Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0393754 (HSA)
 2,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet activating factor (PAF-acether) is released from a variety of inflammatory cell types and has properties appropriate to a mediator of allergy and inflammation. Here, we have examined the interaction between PAF-acether and the prostaglandins, PGE2 and ZK 36374 (a stable analogue of prostacyclin, PGI2) in the skin of guinea-pigs and human volunteers. PGE2 and ZK 36374 significantly potentiated increased plasma protein extravasation induced by PAF-acether in guinea-pigs, assessed by extravasation of I-125-HSA. In addition, PGE2 significantly potentiated the ability of PAF-acether to elicit acute wheal (volume) and flare responses in human skin. The inflammatory properties of PAF-acether should not be considered in isolation since this phospholipid interacts synergistically with prostaglandins which are recognised as modulators of inflammation.
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PMID:Synergistic interaction between prostaglandins and PAF-acether in experimental animals and man. 620 39

Since rat platelets fully responsive to thrombin and collagen did not respond by releasing 3H-serotonin with up to 10 micrograms/ml of synthetic PAF-acether, the rat, contrariwise to the rabbit, was considered to be an appropriate model to study the actions of PAF-acether not mediated through the activation of platelets and the subsequent release of their inflammatory mediators. We developed an experimental approach using 57Co and 113Sn radiolabeled microspheres to assess the effect of PAF-acether on cardiac output, peripheral vascular resistance, and regional flows and resistance. The effect on vascular permeability and blood volume was studied by measuring the clearance of 125I-HSA and the variations of the hematocrit. A significant fall in blood pressure and peripheral vascular resistance was found with doses of PAF-acether ranging from 0.05 to 5 micrograms. Moreover, the higher doses of PAF-acether also induced a marked depletion of blood volume. A significant fall in spleen, coronary, and kidney output, but not in cardiac output, was also found. Our data show that PAF-acether, by itself, induces a drop in peripheral vascular resistance and, at higher doses, also in circulating volume, accounting for both by the hypotensive effect. The redistribution of cardiac output seems to be the expression of a nonuniform action of the compound on the vascular resistance of the different organs.
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PMID:Vascular actions of synthetic PAF-acether (a synthetic platelet-activating factor) in the rat: evidence for a platelet independent mechanism. 708 59

Rat platelets fully responsive to thrombin and collagen did not release 3H-serotonin with up to 10 microgram/ml synthetic PAF. Therefore, an experimental approach using 57Co and 113Sn radiolabelled microspheres was developed to evaluate the effect of PAF on cardiac output (CO), peripheral vascular resistance (PVR) and redistribution of CO among organs. The effect on vascular permeability was studied by measuring the clearance of 125I-HSA and the variations of the haematocrit. A significant fall in blood pressure and PVR was found with doses of PAF from 50 to 5000 ng. Moreover, the highest doses of PAF induced also a marked reduction in blood volume. A significant fall in spleen, coronary and kidney output was found but not in CO. Our data show that PAF, by itself, induces a fall in PVR and at higher doses also in circulating volume, both accounting for the hypotensive effect. The redistribution of CO seems to be the expression of a non-uniform action upon PVR.
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PMID:Non-platelet-mediated vascular actions of 1-O-alkyl-2-acetyl-sn-3-glyceryl phosphorycholine (a synthetic PAF). 734 Apr 43

1. Eosinophil accumulation and plasma extravasation are features of type I allergic responses. In an attempt to characterize the mediators of these responses, we have examined the local accumulation of 111In-eosinophils and leakage of 125I-human serum albumin (125I-HSA) during passive cutaneous anaphylaxis (PCA) reactions and in response to defined inflammatory mediators in the guinea-pig. Animals were passively sensitized by intradermal injection of anti-bovine gamma globulin antibody (50 microliters, 1/50 dilution). After 20-24 h, animals were injected intravenously with 111In-eosinophils and 125I-HSA for the measurement of cell accumulation and plasma leakage, respectively. 2. When injected into sensitized sites, antigen caused a dose-related increase in the accumulation of 111In-eosinophils and plasma leakage in guinea-pig skin. Time course experiments over 24 h revealed that the maximal rate of 111In-eosinophil accumulation occurred over the first 90 min, with little accumulation at later time points. Plasma leakage was completed within the first 30 min after challenge. Responses to the mast cell degranulator, compound 48/80, exhibited very similar responses to the PCA reaction. 3. Co-injection of antigen with the PAF antagonist, WEB 2086 (10(-7) mol/site) or the 5-lipoxygenase inhibitor, PF 5901 (10(-7) mol/site) did not significantly alter the accumulation of 111In-eosinophils or plasma leakage, whereas these drug doses abolished responses to exogenous PAF (10(-9) mol/site) and arachidonic acid (AA, 3 x 10(-8) mol/site), respectively. The H1 receptor antagonist chlorpheniramine (2.5 x 10(-8) mol/site) did not reduce antigen-induced 111In-eosinophil accumulation. Drug combinations were also injected with antigen into sensitized sites, but were unable to reduce "'In-eosinophil accumulation.4. These results indicate that anaphylactic eosinophil accumulation in this model involves mediators other than histamine, PAF or lipoxygenase products. This is in contrast to plasma leakage in this reaction, which can be abolished by a combination of antagonists blocking these mediators.
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PMID:Investigation of the endogenous chemoattractants involved in 111In-eosinophil accumulation in passive cutaneous anaphylactic reactions in the guinea-pig. 781 29

