[Case report of infected lymphocele].

The lymphorrhea is a problem that we face in the early postoperative period in patients undergoing lymph node dissection (LND) for treatment of cervical cancer (CC). The formation of lymphocele most often in the pelvis is as a consequence. The incidence of lymphocele different, ranging from 0.4% to 58.7%. It is diagnosed most common in random checks in the asymptomatic or by presence of complains in symptoms. Ultrasound is most commonly applied together with computed axial tomography. One of the methods for treatment of symptomatic lymphocele is percutaneous drainage under ultrasonic control. As a complication of this procedure are observed cases of infection of lymphocele.

Effect of immobilization, cold and cold-restraint stress on liver monooxygenase activity and lipid peroxidation of influenza virus-infected mice.

The present study provides a direct experimental evidence that the combination of influenza A/Aichi/2/68 (H3N2) infection with different models of "oxidative stress", such as immobilization, cold and cold-restraint, is associated with graduated oxidative disturbances in the liver of mice, despite the absence of virus and inflammation in this tissue. It was found that experimental influenza virus infection is accompanied with a significant increase of lipid peroxidation products, a decrease of natural antioxidants (vitamin E, glutathione) and cytochrome P-450, an inhibition of cytochrome c reductase and liver monooxygenases (analgin- N-demethylase and amidopyrine- N-demethylase). Immobilization and cold stress, applied separately or in combination (cold-restraint), did not influence significantly any of the analysed parameters compared to those of the control group of non-infected mice. Preliminary exposure of mice to immobilization or cold stress and subsequent inoculation of influenza virus resulted in a significant increase of lipid peroxidation products and a significant decrease of vitamin E and reduced glutathione, compared with levels in control (non-infected) animals. Compared to influenza virus-infected and non-stressed animals, the changes in all these parameters were negligible. Immobilization or cold stress, applied in combination with influenza virus infection, partially prevented the suppressive effect of influenza virus on cytochrome P-450 and liver monooxygenases. A tendency towards normalization of these parameters to the control levels was observed. However, after application of cold-restraint plus influenza virus infection, the level of cytochrome P-450 and activity of cytochrome c reductase stayed markedly lower than in infected and non-stressed animals. The activities of liver monooxygenases were slightly increased compared with those of infected and non-stressed animals, but stayed relatively low compared to control (non-infected) mice. Combination of cold-restraint and influenza virus infection resulted in a greater synergistic increase of lipid peroxidation products and a greater synergistic decrease of vitamin E and reduced glutathione compared to controls, as well as to influenza virus-infected and non-stressed animals.

Effect of vitamin E supplementation on lipid peroxidation in blood and lung of influenza virus infected mice.

The influenza virus infection (A/Aichi/2/68) was associated with development of oxidative stress in lung and blood of mice, accompanied by an increase in levels of lipid peroxidation products (conjugated dienes and total malondialdehyde) and a decrease in endogenous amounts of natural antioxidant vitamin E. These effects were most pronounced on the 5th day after virus inoculation, in comparison with those on the 7th. Supplementation of mice with exogenous vitamin E before virus inoculation lead to lung and blood protection against lipid peroxidation. A marked decrease in lipid peroxidation products and an increase in vitamin E content was established in blood and lung on the 5th and 7th day after virus inoculation. The stabilizing effect of vitamin E is dose-dependent in blood and dose-independent in lung, and was most pronounced on the 5th day after virus inoculation in comparison with the 7th day.

Effect of vitamin E on lipid peroxidation and liver monooxigenase activity in experimental influenza virus infection.

Influenza virus infection was associated with development of oxidative stress in liver of mice, viz. increase in amount of lipid peroxidation products, decrease in cytochrome P-450 and NADP. H-cytochrome c-reductase activity, and inhibition of liver monooxygenases (aniline hydroxylase, ethylmorphine-N-demethylase, amidopyrine-N-demethylase and analgin-N-demethylase). These effects were most pronounced on the 7th day after virus inoculation as compared to the 5th one. Supplementation of mice with vitamin E before virus inoculation leads to liver protection against oxidative stress and toxicosis. A marked decrease of lipid peroxidation products and an increase of cytochrome P-450 and activities of monooxygenases was established. The stabilizing effect of vitamin E was dose-dependent and was most pronounced on the 5th day after virus inoculation as compared to the 7th one.

