Effect of cimetidine on the heart conduction system]

An effect of cimetidine on ECG records has been investigated in a group of 40 patients with gastric or duodenal ulcers and coexisting circulatory disorders. For this purpose ECG has been recorded with Holter's technique (Medilog 2000) together with ECG-recording using high amplifying technique. An intravenous injection of 200 mg of cimetidine produced in some of patients inhibition of the sinus rhythm atrio-ventricular conduction disturbances as well as changes in the end phase of ECG ventricular image. The authors suggest, that intravenous administration of cimetidine to patients with cardiac diseases should be monitored with ECG recording.     

Examinations of cell mediated immunity in diffuse peritonitis]

Phagocytic index and rosette test E have been determined in 50 patients, including 15 with diffuse peritonitis and the noncomplicated diffuse peritonitis, 20 patients with septic complications, and 15 patients who underwent abdominal surgery. It was found, that phagocytic index is decreased in all patients after abdominal surgery. The most marked decrease of this index was found in patients with complicated peritonitis. It still decreases in the course of peritonitis and increases in the reference group. The marked decrease in the number of T-cells was observed in complicated peritonitis during the whole period of follow-up while it normalizes in case of noncomplicated peritonitis as in the reference group. Using the tests under study it was possible to assess cell-mediated immunity which is depressed in peritonitis. The tests enable also the prediction of septic complications of peritonitis.     

Results of treating acute myeloblastic leukemia in patients over 60 years of age

An efficiency of the acute myeloblastic leukemia therapy has been assessed in 79 patients aged over 60 years. Twenty six patients out of this group have been treated with usual or reduced doses of doxorubicin and cytarabine (ADR-Ara-C) 35--low doses of cytarabine (LD Ara-C), 11-6-mercaptopurine (6 MP), and 7 patients died before chemotherapy. Complete remission in group treated with ADR-Ara-C was achieved in 23% of patients while partial remission in 42%. Median survival in this group was 5.8 months (range from 0.5 to 16 months). Percentage of the complete remissions in the group treated with LD-Ara-C was 6%, and partial remissions 40%. Median survival was 4.7 months (range from 0.5 to 14.2 months). Partial remission in 5 out of 11 patients treated with 6 MP (36%) and no complete remissions were noted. Median survival was 3.9 months. Therapy with ADR-Ara-C produced marked leucopenia and thrombocytopenia in the majority of treated patients. Vomiting, hemorrhagic complications, and bacterial infections have also been noted. These adverse reactions have been less frequent in patients treated with LD-Ara-C, and 6 MP. Ten patients (38%) treated with ADR-Ara-C and 7 patients treated with LD-Ara-C died during remission inducing therapy.     

Effect of methylguanidine and guanidine succinic acid on methemoglobin reductase activity in human red cells]

Activity of methemoglobin reductase was studied in human red cells treated with methylguanidine and guanidinosuccinic acid in concentrations similar to those in plasma of patients with chronic renal failure. Enzyme activity was measured with Richterich technique following an incubation at 37 degrees C for three hours. Results have shown that methylguanidine in concentration of 5.4 x 10(-5) mol/l decreases activity of methemoglobin reductase in human red cells on average by 13.9%. Higher concentrations potentiate this effect. Similar changes in methemoglobin reductase activity were noted after introduction of guanidine-succinic acid into the mixture. This agent in concentration 5.6 x 10(-5) mol/l inhibited activity of the tested enzyme by 34.2% on average. Combined methylguanidine in concentration of 5.4 x 10(-5) mol/l and guanidine-succinic acid in concentration of 2.8 x 10(-5) mol/l inhibited methemoglobin reductase activity by 33.0% on average. It may be suggested, that methylguanidine and guanidine-succinic acid being low molecular uremic toxins may significantly decrease methemoglobin reductase activity in red cells of patients with chronic renal failure.     

