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S Jancar

Publications and source records attributed to S Jancar.

68 records · Page 4Linked to original sources
PubMed1986

C5 fragments: are they important in polymorphonuclear leucocyte diapedesis?

In the present study the coisogenic C5-sufficient B10.D2/nSn and C5-deficient B10.D2/oSn mice were used to determine the importance of the C5 molecule in the polymorphonuclear leucocyte accumulation in inflammatory sites. Peritoneal exudates were induced by carrageenin, glycogen, zymosan, endotoxin lipopolysaccharides (LPS) and via a passive immediate hypersensitivity reaction. It was found that the temporal profile of PMN accumulation induced by all inflammatory stimuli tested, except by high doses of LPS, is similar in C5-sufficient and C5-deficient strains of mice.

Animals↗
PubMed1985

The anti-oedematogenic effect of SRS as an additional factor in the mode of action of non-steroid anti-inflammatory drugs.

A partially purified preparation of SRS was obtained from peritoneal exudates induced by a non-anaphylactic immediate hypersensitivity reaction. This preparation injected in the rat skin caused vasoconstriction and when administered together with carrageenin reduced oedema formation. Injection of carrageenin into the peritoneal cavity progressively increased exudate formation. Pretreatment of the animals with anti-inflammatory doses of aspirin, indomethacin and salicylate significantly reduced exudate formation and this inhibition was correlated with the appearance of SRS in the exudates. It is suggested that, in some inflammatory exudates, stimulation of the synthesis of vasoconstrictor SRS might be an additional factor to the inhibition of prostaglandin synthesis induced by non-steroid anti-inflammatory drugs.

Animals↗
PubMed1978

Uptake and inactivation of prostaglandin E2 methyl analogues in the rat pulmonary circulation.

1 The fate of (15S)-15-methyl prostaglandin E(2) methyl ester and 16,16-dimethyl prostaglandin E(2) in the pulmonary circulation of rat isolated lungs was compared with that of prostaglandin E(2) by means of bioassay.2 Calculated on the basis of height of response of the assay tissues, the inactivation of prostaglandin E(2) was 96 +/- 1%, of 15-methyl prostaglandin E(2) methyl ester, 53 +/- 6% and of 16,16-dimethyl prostaglandin E(2), 50 +/- 4%.3 Responses of the hamster stomach strip to the prostaglandin E(2) analogues passing through the pulmonary circulation were prolonged and slower in onset than those to the analogue given directly to the tissue. No such difference was observed with prostaglandin E(2).4 Bromocresol green, bromothymol blue, bromocresol purple and thymol blue (10(-5) M) all inhibited the inactivation of the three prostaglandins studied, as did diphloretin phosphate (1.5 x 10(-6) M). All five inhibitors also reversed the shape change in response seen after transpulmonary injection of 16-16-dimethyl prostaglandin E(2).5 We conclude that the inactivation of the methyl analogues is due to uptake, as they are not substrates for prostaglandin dehydrogenase.6 The lung may act as a depot for some compounds taking them up from the pulmonary vessels and later releasing them slowly into the systemic circulation.

Animals↗
PubMed1976

Formation of slow-reacting substance by guinea pig immunoglobulins.

The capacity of guinea pig antibodies to mediate the antigen-induced release of slow-reacting substance (SRS) in the rat peritoneal cavity is restricted to IgG2 and, to a lesser extent, to IgG1 populations of immunoglobulin. IgM and homocytotropic antibody of the reaginic type lacked this activity. The process was partially blocked by previous decomplementation of the rats, was not affected by previous reduction of the circulating leukocytes, and was partially suppressed by previous depletion of circulating platelets with an antiserum to rat platelets.

Animals↗
PubMedDate not supplied

Roles of endothelins and their receptors in immune complex-induced/polymorphonuclear-mediated lung injury (reversed passive arthus reaction) in CD-1 mice.

