Acta medica Polona最新文献

Application of furosemide (F) during peritoneal dialysis had been proposed for enlargement of peritoneal excretion of uric acid (UA), however, localization and mechanism of action of the drug remained obscure. To clarify the problem experimental studies on isolated peritoneum were performed with intention to establish whether and how transperitoneal flux of UA can be modified by F. Experiments were carried out in vitro on fragments of peritoneum taken from rabbits: parietal peritoneum and mesentery were isolated with single layer of mesothelium, and minimal amount of submesothelial tissue. Gradient of UA across the membranes was set up at 0.9-1.1 mmol/l, and flow estimated before and after addition of F (final conc. 10(-4) M) to the medium bathing either side of the membranes. Some differences in the flow between both types of the membranes as quantitative (greater flow in the parietal peritoneum), and qualitative (opposite succession of changes after F) were observed, however, the reaction for the diuretic was significant in both series of the experiments. The results confirm the suggestion that F can affect peritoneal excretion of UA during the dialysis, but at the same time they show that the mechanisms regulating the transperitoneal UA passage are complex.

The percent of bacteria engulfed by blood platelets, surviving in them and killed was determined in these cells taken from 22 patients with pneumonia before the treatment and from 14 patients after the treatment. The mean percent of bacteria phagocytosed by platelets collected before the treatment was 6.28 and by those after the treatment 5.01, being considerably higher than in the control group (3.42). The mean percent of bacteria surviving in platelets taken before the treatment equalled 3.10 and after the treatment 2.36 being also higher than in the control group (1.32). The mean percent of bacteria killed by platelets taken before the treatment was 3.18 and by those taken after the treatment 2.65, being also higher than in the control group. These results seem to indicate that in cases of pneumonia the blood platelets are involved into the antibacterial activity.

Vasopressin (ADH) acts in humans mainly upon renal collecting tubules. By changing their water permeability it plays a key role in regulation of renal water excretion. Acting upon vascular smooth muscle cells, it causes vasoconstriction and raised arterial blood pressure. This hormone was also proven to cause constriction of cultured mesangial cels, it causes vasoconstriction and raised arterial blood pressure. This urea (Seldin, Giebisch 1985), to release the natriuretic hormone as well as to stimulate hepatic glycogenolysis (Abramov et al. 1987). The influence of vasopressin upon peritoneal transport of solutes was studied, too. ADH influenced the passage of phosphate and rubidium through the isolated rabbit mesentery (Berndt, Gosselin 1961) as well as sodium flux through isolated rabbit omentum (Shear et al. 1966). It caused the drop in urea dialysance in dogs subjected to peritoneal dialysis (Henderson et al. 1971). The subject of our study was the assessment of the action of the antidiuretic hormone under "in vitro" conditions upon the peritoneal transfer of urea, the solute present in human body fluids and removable by peritoneal dialysis.

The kinetics of restoration of haemopoiesis was studied in 10 patients prepared for allogenic bone marrow transplantation with busulphan combined with cyclophosphamide. The morphology of peripheral blood after administration of these drugs and transplantation of allogenic bone marrow was similar to that reported elsewhere after irradiation, cyclophosphamide administration and bone marrow transplantation, the cell counts falling almost to zero within several days after the end of the pharmacological preparation, and later rising to normal values within the period from several weeks to several months after transplantation.

CK-MB activity was estimated in 16 patients and infarct size was calculated on that basis using our own computer programme. The infarct size was confronted with ejection fraction calculated in haemodynamic studies (p = 0.01). In the next step the ejection fraction was determined basing exclusively on changes of CK-MB activity. Significant changes between the value of fractions defined in these ways appear in the case when myocardial necrosis simultaneously involves the right ventricle.

