OBJECT: To examine the distribution of mast cells in human placental tissue and to analyse the interactions between mast cell mediators (histamine and serotonin (5-HT)) and contractile activity of the uterus during delivery. DESIGN: 34 placentas were examined. Histamine and serotonin levels in placental samples were estimated using fluorymetric method. Distribution of mast cells were analysed immunohistochemically on the same material. SETTING: Dept. of Pathophysiology, Medical Academy, Warsaw, Poland. (*) Laboratory of Developmental Neuropathology Centre of Experimental and Clinical Medicine, Polish Academy of Sciences, Warsaw. (**) Clinic of Obstetrics and Gynecology, Second Medical Faculty, Medical Academy, Warsaw. SUBJECTS: 34 women, whose pregnancies ended in time and in preterm delivery, with normal, abnormal or without contractile activity of the uterus (elective cesarean section). MAIN OUTCOME MEASUREMENTS: Comparative charts of histamine levels in placental samples in relation to term and course of the labour. RESULTS: Concentration of histamine in placental cuts obtained from maternal surface of the placenta was significantly higher in the case of delivery without contractile activity of the uterus (elective cesarean section). Immunohistochemical identification of mast cells proved, that in regions located close to fetal surface of the placenta and in connective tissue foci, mast cells were most numerous. CONCLUSIONS: It is postulated that the simultaneous release of mast cell mediators (especially histamine) in placental tissue could be an important factor for evoking contractile activity of the human uterus, initiating labour. Further investigations should give answers on the points of these dependences.

Female↗

PubMed1994

Are histamine H1 receptors involved in ischaemia/reperfusion injury in rat heart?

During ischaemia, there was no apparent change in malondialdehyde (MDA) content in rat myocardium. However, reoxygenation resulted in a significant increase in MDA content. The changes evoked by ischaemia and reoxygenation were significantly attenuated by addition of fenistil (histamine H1 receptor antagonist). Enzymatic antioxidant systems were not significantly modified in the different periods of ischaemia and after 30 min of reoxygenation. It is suggested, that maintenance of an adequate endogenous antioxidant reserve during ischaemia may be important in recovery upon reoxygenation.

Animals↗

PubMed1992

Fibronectin and fibrinogen degradation products stimulate PMN-leukocyte and mast cell degranulation.

The ability of various peptides cleaved by plasmin from human fibrinogen and fibronectin or fibrinogen- and fibronectin- related synthetic peptides to induce histamine release from mast cells and collagenase and elastase from PMN-leukocytes was examined. Low molecular weight fibrinogen degradation products showed dose dependent secretion of collagenase. These peptides (mol. wt. 1.4 kD) at the concentration of 10(-5) M released about 47% of collagenase and 13% of elastase. Synthetic fibrinopeptides A and B had a similar strong collagenase releasing potency and also released histamine from mast cells. Peptides from plasmin digestion of fibronectin containing cell attachment site with sequence Arg-Gly-Asp-Ser and also synthetic peptide reproducing this amino-acid sequence at the concentration of 1000 micrograms/ml released about 50% of collagenase and 55% of elastase from PMN-leukocytes. Moreover peptides containing cell attachment and gelatin binding site induced histamine release from mast cells. The association of fibrinogen and fibronectin degradation with activation of mast cells may motivate the treatment with antihistaminic drugs of all pathological conditions where the intensive protein degradation takes place.

Animals↗

PubMed1989

Neutrophil enzyme activities in carrageenan-induced inflammation in rats.

During the course of carrageenan-induced inflammation in rats major changes were observed in the activities of neutrophil granule enzymes. The activities of three enzymes--gelatinase, collagenase and beta-glucuronidase, the markers of three different types of granules, have been measured and compared to those of a control group of animals. Total collagenase and gelatinase activities of control rats were 59.4 +/- 3.6 (mean +/- SD) and 23.0 +/- 2.9 units/mg protein, respectively. Significantly reduced levels of both collagenase (35.6 +/- 2.5 units) (p less than 0.05) and gelatinase (7.1 +/- 0.7 units) (p less than 0.001) were measured in the blood neutrophils of inflamed rats; and the collagenase activity of neutrophils derived from inflamed pleural exudate was also significantly decreased to a level of 19.7 +/- 1.8 units/mg protein (p less than 0.01). However, the gelatinase activity of exudate neutrophils did not differ from that of blood cells of inflamed rats. In contrast, no change was found for the beta-glucuronidase activity in blood neutrophils of control and inflamed rats. These observations support the concept that during the inflammatory response in rats, neutrophils in the circulation may become activated as judged by the extracellular secretion of collagenase and gelatinase. Therefore, neutrophils accumulating in acute inflammatory lesions contain decreased levels of collagenolytic enzymes and the significance of this observation is discussed.