A number of pro-inflammatory mediators (leukotrienes, platelet activating factor, cytokines) participate in the process of neutrophil-dependent lung injury induced by immune complexes. Here, we studied the role of endothelins (ET) in the reversed passive Arthus reaction (AR) as a model of pneumonitis in CD-1 mice. We examined the broncholaveolar lavage fluid (BALF) for signs of inflammation such as the accumulation of cells, myeloperoxidase (MPO) activity and hemoglobin (Hb) levels, as a measure of hemorrhagic lesions, 24 h after injection. We used a selective ETA (BQ-123) or a non-selective ETA/ETB-R (SB 209670) receptor antagonist at various concentrations (2.5, 5 or 10 mg/kg ip at -8, 0, 8 and 16 h) to assess the involvement of ET. Challenged mice revealed signs of acute inflammation and hemorrhagic lesions. Levels of Hb and MPO, total and neutrophil cell counts increased by 9-, 9-, 3.2- and 63-fold, respectively. The lower dose of SB 209670 reduced Hb levels by 21% (P<0.05), without affecting cell accumulation or MPO. The mid-dose had no effect; the highest dose caused 60, 57 and 70% increases in Hb levels, total cell and neutrophil counts, respectively. Conversely, the highest dose of BQ-123 decreased Hb, total cell and neutrophil counts and MPO levels by 36, 35, 42 and 70%, respectively. These results support a role for ET in AR lung injuries. They also suggests that blocking ETA-R may be beneficial, while blockade of ETB-R (using a high dose of SB 209670) may be detrimental. A beneficial ETB-mediated response may exist that naturally interferes with events triggered by the formation of immune complexes such as cell accumulation and their subsequent activation leading to acute lung injury.

Animals↗
PubMedDate not supplied

Effect of platelet-activating factor antagonists (BN-52021, WEB-2170, and BB-882) on bacterial translocation in acute pancreatitis.

Bacterial translocation is an important source of pancreas infection in acute pancreatitis. The effect of platelet-activating factor (PAF) in the pathogenesis of acute pancreatitis has been proved in various studies. The aim of this study was to determine whether potent PAF antagonists influence bacterial translocation in acute pancreatitis. Acute pancreatitis was induced in 62 Wistar rats by injection of 2.5% sodium taurocholate into the biliopancreatic duct. The rats treated with PAF factor antagonists received intravenous injection of WEB-2170 (10 mg/kg), lexipafant (5 mg/kg), and BN-52021 (5 mg/kg) 30 minutes before induction of acute pancreatitis. Six hours after induction of acute pancreatitis, bacteriologic cultures and histologic scoring of tissues were performed. There was a statistically significant reduction in bacterial translocation to the mesenteric lymph nodes and liver but not to the pancreas of the rats treated with PAF antagonists. No significant increase in the intestinal bacterial population of any group was found. There were no statistical differences between the pancreatic histologic scores of the groups. PAF antagonists reduced bacterial translocation to distant sites other than the pancreas, preventing the bacterial dissemination that occurs in the early phase of acute pancreatitis and may have beneficial effects on the evolution of this disease.

Acute Disease↗
PubMedDate not supplied

Inhibition of airway hyperreactivity, edema, and lung cell infiltration by compound U-83836E in sensitized guinea pigs.

Sensitized guinea pigs were used to assess the effect of treatment with the compound U-83836E ((-)-2-[[4-(2,6-di-1-pyrrolidinyl-4-pyrimidinyl)-1-piperazinyl]methyl]-3 ,4-dihydro-2,5,7,8-tetramethyl-2H--benzopyran-6-ol, dihydrochloride) on the antigen-induced late-phase (16 h) airway hyperreactivity, increase in inflammatory cell number, edema, and release of inflammatory mediators in the bronchoalveolar lavage (BAL) fluid. After antigen challenge, an increase of the in vitro reactivity of the trachea and upper bronchi to acetylcholine and histamine and an increase in the number of leukocytes in the BAL fluid, mainly eosinophils and mononuclear cells, were observed. The concentrations of proteins, histamine, and PGE2 in the BAL fluid were also significantly increased by 53, 57, and 216%, respectively, after antigen challenge. Treatment with U-83836E (10 mg/kg) given i.p. 17 and 3 h before and 6 h after antigen challenge inhibited by approximately 80% the total cell number in the airways and the BAL fluid protein content. Moreover, this treatment totally inhibited airway hyperreactivity. Histamine and PGE2 levels in the BAL fluid were not significantly affected by U-83836E treatment. These results indicate that U-83836E is effective against some of the characteristic features of asthma in ovalbumin-sensitized guinea pigs.

