Leukocytic functions in burn-injured patients

Braquet, M.; Lavaud, Philippe; Dormont, Dominique; Garay, Ricardo P.; Ducousso, R.; Guilbaud, J; Chignard, Michel; Borgeat, Pierre; Braquet, P.

doi:10.1016/0090-6980(85)90135-2

Cited by 27 publications

(6 citation statements)

References 35 publications

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“…In our previous receptor binding study using [3H1-PAF and rabbit washed platelets (1), the IC50 value of pinusoiide for PAP-receptor binding was determined to be 2.5 x 107M (0.087 0.009 pg/mi), which is comparable to the reported value of gmnkgoiide B (5.1 x i0 M), a well known, potent PAP antagonist from natural products (17). To determine whether pinusolide is a PAPreceptor binding agonist or antagonist, its inhibitory effect on platelet aggregation in vitro was investigated.…”

Section: Specific Inhibition Of Paf-induced Platelet Aggregation By Psupporting

confidence: 53%

Biological and Pharmacological Effects of Pinusolide, a Novel Platelet Activating Factor Antagonist

et al. 1995

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Pinusolide, a potent platelet activating factor (PAF) receptor binding antagonist, inhibited PAF-induced aggregation of rabbit platelets with an IC50 value of 5 microM, whereas no inhibitory effects on the aggregation induced by ADP, thrombin, and collagen were observed. Pinusolide protected the mice from PAF-induced lethality with ED50 values of 1.1 mg/kg, i.v. and 69 mg/kg, p.o. Topically given pinusolide at 2 mg/ear effectively inhibited croton oil induced mouse ear edema. All the pinusolide treated ears recovered to normal healthy appearance in a sharp contrast to totally necrotized untreated ears. These results indicated that pinusolide is a potent and specific PAF antagonist in all experimental models as shown in vitro, in vivo, and in animal tests.

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Section: Specific Inhibition Of Paf-induced Platelet Aggregation By Psupporting

confidence: 53%

Biological and Pharmacological Effects of Pinusolide, a Novel Platelet Activating Factor Antagonist

et al. 1995

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“…First, the presence of morphologic changes could readily be dissociated from the insulin release induced by lyso-PAF or other lysophospholipids (e.g., lysophosphatidylserine or -ethanolamine induced microscopic changes but little or no insulin release, whereas NiCI 2 or lowered ambient temperature reduced secretion without preventing morphologic changes). 27 It seems reasonable, therefore, to consider lyso-PAF and other related lysophospholipids (such as LPC) as putative physiologic insulin secretagogues, although additional studies will be required to establish this conclusively. Finally, no or insignificant amounts of 51 Cr release were induced by lyso-PAF concentrations clearly capable of evoking insulin release.…”

Section: Discussionmentioning

confidence: 99%

Ether-Linked Lysophospholipids Initiate Insulin Secretion: Lysophospholipids May Mediate Effects of Phospholipase A2 Activation on Hormone Release

Metz¹

1986

Diabetes

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Phospholipase A2 activation may be a pivotal step in glucose-induced insulin secretion; however, recent studies have focused on only one by-product (arachidonic acid). To examine the possible role of the other by-product (lysophospholipids), the lysoderivatives of alkylacyl- (ether linked) or diacylphospholipids were applied to rat islets in static incubations. 1-O-alkyl-2-lyso-sn-glyceryl-3-phosphorylcholine [lyso-PAF, the precursor of platelet-activating factor (PAF)] or lysophosphatidylcholine initiated insulin release at 1.7 mM glucose. Two preparations of PAF itself (0.005-5000 ng/ml) were without effect at 1.7 or 16.7 mM glucose, but PAF was nearly equipotent to lyso-PAF at greater than or equal to 20 micrograms/ml. A precursor-product relationship was suggested because the precursors (alkylacyl- or diacylglyceryl-phosphorylcholine) of all three active metabolites were inactive. The stimulatory effect of lyso-PAF is largely independent of any toxic or lytic effect, being biphasic, reversible, unassociated with impairment of the subsequent physiologic functioning of treated islets, and inhibitable (by Ni2+, La3+, or nordihydroguaiaretic acid but not by other lipoxygenase inhibitors). It also occurred at threshold concentrations at which islet morphology and 51Cr retention were preserved. Furthermore, lyso-PAF-induced insulin secretion was markedly impaired by reduced ambient temperature (16 degrees C) or by the impermeant anion isethionate, further implying initiation of true exocytotic granule release and fission. Lyso-PAF (but not arachidonic acid) also circumvented the inhibition of glucose-induced insulin release caused by phospholipase inhibitors. Generation of endogenous lysophospholipids through exogenous application of phospholipase A2 also initiated insulin release, an effect responding to a panel of potential inhibitors identically to that induced by exogenously provided lysophospholipids. We propose that glucose activates phospholipase A2 in the pancreatic islet, leading to the generation of lysophospholipids; the latter may couple energy production to insulin release, at least in part via the promotion of Ca2+ translocation.

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“…This reduction may contribute to the susceptibility to infection associated with thermal injury. Lastly, a profound inhibition of LTB4 and oxygen release in PMNs was noted in patients who suffered total body surface area burns of 40 to 80% [24].…”

Section: Group Daymentioning

confidence: 91%

Depression of Phagocytic Activity of The Immune System Following Traditional Cautery in Experimental Animals

1991

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Traditional cautery, which is practiced widely in Saudi Arabia and some other countries, has not been exposed to detailed scientific investigation. In an attempt to elucidate some of its physiological aspects, we assessed the effect of cautery on a normal animal's nonspecific immune system. Male Wistar rats and guinea pigs were cauterized to simulate traditional cautery in size and percentage of cauterized area. Using radioactive sulfur colloid uptake and clearance, the effect of cautery on the mononuclear phagocyte system was evaluated in rats. The respiratory burst in peripheral polymorphonuclear leukocytes (PMNs) after cautery was measured in the guinea pigs using the chemiluminescence technique. The results showed marked reduction in the intravascular clearance of the colloid with prolonged clearance time following cautery. In addition, the liver uptake of the colloid was reduced in cauterized animals compared with control animals and the white cell count was also significantly reduced. The study showed marked inhibition of phagocytic function in guinea pigs in both whole blood and isolated PMNs. These results indicate that traditional cautery reduces the physiological function of the phagocytic system in normal experimental animals. The influence of traditional cautery on infected animals deserves further investigation.

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Leukocytic functions in burn-injured patients

Cited by 27 publications

References 35 publications

Biological and Pharmacological Effects of Pinusolide, a Novel Platelet Activating Factor Antagonist

Biological and Pharmacological Effects of Pinusolide, a Novel Platelet Activating Factor Antagonist

Ether-Linked Lysophospholipids Initiate Insulin Secretion: Lysophospholipids May Mediate Effects of Phospholipase A2 Activation on Hormone Release

Depression of Phagocytic Activity of The Immune System Following Traditional Cautery in Experimental Animals

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