Biomedical subjects

L Chyczewski

Publications and source records attributed to L Chyczewski.

At least 19 recordsLinked to original sources

PubMed1991

The effect of platelet activating factor antagonist (BN 52021) on cerulein-induced acute pancreatitis with reference to oxygen radicals.

Acute edematous pancreatitis was induced in Wistar male rats by iv infusion of cerulein (CR) in the dose of 5.10(-6)g.kg-1.h-1 during 3 or 6 h. The effect of BN 52021--platelet activating factor (PAF) receptor antagonist, against this model of disease was examined. BN 52021 was applied iv as a bolus injection in the dose of 5.10(-3)g.kg-1 at 0 time. Treatment with this agent significantly ameliorates cerulein-induced acute pancreatitis in rats. The effect of BN 52021 was expressed by significant reduction of pancreas edema, diminution of hyperamylasemia, lack of superoxide dismutase activity depletion, and inhibition of lipid peroxidation in pancreatic tissue. These changes were accompanied by significant reduction of acinar cells vacuolization and remarkable inhibition of infiltration with inflammatory cells in the interacinar space. We suppose that beneficial effect of BN 52021 against cerulein-induced acute pancreatitis in rats depends on the prevention of inflammatory cells activation and subsequent generation of oxygen radicals within pancreatic tissue.

Animals↗

PubMed1991

Effect of dimethylsulfoxide-hydroxyl radical scavenger on cerulein-induced acute pancreatitis in rats.

Acute oedematous pancreatitis was induced in Wistar male rats by intravenous (i.v.) infusion of cerulein at the rate of 5.10(-6)g.kg-1.h-1 for 3 or 6 hrs. The effects of dimethylsulfoxide (DMSO)-hydroxyl radical scavenger in this model of disease were examined. DMSO was injected i.v., 0.75 g.kg-1, at 0 and 3 hrs during cerulein infusion. Treatment with this agent exerted a protective effect on the rat pancreas in the cerulein-induced acute pancreatitis. This effect is expressed by inhibition of lipid peroxidation in pancreatic tissue, less oedema formation, diminution of hyperlipasemia and a significant reduction in acinar cell vacuolisation. Our data suggest that besides the hydroxyl radical, other oxidants (secondary?) may cause cytotoxicity in this model of disease. We suggest that phagocytic inflammatory cells provide such oxidants.

Acute Disease↗

PubMed1991

Megakaryocyte cumulation in rabbit lungs after intraperitoneal administration of casein.

In the lung capillary vessels of rabbits, 24 hr after intraperitoneal administration of saturated casein solution, megakaryocyte cumulation (MK) was observed (22 MK/cm2 of section area in treated group and 2,5 MK/cm2 of section area in control group). Megakaryocytes were found most often in the form of an elongated nucleus without cytoplasm. The authors suppose, that MK liberation from the marrow into the venous vessels may be caused by casein degradation products.

Animals↗

PubMed1990

Branched-chain amino acid enriched diet given simultaneously with ethanol partially prevents morphological and biochemical changes in the liver.

Morphological examination of the liver and biochemical studies of the serum were carried out on rats fed: a) ethanol p.o. in the daily dose of 6 g/kg for 4 weeks and maintained on standard diet (Et-OH) and b) ethanol in the same doses but fed the BCAA enriched diet (to amount of 1.174 mM/day/rat) were carried out. It can be concluded that BCAA enriched diet given simultaneously with ethanol prevent in part the morphological and ultrastructural changes in liver and improve positive body weight gain of experimental animals.

Amino Acids, Branched-Chain↗

PubMed1989

[Megakaryocytes in human lungs in non-selected autopsy specimens-- topography of their occurrence and correlation with pulmonary thrombosis].

In a 100 lungs of patients died in hospital (61 males, 39 females including 4 children) consecutively studied at autopsies in 1986 topographic quantification of megakaryocytes (MK) was performed. Mean number of MK was 31 cells per 1 cm2 of the studied sections (the range from 0 to 336 MK/cm2). More numerous MKs were observed in the upper pulmonary lobes and fibrous foci. The greatest accumulation of MK was found in the patients died from various types of shock. In the lungs with a large number of MK we found enhanced microthrombosis of the pulmonary vessels.

Adolescent↗

PubMed1989

[Pulmonary megakaryocytes (MK) in experimental hemorrhagic shock].

Quantification of MK in blood and pulmonary sections was performed in rabbits with induced hemorrhagic shock (group I) and in control rabbits (group II). In electron transmission microscopy we studied the ultrastructure of pulmonary capillaries. Animals in group I were exsanguinated to achieve systemic blood pressure level of 40 mm Hg. This level was maintained for 1.5 hours and then the rabbits from both groups were sacrificed. Pulmonary arterial and venous blood was sampled in the amount of 10 ml and two sections from each pulmonary lobe were taken. The blood samples were then treated with Streptolysine 0 in order to isolate MK which were counted in the smears. In pulmonary sections MKs were counted per 1 cm2. In animals with shock we found an increase in MKs in the pulmonary artery (means = 4.9 MK/ml against means = 1 MK/ml in venous blood; corresponding values for group II were means = 1.7 MK/ml and 1 MK ml respectively). In the lungs of rabbits in group I we found considerable accumulation of MKs means = 22.4 MK/cm2 (corresponding value for group II means = 2 MK/cm2). It was found that hemorrhagic shock was probably the factor activating the release of MK from the bone marrow to the periferal blood, whereas pulmonary capillaries were an effective filter uptaking circulating MKs. Edematous changes in the capillary endothelium were probably the factors intensifying the process of pulmonary uptake of MK. We discussed the value of pulmonary accumulation of MK in the development of mechanisms leading to adult respiratory distress syndrome.

Animals↗

PubMed1988

Oxygen-derived free radicals in cerulein-induced acute pancreatitis.

Conscious rats were treated with a supramaximal dose of 5.10(-6)g.kg-1.h-1 of cerulein for periods of 3 and 12 h. In both groups of animals typical features of acute oedematous pancreatitis were proved by biochemical and histologic examinations. The most important finding of our study was the decrease of superoxide dismutase (SOD) activity in pancreatic tissue, accompanied by a slight increase of this scavenger enzyme in serum of rats stimulated with cerulein during 3 h. Parallelly, evident elevation of malondialdehyde (MDA) concentration in pancreatic tissue was noted. After the 12-h infusion of cerulein we were not able to detect any SOD activity in pancreatic tissue, whereas this activity appeared in ascitic fluid of tested animals. Further increase of MDA concentration in pancreatic tissue, in comparison with 3-h pancreatitis, was found. These data suggest that in 3-h and 12-h cerulein-induced pancreatitis the oxygen-derived free radicals mediate the increased lipid peroxidation in pancreatic tissue. We think that the depletion of the scavenger enzyme SOD may be responsible for such a disturbance of lipid metabolism.

Acute Disease↗

PubMed1979