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E Pirotzky

Publications and source records attributed to E Pirotzky.

49 records · Page 3Linked to original sources
PubMed1987

Renal anaphylaxis. I. Antigen-initiated responses from isolated perfused rat kidney.

Isolated perfused rat kidneys were passively sensitized by addition of either mouse ascitic fluid containing monoclonal IgE against dinitrophenol (DNP) or DNP-specific purified IgE. After washing the organ, defined doses of DNP-bovine serum albumin were given as bolus injection via the kidney artery. Antigen challenge of IgE-sensitized kidneys resulted in a dose-dependent increase of perfusion pressure starting with 5 micrograms antigen (2.46 +/- 0.2 mm Hg) and reaching a maximum at dose higher than 100 micrograms (10.3 +/- 1.6 mm Hg) (N = 4, means +/- 1 SD). A decrease of glomerular filtration rate was also observed which reached a plateau at 100 micrograms antigen (-68.5 +/- 2.9%) (N = 4). Regardless of the dose of antigen used, the urinary protein excretion markedly increased for the first five minutes following antigen injection and returned to basal values after 10 minutes. The total amounts of histamine, PGE2 and paf-acether (platelet-activating factor) released upon antigen challenge (1 mg) for 15 minutes reached maximal values of 405 +/- 21.1 ng, 286 +/- 19.4 pg and 12.3 +/- 3.2 ng (N = 5), respectively. None of these hemodynamic and biochemical effects were observed using IgG1 monoclonal antibodies or when the ascitic fluid containing monoclonal IgE used to sensitize the organ was heated at 56 degrees C for two hours. Thus, we have described a pure IgE-dependent rat kidney anaphylaxis. Antigen challenge markedly altered renal parameters and triggered the release of various mediators from the organ, suggesting that type I-hypersensitivity reactions may play a role in renal pathophysiology.

Anaphylaxis↗
PubMed1985

Ultrastructural evidence for extravascular platelet recruitment in the lung upon intravenous injection of platelet-activating factor (PAF-acether) to guinea-pigs.

Bronchoconstriction and degenerative lesions of the bronchial epithelium were observed microscopically 1 min after the i.v. injection of 100 ng/kg of platelet-activating factor (PAF-acether) to the anaesthesized guinea-pig. Constricted arterioles containing marginated polymorphonuclear neutrophils and platelet aggregates were seen, as well as alveolar capillaries obstructed by thrombi formed by partially or totally degranulated platelets. Three minutes after the injection of PAF-acether, platelet diapedesis to the alveolar septa and lumen was clearly observed. Bronchoconstriction was still present at 3 min, but subsided after 60 min, whereas oedema of the submucosa persisted accompanied by an infiltration of eosinophils and neutrophils. The infusion of prostacyclin prevented the formation of platelet aggregates and platelet diapedesis due to PAF-acether, but the morphological evidence of bronchial constriction was not modified. Aspirin failed completely to modify the effects of PAF-acether. Our results show that PAF-acether causes early formation and deposition of platelet aggregates, accompanied by the margination of polymorphonuclear neutrophil leucocytes in pulmonary vessels of the guinea-pig. Since bronchoconstriction persisted when platelet aggregation was inhibited with prostacyclin, aggregation by itself would not account for this effect. Early platelet diapedesis in the vicinity of bronchial smooth muscle corroborates previous evidence that platelets contain and release bronchoconstrictor substances, which operate by cyclo-oxygenase-independent mechanisms and are possibly involved with the physiopathology of lung inflammation during immediate hypersensitivity.

Adenosine Diphosphate↗
PubMed1984

Release of platelet-activating factor, slow-reacting substance, and vasoactive amines from isolated rat kidneys.

