[Unithiol in the therapy of poisoning caused by cardiac glycosides].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVE: To investigate the activity of ChE in rats poisoned by dimehypo and then treated with pralidoxime methylchloride or unithiol. METHOD: Rats were divided into control group (dimehypo); intervention groups [dimehypo plus pralidoxime methylchloride or dimehypo plus unithiol (sodium dimercaptopropanesulphonate)]. Rats were dosed with 4 different doses of dimehypo: 1/16, 1/8, 1/4 and 1/2 of LD50 respectively(the LD50 of dimehypo is 342 mg/kg). After being poisoned with dimehypo orally, rats were immediately injected intramuscularly with pralidoxime methylchloride or unithiol. The activity of ChE in blood was detected before and 1/2, 1, 2, 4 and 24 h after poisoning in dimehypo and intervention groups. RESULT: The ChE activity of four dose subgroups at 1 h after poisoning were (1.04 +/- 0.21), (0.84 +/- 0.12), (0.71 +/- 0.12), (0.66 +/- 0.07) U/ml respectively; the ChE activity of pralidoxime methylchloride intervention groups were (1.01 +/- 0.18), (1.17 +/- 0.11), (1.01 +/- 0.04), (1.03 +/- 0.12) U/ml respectively; and the ChE activity of unithiol intervention groups were (1.15 +/- 0.15), (1.26 +/- 0.27), (1.08 +/- 0.08), (1.04 +/- 0.12) U/ml respectively. The inhibited ChE in blood was recovered by either treatment with pyraldoxime methylchloride or unithiol. These two drugs had similar effects of recovering the activity of ChE(P > 0.05), but at higher doses(1/4 and 1/2 of LD50) the effects of both were not so good. CONCLUSION: Pralidoxime methylchloride and unithiol could partly recover the activity of ChE inhibited by dimehypo.
The authors describe the status of lipid peroxidation (diene conjugates and malonic dialdehyde) and the endogenous antioxidant enzyme superoxide dismutase in the course of the treatment of patients with acute focal pneumonia by means of the use of transthoracic intrapulmonary injections of unithiol and autologous ultraviolet blood radiation (AUVBR). Three groups of patients were entered into the study. The first group included 64 patients who were given transthoracic intrapulmonary injections of unithiol, the second group 58 patients who received 5-7 sessions of AUVBR, in the third group, 52 patients were given transthoracic intrapulmonary injections of unithiol coupled with 3-5 sessions of AUVBR. The control group was made up of 40 patients given intravenous unithiol injections in routine therapeutic doses. The results of the treatment evidence that combined correction of lipid peroxidation carried out in the third group patients was most effective. As regards the times, the positive dynamics of lipid peroxidation and superoxide dismutase activity correlated with the clinical, biochemical and x-ray improvement. Therefore the method of correction in question is a pathogenetically based approach, permitting one to enhance the clinical efficacy of the treatment of patients suffering from acute focal pneumonias and to reduce the times of their stay in the hospital by 5-7 days, on the average.
The effects of potassium ethylxanthogenate (PEX) and 2,3-Dimercaptopropane sulphonate sodium (Unithiol) on the pentobarbital (40 mg/kg, body weight i.v.) (PB) sleeping time, pharmacokinetics, and metabolism, were studied in comparative experiments on male albino mice. It was established that the pretreatment of animals with PEX (80 mg/kg of body weight s.c.) potentiated the PB sleeping time. Unithiol in an equimolar dose (105.2 mg/kg of body weight s.c.) had no effect. The pharmacokinetics of PB could be fitted to be a biexponential equation of the type Cp(t) = A.e-alpha t + B.e-beta t. PEX caused an almost two-fold decrease in the elimination rate constant of plasma PB, which led to a higher half-time and a lower total clearance compared with the controls. The curve for the plasma PB metabolites in the PEX-pretreated mice was significantly lower than of the controls. A higher PB level and decreased rate of elimination in PEX-pretreated animals was observed also in the: liver, lungs, kidney, and brain. A conclusion was drawn that the potentiating effect of PEX on the PB sleeping time is mainly due to inhibition of PB liver metabolism. It was suggested that the differences in the biological effects of the two thiol compounds are due to the differences in their chemical structures: PEX possesses a C = S group but Unithiol lacks this group.