Effect of hydrocortisone and desoxycorticosterone on some reductases, esterases and synthetases.

Corticosteroids, applied in single high doses, are known to inhibit the activity of mixed function oxidases. Experiments on male rats have been performed in order to clarify their effect on other drug-metabolizing enzyme systems. It is found that hydrocortisone (HC) and desoxycorticosterone (DOCA), applied in a single dose of 50 mg/kg, do not change the activity of the liver microsomal NADPH-dependent neotetrazolium reductase. HC inhibits the intestinal acetylsalicylic esterase B, whereas DOCA does not change it significantly. This effect should be borne in mind when combining corticosteroids with acetysal. No significant changes are observed in the activity of liver esterase A under the effect of the two corticosteroids. DOCA inhibits the liver cytosol glutathione-S-transferase. The reduced enzyme activity of the liver microsomal UDP-glucuronyl-transferase by the two corticosteroids and of the glutathione-S-transferase by HC is manifested only as an insignificant tendency.

Enzyme-inhibiting action of hydrocortisone and desoxycorticosterone of mixed function oxidases.

Comparative studies have been carried out on the action of two corticosteroids: the mineralocorticoid desoxycorticosterone and the glucocorticoid hydrocortisone, upon single administration in male albino rats, on the hexobarbital sleeping time and the activity of the mixed function oxidases. Applied in equimolar doses, the two steroids prolong the hexobarbital sleeping time, the effect of desoxycorticosterone being stronger. The potentiation of hexobarbital sleeping time by hydrocortisone differs in degree in animals from the different age groups, being most pronounced in mature animals compared with two-week-old immature and old animals. Unlike hydrocortisone, the potentiating effect Of desoxycorticosterone is close in intensity for all age groups studied. Both corticosteroids in single doses (50 mg/kg) inhibit the activity of mixed function oxidases, metabolizing type I substrates--hexobarbital and morphine, the inhibitory effect of desoxycorticosterone being stronger. Hydrocortisone does not influence the metabolism of type II substrates (aniline), while desoxycorticosterone inhibits it considerably. The reasons for the differences observed in the effects of the two compounds are sought in the different involvement of the enzyme systems studied in their metabolism.

Effect of hydrocortisone on oxidative degradation of hexobarbital and ethylmorphine.

In experiments on albino rats of both sexes it has been established that hydrocortisone applied in a single dose of 50 mg/kg i.p. inhibits hexobarbital oxidase and ethylmorphine-N-demethylase and applied repeatedly in a dose of 10 mg/kg increases the activity of both enzymes. In castrated male rats the enzyme-inhibiting action of the single dose of hydrocortisone is much reduced, while its enzyme-inducing action on repeated application remains the same (the two effects are evaluated by the hexobarbital sleeping time).

[Mechanisms of hexobarbital anesthesia potentiation by hydrocortisone]. / Vurkhu mekhanizmite na potentsrane na kheksobarbitalovata narkoza ot khidrokortizona.

The authors carried out studies on white rats of Wistar strain and investigated some of the mechanisms, metabolic and central, by means of which hydrocortisone affected hexobartital sleep. They established that hydrocortisone in dose of 25 and 50 mg, administered singly, together with hexobarbital or after a 30-minute interval, potentiated hexobarbital sleep significantly. The concentrations of hexobarbital in blood serum and in brain on the 30th minute after its administration were higher in the experimental animals, treated with hexobarbital in comparison with the controls of both sexes. The experiments with determination of the activity of liver microsomal hexobarbital enzymic system showed convincingly a considerable inhibition of enzymic activity (with 53%) of hydrocortisone after 20 minutes after its application in vivo. Subthreshold sreep dose of hexobarbital, determined by the method of Lewy, was lowered than that of the experimental group and higher in the control rats. Hexobarbital concentrations in blood serum and in brain at the moment of waking were lower in experimental animals, treated with hydrocortisone, and higher in the control animals. The obtained results gave foundations to the authors to assume that metabolic and central nervous mechanisms participated in potentiation of hexobarbital sleep.