Echocardiographic evaluation of delayed outcome of artificial valve implantation in patients with aortic semilunar valve insufficiency]

An average follow-up period of 16 patients was 28 months following an implantation of the artificial aortic valve for its insufficiency. In 10 operated patients who were able to continue their occupation exercise tolerance increased by two classes, according to NYHA. Blood pressure gradient decreased significantly from 61.8 to 37.5 mmHg, cardiac volume index decreased from 639 to 602 ml/m2. Echocardiographically measured muscle mass of the left ventricle, end-diastolic and end-systolic volumes, and the left atrial dimensions decreased significantly following surgery. A significance of the relation of the left ventricle volume to its mass <4 as a prognostic factor in aortic valve replacement has also been confirmed.     

Factors effecting recurrence of duodenal ulcers after highly selective vagotomy]

Recurrence of duodenal ulcer was diagnosed in 15 patients who underwent highly selective vagotomy before 6-13 years, i.e. in 12.2%. Factors possibly contributing to such a recurrence were analysed. Patients with ulcer recurrence were: 1) non-qualified workers, 2) tobacco smokers, 3) heavy drinkers, 4) users of ulcerogenic medicines, and 5) were involved into conflict situations.     

Microbial transformation of neutral fraction and upgraded neutral fraction of Polish tall oil

Summary Microbial transformations of neutral fraction (NF) and upgraded neutral fraction (UNF) of Polish tall oil byMycobacterium sp. MB 3683 were performed. Final metabolites and yields were compared to bioconversion of pure -sitosterol. Additionally, origin of a new metabolite —5-androsta-3,6,17-trione was proved by transformation of UNF in the presence of labeled -sitosterol.     

Phenylarsine oxide induces the cyclosporin A-sensitive membrane permeability transition in rat liver mitochondria

This paper reports an investigation on the effects of the hydrophobic, bifunctional SH group reagent phenylarsine oxide (PhAsO) on mitochondrial membrane permeability. We show that PhAsO is a potent inducer of the mitochondrial permeability transition in a process which is sensitive to both the oxygen radical scavanger BHT and to cyclosporin A. The PhAsO-induced permeability transition is stimulated by Ca²⁺ but takes place also in the presence of EGTA in a process that maintains its sensitivity to BHT and cyclosporin A. Our findings suggest that, at variance from other known inducers of the permeability transition, PhAsO reacts directly with functional SH groups that are inaccessible to hydrophilic reagents in the absence of Ca²⁺.     

Quinolinate-like neurotoxicity produced by aminooxyacetic acid in rat striatum

Summary The endogenous tryptophan metabolite quinolinic acid elicits in rodent brain a pattern of neuronal degeneration which resembles that caused by L-glutamate. Its qualities as a neurotoxic agent raised the hypothesis that quinolinic acid might be involved in the pathogenesis of human neurodegenerative disorders. Kynurenic acid, another endogenous tryptophan metabolite and preferential N-methyl-D-aspartate (NMDA) antagonist, has been shown to block quinolinic acid neurotoxicity. Here we report that microinjections of aminooxyacetic acid (AOAA), an inhibitor of kynurenine transaminase and of other pyridoxal phosphate-dependent enzymes, into the rat striatum produce neuronal damage resembling that caused by quinolinic acid. AOAA-induced striatal lesions can be prevented by kynurenic acid and the selective NMDA antagonist 2-amino-7-phosphonoheptanoic acid. These results suggest that AOAA produces excitotoxic lesions by depleting brain concentrations of kynurenic acid (inhibition of synthetic enzyme) or due to impairment of intracellular energy metabolism (depletion of cell energy resources). The concept of deficient neuroprotection due to metabolic defects might help to clarify the pathogenesis of human neurodegenerative disorders and to develop strategies that may be useful in their treatment.This work was supported by research grant from the Polish Academy of Sciences.These data have been communicated to the International Congress on Amino Acid Research held in Vienna in August 7–12, 1989.