Acta medica Academiae Scientiarum Hungaricae最新文献

The effect of phenobarbital pretreatment (PB; 75 mg/kg i.p. once daily for 5 days) and the simultaneous administration of taurocholate (TC; 200 mumol/kg i.v.), eosin(EO; 40-160 mumol/kg i.v.) and iodoxamic acid (IA; 125--500 mumol/kg i.v.) on the hepatic uptake and biliary excretion of BSP (30--120 mumol/kg i.v.) and BSP--GSH (40--160 mumol/kg i.v.) was investigated on diethyl maleate (DEM)-pretreated rats. The biliary excretion of BSP was not influenced by PB and EO, while it was increased by TC and decreased by IA. In contrast, the excretion of BSP--GSH was not influenced by TC or IA, it was stimulated by PB and inhibited by EO. In the different experimental conditions the hepatic uptake of BSP and BSP--GSH changed similarly: PB did not influence, TC, EO and IA decreased the accumulation of BSP and BSP--GSH in the liver. These results indicate that qualitative differences exist in the hepatobiliary transport of BSP and BSP--GSH, which manifest themselves following their hepatic uptake.

A fundamental role is attributed to the pathological immune response in the development of chronic hepatitis B. By virtue of its non-specific immune modulatory effect, levamisole is capable of improving impaired T-cell function. Hence, studies with treated and control groups were performed in determine the effect of levamisole in acute viral hepatitis and chronic active hepatitis B. In acute hepatitis B, levamisole promoted the normalization of GPT, the elimination of HBsAg; this improvement was preceded by higher GPT values and increased titres of IgG, IgA, and of anti-HBcore. In chronic active hepatitis in the first few months of treatment a moderate increase of the GPT and HBsAg levels occurred, followed later by a decrease of these values. At the same time the phytohaemagglutinin reactivity of lymphocytes increased, and so did the ratio of circulating active T-cells.

Biliary flow and the biliary excretion of bromcresol green were measured in rats injected i.p. with a single dose of phenobarbital, 75 mg/kg. Biliary flow began to increase 6 h after the injection, it reached a peak at 36 h and returned to the control level at 72 h. In the same rats, the enhanced biliary excretion of bromcresol green was first observed at 12 h, it reached a peak at 24 h and returned to the control level at 72 h. Other groups of rats received 75 mg/kg phenobarbital as daily i.p. dose over 5 days. In these groups, the increase in biliary flow did not exceed that measured in the rats given the single dose, however, the biliary excretion of bromcresol green reached its peak after a 4-day phenobarbital treatment. After the 5th day of treatment the biliary flow and the biliary excretion of bromcresol green remained significantly stimulated for 4 days and the changes in these parameters regressed on the fifth day following the last injection of phenobarbital. The changes in liver weight appeared not to run closely parallel either with the increase in biliary flow or with the enhancement of biliary excretion of bromcresol green. It is suggested that the changes in biliary flow and in the biliary excretion of bromcresol green take place by different mechanisms after phenobarbital administration.

In a 34-year-old woman a non-Hodgkin malignant lymphoma with extreme splenomegaly and monoclonal IgM paraproteinaemia was seen. The removed spleen and splenic hilar lymph glands showed a nodular centroblastic-centrocytic malignant lymphoma with large numbers of plasmocytoid cells containing monotypical (monoclonal) IgM-kappa type immunoglobulin. The case represents a borderline non-Hodgkin malignant lymphoma with features of a follicular tumour and an immunocytoma. The appearance of peculiar intracytoplasmic inclusions would support this assumption. Therapeutic measures (splenectomy and/or cytostatic treatment) and prognostic features (nodularity of the tumour) are discussed.

Fifteen cases of female infertility, probably connected with luteal insufficiency, are reported. This abnormality was found to be fairly common in hyperprolactinaemic and clomiphene-treated normoprolactinaemic women with galactorrhoea. Bromocryptine reduces the prolactin-level, prolongs the luteal phase and increases the secretion of progesterone. According to the observations thus far reported, some optimum prolactin concentration seems to be desirable for an adequate luteal function. In the case of luteal insufficiency, estimation of the prolactin and progesterone level in the luteal phase is advocated. The basal temperature curve the hyperthermic phase to be followed up before and after treatment allows.