In the present study the influence of interleukin 3 and interleukin 5 on the migration of normal eosinophil and neutrophil granulocytes has been investigated. LTB4, PAF, f-MLP, C5a and ZAS were used as chemoattractants, and HSA and pooled normal human serum were used as chemokinetic agents. Recombinant human IL-5 (rh-IL5) at a concentration of 4 x 10(-12) mol/l was chemotactic for eosinophils, while recombinant mouse IL-5 (rm-IL5) attracted both eosinophils and neutrophils. IL-3 (rh-IL3) at a concentration around 10(-12) mol/l exerted a priming effect on eosinophil and neutrophil migration, i.e. chemotactic and chemokinetic responses to all agents tested. Human IL-5 at a concentration of 2 to 20 x 10(-12) mol/l primed the chemotactic and chemokinetic responses of eosinophils to all agents tested. The migration of neutrophils was also primed by rh-IL5, but at higher concentrations, i.e. around 10(-10) mol/l. IL-5 of mouse origin primed the migration of both eosinophils and neutrophils. In conclusion, IL-3 primed the migratory function of both eosinophils and neutrophils, while IL-5 was a more potent primer of eosinophil than of neutrophil migration.
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PMID:Priming of eosinophil and neutrophil migratory responses by interleukin 3 and interleukin 5. 801 8

Oxidized low density lipoprotein (LDL) plays an important role in atherogenesis. It is generally thought that LDL is mainly oxidized in the intima of vessel walls, surrounded by hydrophilic antioxidants and proteins such as albumin. The aim of this study was to investigate the possible interrelationships between oxidation resistance of LDL and its protein and lipid moieties. Proteins and to a lesser extent lipids, appeared to be the major determinants in the LDL Cu2+-oxidation resistance, which in turn depend on the ultracentrifugation (UC) procedure used. Comparing high speed/short time (HS/ST, 4 h), high speed/long time (HS/LT, 6-16h) and low speed/long time (LS/LT, 24h) conditions of UC, HS with the shortest time (4h) led to prepare LDL (named LDL.HS-4 h) with higher total protein and triglyceride contents, unchanged total cholesterol, phospholipids and Vitamin E, and higher Cu2+-oxidation resistance. Among proteins, only albumin allows to explain changes. PAF acetyl hydrolase appeared to be unaffected, whereas its pro-oxidant role was established and found only in the absence of albumin. In contrast the pro-oxidant role of caeruloplasmin took place regardless of the albumin content of LDL. The antioxidant effect of albumin (the oxidation lag time was doubled for 20mol/mol albumin per LDL) is assumed to be due to its capacity at decreasing LDL affinity for Cu2+. Interestingly, the LDL.HS-4 h albumin content mirrored the intrinsic characteristics of LDL in the plasma and was not affected by added free albumin. Moreover, it has been verified that in 121 healthy subjects albumin was the best resistance predictor of the Cu2+-oxidation of LDL.HS-4 h, with a multiple regression equation: lag time (min) = 62.1 + 0.67(HSA/apoB) + 0.02(TG/apoB)-0.01(TC/apoB); r = 0.54, P < 0.0001. Accounted for by lag time, the oxidation resistance did not correlate with alpha-tocopherol and ubiquinol contents of LDL. The mean albumin content was about 10mol/mol, and highly variable (0-58 mol/mol) with subjects. The LDL.HS-4h may account for the status of LDL in its natural environment more adequately than LDL resulting from other conditions of UC.
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PMID:New insight on the relationship between LDL composition, associated proteins, oxidative resistance and preparation procedure. 1199 80