The present work brings the first evidence for the simultaneous release of Paf-acether (platelet-activating factor), slow-reacting substance (SRS), histamine, and serotonin from isolated rat kidneys stimulated with ionophore A 23187. However, with compound 48/80 we detected only SRS, histamine, and serotonin. Upon addition of antigen, kidneys from sensitized rats released Paf-acether and SRS of anaphylaxis. Paf-acether released in the perfusate was identified by its ability to aggregate aspirin-treated washed rabbit platelets in the presence of an ADP scavenger complex. It was also characterized by its inactivation by phospholipase A2, and it was eluted from high pressure liquid chromatography (HPLC) after 16 to 18 min, a retention identical to that of synthetic Paf-acether, that is, between sphingomyelin and lysophosphatidylcholine. The biological activity of SRS was detected after several purification steps including Amberlite XAD-2 and reverse phase HPLC (RP-HPLC). Kidney SRS exhibited a typical spasmogenic activity in isolated guinea-pig ileum preparation that was reversed by FPL 55712. When kidneys were incubated with [3H]arachidonic acid, radioactivity and biological activity comigrated in RP-HPLC with leukotrienes C and D. These results indicate that the kidney is capable of actively released inflammatory mediators.

Animals↗
PubMed1984

Biosynthesis of platelet-activating factor. VI. Precursor of platelet-activating factor and acetyltransferase activity in isolated rat kidney cells.

Isolated glomeruli and tubular and medullary cells obtained from perfused kidneys from Wistar rats were stimulated with ionophore A 23187 (0.5 to 6 microM) or kept overnight at pH 9.5. The amount of platelet-activating factor (Paf-acether) formed was measured in the ethanolic cell extracts using aggregation of washed rabbit platelets. 2-Lyso Paf-acether present in cells was transformed into Paf-acether by chemical acetylation and measured in the same manner as Paf-acether. Microsomes from glomeruli and medullary and tubular cells were prepared, and the acetyltransferase activity was measured. Paf-acether was formed in a dose-dependent fashion by glomeruli and medullary cells, and maximal formation with 3 microM ionophore A 23187 was 1.9 +/- 0.2 and 1.1 +/- 0.2 pmoles/mg of protein, respectively. Paf-acether was not recovered from tubular cells. Three cell types produced large amounts of 2-lyso Paf-acether when incubated at alkaline pH. Only glomeruli generated appreciable quantity of 2-lyso Paf-acether upon ionophore A 23187 stimulation. The acetyltransferase specific activities in ionophore A 23187-stimulated glomeruli and medullary and tubular cells were 3.8 +/- 0.8, 0.3 +/- 0.1, and 0.2 +/- 0.1 nmoles of Paf-acether/10 min/mg of protein, respectively. This study demonstrates the formation of Paf-acether by two distinct populations of kidney cells, pointing out the glomerular cells, besides the already known medullary cells, as capable of forming Paf-acether.

Acetyltransferases↗
PubMed1984

PAF-acether-induced plasma exudation in rat skin is independent of platelets and neutrophils.

The ability of Paf-acether to induce increased plasma protein extravasation (IPPE) was assessed in the skin of rats by measuring extravasation of 125I-bovine serum albumin. Paf-acether elicited dose-dependent IPPE with a threshold of 0.04 pmol and a maximum at 4.5 nmol, with an effective concentration (EC50) of 23 pmol. The EC50 of the 1-0-ester Paf-acether analog was 1.5 nmol whereas 2-lyso Paf-acether was ineffective in inducing IPPE. Serotonin and histamine were respectively 100 and 1,00-fold less potent than Paf-acether. High doses of Paf-acether also resulted in a dose related accumulation of III-indium oxine labeled platelets. Ultrastructural and radioisotopic studies showed that Paf-acether-induced IPPE was not dependent upon platelet accumulation. In addition, platelet release products were ruled out in this phenomenon, since a "cocktail" of indomethacin, methysergide and pyrilamine-maleate failed to significantly reduce Paf-acether-induced IPPE. Neutrophils were not involved in Paf-acether -induced IPPE since nitrogen mustard-treated animals presented with IPPE not significantly different from controls. Finally, the specificity of Paf-acether on IPPE formation was demonstrated by its complete prevention by prior intravenous injection of Paf-acether (6 ug/kg), but not of Paf-acether analogs, histamine or serotonin.

Animals↗
PubMed1984

[Frequent positivity of the human basophil degranulation test in idiopathic nephrotic syndromes (minimal glomerular changes and segmental and focal glomerulosclerosis)].