Incubation of human peripheral blood mononuclear cells in the presence of 25 mg/l concanavalin A (Con A) or 2 mg/l phytohaemagglutinin (PHA) suppressed their ADCC activity. Thirty-minute incubation with the mitogens resulted in a significant decrease in ADCC activity. The effect was more striking with longer (24 and 48 h) incubation. The suppressive effect of PHA was abolished after 6 days incubation, while no such phenomenon was observed with Con A. Macrophages participating in the ADCC reaction were not influenced by the lectin treatment, though their removal increased the suppressive effect. The lectin-induced suppression of ADCC activity did not correlate with the suppression of Con A-induced blastogenesis. The suppressive effect of lectins on ADCC is not mediated through suppressor cells, but rather represents a direct action of ligands on the (killer) lymphocyte membranes, resulting probably in an altered metabolism, or inhibition of membrane mobility or lymphocyte locomotion.

Synthetic salmon calcitonin infused intravenously in a pharmacological dose of 2 MRCU/kg/hour resulted in an abrupt and profound inhibition of basal and pentagastrin and calcium induced gastric acid secretion in patients with duodenal ulcer. The inhibition in the sixth 15-minute period of the intravenous infusion of calcitonin amounted to 98.7% (basal acid secretion), 51.8% (pentagastrin-stimulated acid secretion) and 80.9% (calcium-induced acid secretion). There were no significant alterations in the serum calcium and gastrin levels during the intravenous infusion of calcitonin. The slight decrease in serum gastrin concentration in the first 30 minutes of calcitonin infusion cannot explain the strong inhibition of gastric acid secretion produced by calcitonin. It is assumed that calcitonin inhibits directly the parietal cells.

The difficulties of differentiating functional disorders from organic diseases of the intestinal tract in old age are well known. It is also known that the age-related structural changes of the digestive tract are inconclusive of any functional disorder. This has raised the question whether the process of aging is bound to affect the absorption of d-glucose and the amino acids (gly, ala, val, thr, leu, phe, try, pro, his, lys and arg). The results of the present rat experiments, which have been undertaken under a kinetic approach, indicate that the intestinal carrier affinity to the molecules available for transport declines with aging. This implicates that in the young animal the transport of the absorbed molecules from the intestinal lumen at low (initial) concentrations proceeds at a higher rate than it does in the old animal. The reverse was found to be the case for the basic amino acids.

The chemotactic response of polymorphonuclear leukocytes of normal subject, to corneal extracts of 0.2 and 0.4 mg/dl protein concentration were studied in blind-well type chemotactic chambers. E. coli endotoxin served for the positive, Rindex-5 fluid for the negative controls. The chemotactic response to corneal tissue extracts, as compared to random migration in the Rindex-5 medium, proved significant. It is suggested that chemotactic factors may be released from corneal grafts in vivo too, in consequence of diverse noxae. These factors are supposed to elicit a granulocytic invasion and to lead to an opacification of the graft as a result of a cellular reaction.

The inhibitory effect of atropine on the gastric mucosal damage produced by topical aspirin has been studied in the rat, in the presence and in the absence of intragastrically applied 160 mmole/l HCl. The gastric mucosal damage was produced by aspirin given intragastrically in doses of 192 mg/kg. The topical application was done alone or in the presence of 160 mmole/l HCl. The ulcer incidence, the number and size of gastric mucosal damage were studied during 4 h. The aspirin solutions were administered with or without atropine (in doses of 4 and 10 mg/kg). The atropine was added immediately after the administration of aspirin. The results were as follows 1. A dose-dependent inhibition of ulcer incidence, number and size of gastric mucosal damage was produced by atropine in both groups of animals, when the aspirin was given alone or together with 160 mmole/l HCl; 2. The inhibitory effect of atropine was significantly weaker in the group treated with aspirin plus 160 mmole/l HCl than in th aspirin-treated group. It has been concluded the ulcer-preventing effect of atropine is mediated partly through the inhibition of gastric H+ secretion, and partly some "cytoprotective effect"; the extent of the "cytoprotective effect" of atropine was about half that on gastric H+ secretion.