Sodium nitrite induced poisoning resulted into oxidation-reduction disorders with concomitant changes in the ratio of the oxidated and reduced forms towards accumulation of the oxidated equivalents. Antioxidants unithiol, tocopherol acetate, ascorbic acid, methylene blue, violuric acid influenced the oxidation-reduction balance in different ways. The protective action of violuric acid was comparable with that of methylene blue and exceeded the unithiol protective properties. Violuric acid, as compared with unithiol, ascorbic acid and tocopherol, was more effective in decreasing methemoglobin and nitrates contents in blood in methemoglobinemia cases. The violuric acid and methylene blue protective mechanisms are in all probability influenced by the antioxidant properties of these substances and their reductase activity.
Unithiol (2,3-dimercaptopropan-sodium sulphonate) has been found to be an effective, nontoxic stabilizer of antiviral activity of labile interferons. The optimum stabilizing concentration of unithiol is 0.07%: at this concentration its protective effect is maximum with the lowest content of the substance. Unithiol at this concentration retains about 66% of the initial antiviral activity in acid medium (pH 2.0) and up to 75% of the initial antiviral activity on mechanical exposure.
A one-time addition of gutimine (0.5 g/l), amtizol (0.2 g/l), and unithiol (0.25 g/l) to the medium at early stages of tadpole development was shown to inhibit metamorphosis only upon addition of unithiol. Repeated addition of gutimine, amtizol, and unithiol to the medium leads to reliable delay in metamorphosis. The delay is more pronounced at addition of the compounds to the medium at late stages of tadpole development (beginning at 40 stage). This suggests that the studied compounds may have anti-thyroid activity. All drugs under study induce the skin clearing.
The effect of type C botulinum toxin on Na, K, Mg-ATPase activities of erythrocyte membranes of white rats was studied in experiments in vivo and in vitro. The activity of Na, K, Mg-ATPase was found to be markedly inhibited in the preclinical period of poisoning, 2 hours after intraperitoneal injection of the toxin. In this case Mg-ATPase activity noticeably increased. In the presence of the development of a grave paralytic syndrome one day after intraperitoneal injection of the toxin, the activity of Na, K-ATPase of the erythrocyte membrane remained decreased as was the case in the preclinical period of poisoning, whereas the activity of Mg-ATPase returned to normal. The experiments in vitro with preincubation of erythrocyte membranes with botulinum toxin in the concentrations corresponding to the mean calculated ones in the experiments in vivo demonstrated inhibition of Na, K-ATPase. The magnitude of Mg-ATPase activity remained virtually unchanged in all the modifications of the experiments with boiled and native botulinum toxin. The in-vivo experiments with intraperitoneal injection of glutathione and unithiol to the pretreated animals attested to normalization of Na, K-ATPase in the preclinical period of poisoning, with this normalization being brought about by unithiol. In the in-vitro experiments with addition of unithiol or glutathione into the incubation medium, each of the donators of sulphhydryl groups prevented Na, K-ATPase inhibition with botulinum toxin.
It was shown in experiments with three types of cells (dog red cells, hepatic cells of newborn Wistar rats, and culture of the renal epithelium of Vero monkeys) that cadmium in complexes with dimercaptoethanol penetrates the cells in an 8-33-fold greater amounts than free cations of metal. Unithiol increases cadmium penetration in the cells by 1.6-3 times only. The strength of cadmium binding with dimercaptopropranolol in the cells is greater than that with unithiol and free cations. Albumin limits penetration of free cations of cadmium and of complexes with dimercaptothiol to a greater degree than that of cadmium complexes with unithiols. The reasons for the differences revealed are discussed.
The method is infusing an isolated jejunal strip with heparinized blood (3-5 units/ml) was used to determine total free kinins in peripheral blood of man and animals to a high precision (+/- 6.9%). Kinin formation was inhibited by trypsin inhibitor obtained from soybean (100-200 microgram/ml). Destruction of kinin was blocked by 8-hydroxyquinoline (0.03-0.05 ml of saturated solution per 1 ml of blood) or by unithiol (2,3-dimercaptopropanol-2 mg/ml). Since these inhibitors can induce hypesthesia of the jejunum to bradykinin (8-hydroxyquinoline in 47% of cats) or to potentiate contractility of the jejunal strip (unithiol in 50% of cats) it is advisable that appropriate corrections is made in order to restrict the number of tests, to raise the interval between the tests and to carry out additional analysis of jejunal sensitivity to bradykinin in the presence of 8-hydroxyquinoline or unithiol.