The purpose of this study was to evaluate the effect of various therapeutic regimens on: 1) intrathecal IgG synthesis on the basis of IgG Index value, 2) oligoclonal IgG spectrum visualized by SDS-PAGE of unconcentrated CSF, 3) CSF antibody specific activity against MBP estimated by solid phase RIA and expressed in cpm/micrograms IgG, and 4) immune complex (CIC) level in the CSF estimated by C1q binding solid phase RIA. CSF antibody against Gal-C and ganglioside was also estimated. Patients with clinically definite MS were selected according to 4 therapeutic regimens: group 1, subjected to Mega-dose prednisone therapy (4000 mg over 54 days), group 2, subjected to moderate dose prednisone therapy, group 3 subjected to Mega-dose Solu-Medrol therapy (7500 mg over 10 days), and group 4, subjected to intravenous Cyclophosphamide therapy (4000 mg over 10 days). This last group was characterized by chronic progressive course of disease. Intrathecal IgG production was significantly reduced in all 4 groups as a result of therapy. More pronounced reduction was obtained in Mega-dose prednisone (p below 0.001) and CY (p below 0.001) treated group. Therapeutic regimens did not influence the IgG oligoclonal pattern. The moderate dose prednisone therapy and Mega-dose Solu-Medrol therapy on CSF IgG anti-MBP antibody specific activity were less effective than the Mega-dose prednisone medication. CY therapy did not influence anti-MBP antibody specific activity in MS group characterized by chronic progressive course of disease. The influence of therapeutic regimens on elevated CIC level in the CSF was insignificant. In our study CSF the anti-galactocerebroside antibody appeared to be of IgM class.

Atrial natriuretic peptide (ANP) is a hormone release into the circulation by atrial cardiocytes (Gutkowska et al. 1984). Extracellular fluid volume expansion acts as a powerful stimulus for ANP secretion and results in the augmentation of its plasma concentration (Lang et al. 1985). Patients with active acromegaly demonstrate the increased extracellular fluid volume (Falkheden et al. 1964), while a successful treatment of the disease results in the disappearance of hypervolemia (Strauch et al. 1977). We have recently demonstrated that in patients with active acromegaly the increased total body plasma volumes are accompanied by the elevated plasma ANP concentrations, whereas, in the successfully treated patients, both: total plasma volumes and plasma ANP levels do not differ significantly from these in healthy subjects (Czekalski et al. 1988b).

Sodium valproate, a gamma-aminobutyric acid (GABA) agonist, was found to decrease plasma ACTH concentration in some cases of Cushing's disease and Nelson's syndrome. In this study we have investigated the influence of magnesium valproate (MV), a newly introduced salt of valproic acid, on plasma ACTH levels in 8 patients with Nelson's syndrome. The daily dose, 1200 mg of MV, significantly decreased plasma ACTH level at 10 p.m. compared with placebo. A single dose of 400 mg of MV, led to a reduction in plasma ACTH concentration only in two out of seven patients during a four-hour observation. The fall in plasma ACTH level in the same patients at 10 p.m., after the next two doses of this drug, suggests that single dose may be insufficient for introducing GABA-dependent reduction in ACTH release. During a long-term therapy with MV, in all three patients investigated a marked decrease in plasma ACTH was observed. Our results suggest that magnesium valproate may be useful during chronic therapy in some patients with ACTH hypersecretion.

The effect of prolonged treatment with captopril on some parameters of pulmonary circulation was studied in a group of 17 patients with secondary pulmonary hypertension due to mitral stenosis. Each patient received 25 mg of captopril four times daily for mean time of means = 12.5 +/- 2.1 days. A drop in pulmonary artery mean pressure of at least 20% was observed in 5 patients (29.4%). In 4 patients (23.5%) captopril had adverse effect on the hemodynamics of the pulmonary circulation, and in 8 patients no effect of captopril on the pulmonary hypertension was noticed. Our model of the experiment did not allow us to select before the treatment the group of patients in whom positive effects of captopril could be expected.

The activity of urinary total alpha-amylase (EC 3.2.1.1) as well as of its pancreatic and salivary isoenzymes was determined in Marathon runners using the Labordiagnostica Gödecke "Enz-Amyl-Isoamylase" test set with specific inhibitor extracted from wheat germs. Initial total alpha-amylase activity equals about 20 U/l with the 56% share of type P isoenzyme. The correlation was found between the race score and changes in enzymatic activity after subgrouping the racers according to their scores in Marathon race. After the race total alpha-amylase activity rose respectively 3.14 and 8 times in particular groups, the proportion of isoenzymes being also changed. The activity of type P isoenzyme rose 16 times immediately after the race, and that of type S one 11 times 24 h after the race. The determination of the activity of these enzymes may be helpful in the evaluation of physical effort.