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Biomedical subjects

S N Chuklin

Publications and source records attributed to S N Chuklin.

8 recordsLinked to original sources

[Contents of prostaglandins F2alpha, I2 (prostacyclin) and thromboxane A2 in the dog liver during development of hemorrhagic shock].

Contents of prostaglandins (PGs) F2 alpha, I2 and thromboxane (TH) A2 in the liver of 6 dogs has been studied in dynamics of hemorrhagic shock development. The results show that acute haemorrhage (31.9 +/- 1.6 ml/kg) stimulates the synthesis and release of all the eicosanoids studied. Nevertheless, in the progression of shock a significant difference was noticed between the high TXA2 and PGF2 alpha rates and comparatively lower rise of PGI2 production. The late stage of shock (201 +/- 44 minutes after haemorrhage) was characterized by a further rise in TXA2 and PGF2 alpha rates with simultaneous lowering of PGI2 as a result of vascular endothelium affection which is the main source for prostacyclin synthesis. In view of the antagonism of PGI2 to TXA2 and PGF2 alpha and its cytoprotective effects, the results of present investigation give the experimental background for using prostacyclin or its synthetic analogues in a complex therapy of acute liver failure in clinic.

Animals↗

[The prostaglandin I2 and thromboxane A2 content of the blood of dogs in the dynamic development of hemorrhagic shock].

The content of prostaglandin I2 (PGI2) and thromboxane (Tx) A2 in the venous blood was studied in 5 dogs in the time course of hemorrhagic shock simulated by a single jet blood-letting from the femoral artery. PGI2 and TxA2 concentrations were estimated by the levels of their stable metabolites in RIA. It was found that acute hemorrhage stimulated the synthesis of prostanoids studied up to the animals' death. However, with the shock progressing, a shift took place in the ratio PGI2/TxA2 from 1:3.8 to 1:5.2, due to a higher rise of TxA2. Possible causes of PGI2 synthesis decrease and TxA2 production increase in hemorrhagic shock were considered. Basing on the data obtained a conclusion has been made on the necessity of exogenous PGI2 (prostacyclin) inclusion into the combined therapy of hemorrhagic shock.

Animals↗

[The content of prostaglandins A and E in the blood and renal tissues in the early phase of experimental acute renal failure caused by the crush syndrome].

Prostaglandin (PG) A and E content in the blood and renal tissues (cortex and medulla) has been studied in 25 dogs in the early phase of acute renal failure (ARF). It has been found that by the 4th hour of compression PG content increases drastically in the blood and renal cortex and decreases in the renal medulla. Compression relief and ARF progress were accompanied by a drop in PG concentration both in the blood and the renal cortex and medulla. It is concluded that enhanced PGE2 synthesis is a protective reaction preventing the damage of the renal structure and function. The following decrease in PGE2 level is mediated by progressing effect of aggressive factors on the interstitial cells of the renal medulla and the endothelial cells of the cortex vessels--as a basic source of endogenous PG synthesis. The results obtained are experimental proof of PGE2 use in the complex therapy of ARF.

Animals↗