Atopic factors play an important role in minimal changes idiopathic nephrotic syndrome ( MCINS ). We therefore studied human basophil degranulation test ( HBDT ) in MCINS and also in patients with segmental and focal glomerulosclerosis ( SFGSNS ) whose relation with MCINS is debated. HBDT was performed with 5 or 6 allergens chosen according to the history of patients and results of cutaneous tests. HBDT was positive in 16 out of 28 MCINS and in 14 among 18 SFGSNS subjects. The difference versus 29 Immune Complex glomerulonephritis and 11 blood donors was significant with the chi 2 test. Because the basophil count was low (less than 10/microliter) in 5 cases, 4 of which had a severe nephrotic syndrome, the HBDT was performed later. The allergen most frequently involved was house dust. This was responsible for a significant degranulation in 10 MCINS (45%) and in 11 SFGSNS (68%) patients; degranulation was obtained more frequently with 2 allergens than with a single one. Obviously such a basophil sensitisation does not prove the responsibility of these allergens.

Adolescent↗
PubMed1982

Basophil sensitisation in idiopathic nephrotic syndrome.

The degranulation of basophils in the presence of a specific allergen (human basophil degranulation test, HBDT) is an index of IgE-dependent cellular response and it was tested in 46 unselected idiopathic nephrotic syndrome (INS) patients with or without atopic manifestations. 28 of the INS patients had "minimal change" nephrotic syndrome (MCNS) and 18 had focal segmental glomerular sclerosis (FSGS). 29 patients with different types of primary glomerulonephritis (GN) and 11 healthy donors acted as controls. The HBDT was positive in 16 (57%) of 28 MCNS and in 14 (77.8%) of 18 FSGS patients. Only 5 (17.2%) of 29 GN and 1 (6%) of 11 blood donors exhibited positive HBDT. House dust was the commonest allergen to which MCNS and FSGS subjects were sensitive, whereas sensitivity to grass pollen, moulds, and animal danders was less common. 8 MCNS and 8 FSGS subjects were sensitive to house dust plus another allergen. 4 MCNS and 1 FSGS patient had fewer than 5/microliters basophils; 4 of these 5 patients were having a relapse of their nephrotic syndrome at the time. The demonstration of enhanced IgE-basophil sensitisation in INS patients suggests than an anaphylactic process plays a part in the pathogenesis of INS.

Adolescent↗
PubMed1980

[Release of platelet activating factor (P.A.F.-acether) by isolated perfused rat kidney].

Platelet-activating factor (a 1-0-alkyl-2-acetyl glyceryl-3-phosphorylcholine, P.A.F.-acether) causes the aggregation of platelets from various Mammalian species and the release of their granule content. P.A.F.-acether activity has been recovered in vitro from perfused isolated Rat kidneys, stimulated by the ionophore A 23187. The maximum release was reached 10 min. after addition of the ionophore. P.A.F.-acether from kidney exhibited the same physico-chemical and biological characteristics as P.A.F.-acether from leucocytes. These data demonstrate that the kidney secretes a mediator of immediate hypersensitivity (P.A.F.-acether) in the veinous vasculature. Therefore the kidney itself has the ability of inducing intravascular platelet aggregation with subsequent local increase in vasopermeability.

Animals↗
PubMedDate not supplied

Complement activation in acute glomerulonephritis in children.

Serial determinations of complement components (C1q, C4, C3, C5 and factor B) were performed in 32 children with acute glomerulonephritis. Low levels of C3 were found in 30 patients and low levels of C5 in 26. The findings of reduced C1q and/or C4 levels (25 patients) in the first days of the disease suggest activation of the classical pathway. Depressed Factor B levels were found rarely (4 patients). In all patients, the presence of a C3 splitting activity and/of a C3 nephritic factor-like activity was investigated. Both activities were demonstrated in 7 patients whereas in another patient, only C3 splitting activity was noted. A disappearance of both activities was observed in all patients. In 3 patients tested, the C3 nephritic factor-like activity was heat-labile and was therefore not related to true C3 nephritic factor. Both pathways are implicated in the early phases of the disease but continued C3 depression is probably through alternate pathway.

Acute Disease↗