATERIAL: 22 juvenile pigs. INTERVENTIONS: 15 animals received 0.01 mg/kg endotoxin infusion, the rest being given the same volume of saline. 10 received no treatment, and 5 were given a combination of methylprednisolone, naloxone, ketanserin, promethazine, C1 esterase inhibitor, antithrombin III and aprotinin. MAIN OUTCOME MEASURES: Assessment of the liberation of tumour necrosis factor, generation of plasma kallikrein, and haemodynamic and cellular effects of endotoxaemia. RESULTS: There was a linear statistical relationship between decreases in cardiac output and increases in packed cell volume, and between increases in packed cell volume and plasma kallikrein activity. The combination treatment totally blocked all the effects of the infusion of endotoxin. CONCLUSION: Endotoxin affects several mediators, but combination treatment can prevent some of these effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8193212&dopt=Abstract
Acta Microbiol Acad Sci Hung. 1976;23(1):45-54.
Antibacterial effect of some phenothiazine compounds and R-factor elimination by chlorpromazine.
Molnar J, Mandi Y, Kiraly J.
Chlorpromazine, levopromazine and promethazine exerted a bacteriostatic effect on Gram-positive bacteria at 20-60 mug/ml, on Gram-negative bacteria at 130-180 mug/ml concentration. Of the three compounds, chlorpromazine had the most marked bactericidal effect on cultures of Bacillus anthracis growing in minimal medium. In addition, chlorpromazine had a significant bactericidal effect on the resting cells of Escherichia coli suspended in saline. Pseudomonas aeruginosa was resistant to phenothiazines. Experiments have failed to derive resistant mutants from the highly sensitive B. anthracis. An effective R-factor elimination was observed at chlorpromazine concentrations of 50 mug/ml, practically not affecting the growth of multiple resistant E. coli.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=820163&dopt=Abstract
J Rheumatol. 1993 Aug;20(8):1374-7.
Platelet activating factor and histamine effects in synovial blood flow evaluated by laser-Doppler flowmetry.
Rocha FA, Jancar S, Fraga CA, Timo-Iaria C, De Brum-Fernandes AJ.
Department of Medicine, University of Sao Paulo, Brazil.
OBJECTIVE. To investigate platelet activating factor (PAF) and histamine effects in synovial circulation of rabbits. METHODS. A laser-Doppler flowmeter was adapted to study the synovial blood flow. Either PAF or histamine were infused in the first femoral artery branch. The effects of PAF and histamine antagonists as well as of inhibitors of cyclooxygenase products were evaluated. RESULTS. PAF induced a vasoconstriction in synovial circulation, which was inhibited by the PAF antagonist, WEB 2170, a cyclooxygenase inhibitor, indomethacin or a thromboxane synthesis inhibitor, dazmegrel. Histamine induced vasoconstriction in the synovial vessels. Promethazine not only inhibited this vasoconstriction but also induced a vasodilation, that was blocked by a combined treatment with promethazine and cimetidine. Pretreatment with WEB 2170 did not interfere with histamine effect. CONCLUSIONS. Our data indicate that PAF induces vasoconstriction in synovial blood flow through a receptor mediated mechanism and that thromboxane is involved in this effect. Histamine induces constriction or dilation in synovial vessels, through action on H1 or H2 receptors, respectively. This effect is not dependent on PAF.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8230022&dopt=Abstract
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