Animals↗

PubMed1988

Is histamine involved in ethanol-induced inflammation?

The participation of histamine in ethanol-induced inflammation has been estimated in rats. Administration of ethanol caused an increase in the total number of blood leukocytes and changed the composition of the leukocyte population. The histamine receptor antagonists mepyramine and cimetidine did not affect the changes in cellular composition. Pretreatment with the anti-allergic drug Tritoqualine had no effect on the total number of leukocytes and PMN-leukocytes. PMN-leukocytes from ethanol treated rats had a greater capacity to activate latent collagenase. This ability was partially inhibited by the histamine receptor antagonists mepyramine and cimetidine, particularly in combination. Pretreatment with Tritoqualine apparently protected the latent collagenase against ethanol activation. Thus we conclude that histamine is possibly implicated in the process of generating activity for latent collagenase.

Animals↗

PubMed1988

Anti-inflammatory drugs modulate histamine release from mast cells induced by fibrinogen degradation products.

The products resulting from proteolytic degradation of human fibrinogen (FDP) were found to induce the release of histamine from rat peritoneal mast cells. Low molecular weight, dialysable peptides (FDP) showed the highest dose dependent, histamine releasing activity. Histamine release induced by FDP was effectively inhibited by the gold compound auranofin at a concentration of 10(-5)-10(-7) mol/l and also by the non-steroidal anti-inflammatory drugs BW 755c, timegadine, medosan, naproxen, and aspirin at the higher concentration range of 10(-4)-10(-6) mol/l. It is concluded that the release of histamine from mast cells may be modulated to some extent by anti-inflammatory drugs, especially auranofin, BW 755c and timegadine, a functional property which may be beneficial in the management of joint disease.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

PubMed1987

Inhibitory effect of tritoqualine on activation of latent polymorphonuclear leukocyte collagenase.

Treatment of rats with histamine releaser compound 48/80 caused changes in blood leukocyte populations. An increased number of PMN-leukocytes was observed. Tritoqualine only modestly reduced the number of granulocytes. In animals treated with compound 48/80 an activation of PMN-leukocyte latent collagenase of up to 80% was observed. This activation was partially inhibited (about 40%) in animals pretreated with tritoqualine. The results presented suggest that the beneficial effect of tritoqualine in allergic diseases may be in part connected with an indirect inhibition of collagenase activity.

Animals↗

PubMed1987

Auranofin modulates gelatinase release from rat neutrophils.

We have examined the effects of auranofin and some nonsteroidal anti-inflammatory drugs (NSAID) on the release of gelatinase from rat neutrophils. Two preparations of neutrophils were used, one derived from normal blood and the other from the inflamed pleural fluids of carrageenin-elicited pleurisy. Both neutrophil preparations released gelatinase in response to stimulation by serum-treated zymosan (STZ) or concanavalin A (Con A). Control, blood-derived neutrophils exposed to STZ produced more than a four-fold increase in the release of gelatinase, a response significantly inhibited by the presence of auranofin at 10(-5) and 10(-4) M. Inflamed, pleural neutrophils exposed to STZ produced a doubling in gelatinase release and this was also inhibited by auranofin at 10(-5) and 10(-4) M. The release of gelatinase by control neutrophils (no stimulation) or by neutrophils exposed to Con A was enhanced by 10(-6) M auranofin. In contrast, the NSAIDs aspirin, piroxicam, sulindac, indomethacin and naproxen had no inhibitory action on neutrophil gelatinase release. We conclude that auranofin is an effective inhibitor of gelatinase release from neutrophils and this property may represent a contributory factor assigned to the beneficial therapeutic action of gold salts.

Animals↗