carrageenan pleurisy
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Author(s):  
O. M. Larycheva ◽  
L. D. Chebotar ◽  
T. Ya. Yaroshenko

Introduction.Pathological changes in human body due to light exposure at night are triggered by circadian disruption, inhibition of melatonin secretion by the pineal gland at night that leads to its reduction in blood. Clinical and experimental data indicate high importance of free radical oxidation inthe pathogenesis of pulmonary diseases. The aim of the study – to explore the influence of a melatonin deficiencyin addition to pleurisy on free radical oxidation in the tissues of the lungs of rats exposed to light for 30 days.Research Methods. Experiments were carried out on male albino Wistar rats. The animals were randomized into four groups with 7 animals in each: an intact group, 30 day pineal gland hypofunction, carrageenan pleurisy, 30 day pineal gland hypofunction with carrageenan pleurisy. Pineal gland hypofunction was modeled by 1500 lx fluorescent lamps around the clock. The experimental pleurisy was induced in anesthetized animals by intrapleural injection of 0.1 ml of carrageenan. Superoxide (•О2-) products were determined by the reaction with nitro blue tetrazolium under the influence of NADH, NADP and pirogenal. The concentration of diene conjugates was determined by I.D. Stalna technique, TBA-active products – by I.D. Stalna, T.H. Harishvili method, trienes, ketodienes, - by a modified method based on the molar extinction coefficient.Results and Discussion.Assessingthe intensity of the reactive oxygen species (ROS) generation, a significantincrease of the •О2-level in all sources of its generation in the tissues of the lungs has been observed both in the control group with pleurisy and in the rats with 30-day pineal gland hypofunctionandpleurisy, compared to the intact animals.The chronic pineal gland hypofunction in the animals with experimental pleurisy lead to •О2- generationby the microsomal electron transport chain (ETC) by 54.6 % (р<0.05) when compared with carrageenan group of rats. No significant changes in concentration of the lipid peroxidation products has been observed in the animals with pleurisy during long-term light exposure.Conclusions. Chronic hypofunction of the pineal gland with the carrageenan-induced pleurisy causes activation of the free radical processes in the rats’ lung tissues and occur as hyperproduction of the superoxide anion radical by the microsomal chain of oxidation. This fact denotes probable abnormalities in the function of the microsomal electron transport chains especially under the condition change of properties of dehydrogenases. 


1994 ◽  
Vol 41 (1-2) ◽  
pp. 53-56 ◽  
Author(s):  
C. A. Allen ◽  
D. M. Ferry ◽  
V. S. Chadwick

1993 ◽  
Vol 2 (1) ◽  
pp. 33-39 ◽  
Author(s):  
R. Goodman ◽  
L. R. Mantegna ◽  
C. L. McAIlister ◽  
E. Bruin ◽  
R. L. Dowling ◽  
...  

The carrageenan pleurisy model, which is characterized by cellular influx and oedema, has been used to examine the effects of anti-inflammatory compounds such as naproxen. Interleukin-1α and β (IL-1) are known to be pro-inflammatory mediators, and their roles in this model are unknown. Intrapleural injection of 1% viscarin carrageenan or saline was administered to male Lewis rats. Four to 24 h later, cell counts, fluid volumes and IL-1β levels (measured by ELISA) were determined in the pleural cavity. Serum corticosterone levels were measured only at 4 h. Significant increases in IL-1β levels precede cell influx suggesting IL-1β plays a role in the maintenance of cell accumulation in the pleural cavity. None of the drugs tested, including the IL-1 receptor antagonist, maintained pleural cell influx and IL-1β levels at control levels. When human IL-1α or β or rat IL-1β were injected individually into the pleural cavity, none of these cytokines were pro-inflammatory, as measured by increased cell influx and fluid extravasation. These results suggest that although IL-1β levels increase in the pleural cavity in response to carrageenan, IL-1 per se is not the initiator of the pro-inflammatory events of cell influx and oedema in this model.


1988 ◽  
Vol 20 (7) ◽  
pp. 629-630 ◽  
Author(s):  
M. Marrella ◽  
U. Moretti ◽  
E. Concari ◽  
G.P. Velo ◽  
R. Milanino

1985 ◽  
Vol 7 (3) ◽  
pp. 395
Author(s):  
D. Bradshaw ◽  
B.B. Dodge ◽  
P.H. Franz
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