Acetylcholine↗
PubMedDate not supplied

Airway and pulmonary tissue responses to platelet-activating factor in rats.

We studied airway and pulmonary tissue responses to platelet-activating factor (PAF) in rats by measuring alveolar pressure with the alveolar capsule technique. We calculated airway resistance (Raw), dynamic elastance (Edyn), and pulmonary tissue resistance (Rtis). PAF was administered intravenously in doses of 0.1, 1, 10, and 30 micrograms (1 dose per animal, 5 rats for each dose). Infusion of PAF resulted in a significant increase in Rtis and Edyn (p < .05). Maximal values of Edyn were observed with the infusion of 10 micrograms of PAF (p < .02). Rtis presented a significant increase after infusion of 1 microgram of PAF (p < .05). The observed increase in Raw was transient and did not reach statistical significance. After infusion of PAF lungs were fixed by a quick-freezing method. Morphometric analysis showed that PAF infusion resulted in significant increases in intraluminal secretion (p = .001) and peribronchiolar edema (p < .001) but did not result in significant airway contraction. We conclude that intravenous infusion of PAF results in significant effects on lung tissue mechanics. The effects of PAF on the mechanical properties of lung parenchyma reflect the inflammatory alterations induced by this agonist in distal airspaces.

Airway Resistance↗
PubMedDate not supplied

[Lung injury in acute pancreatitis. Influence of pancreatic enzymes reduction].

UNLABELLED: A previous report has show that cerulein in physiological doses reduces the rate mortality of pancreatitis by decreasing the enzyme content of the pancreas. Clinically detectable signs of lung injury develop in up to 50-70 percent of patients with acute pancreatitis. The aim of the present study was to assess the effect of acute reduction of pancreatic enzyme content on the pancreatitis pulmonary injury. Experimental haemorrhagic pancreatitis was induced by intraductal injection of 5 per cent sodium taurocholate in two groups of Wistar rats: group I (pancreatitis) and group II (pancreatitis after decreasing pancreatic enzyme content). Dye Evans blue was used to evaluate the lung injury. The degree of histologically observed lesions were similar in both groups, but the pulmonary lesion was smaller in group II than group I (p < 0.05). IN CONCLUSION: 1) pancreatitis' pulmonary lesion may be related with pancreatic enzymes that reach the blood stream and 2) the reduction of the pancreatic enzyme content has a beneficial effect on acute pancreatitis and reduces its pulmonary injury.

Acute Disease↗
PubMedDate not supplied

[Physiopathology of lung injury in acute pancreatitis].

Clinically detectable signs of lung injury develop in up to 50-70 percent of patients with acute pancreatitis. Despite that, the physiopathology of the lung injury associated with acute pancreatitis is unclear so far. Pulmonary edema is the main respiratory complication in acute pancreatitis. Increased permeabilities of the pulmonary endothelial and alveolar epithelial barriers are the causes of the pulmonary edema. Several factors have been regarded as the cause to pulmonary edema: release of pancreatic-derived proteolytic enzymes, oxygen-free radicals, phospholipase A2, free fat acids, tumor necrosis factor, platelet activating factor, arachidonic acid metabolites and pulmonary embolization. Understanding lung injury physiopathology enables physicians to a better therapeutic approach of the patients with acute pancreatitis. The aim of this paper is to expose the theories that explain the pancreatic-derived lung injury.

Acute Disease↗