Maternal alloanti-hrS--an absence of HDN.

A 24-year old female, gravida III, para III, delivered a full-term infant by cesarean section. A maternal blood sample at the time of admission showed antibody in her serum that had apparent anti-e specificity and that her RBCs were e+. Further studies determined that the antibody was anti-hrS. Cord RBCs had a negative DAT and a normal Hb level. There was no clinical evidence for increased hemolysis in the infant. We describe an hrS+ infant with no evidence of HDN due to anti-hrS.

[Results of surgical treatment of gastric cancer]. / Nase výsledky chirurgickej liecby rakoviny zalúdka.

The authors retrospectively analyse a group (1991-2000) of 129 patients with malignancies of the stomach operated at the Surgical Department of The District Hospital in Lucenec. The operated patients were: males 83 (64%), females 46 (36%), mean age--63.4 years. Elective operations were performed in 78.2% and acute operations in 21.8%. We were able to make resections in 90 (69.8%) patients and palliative operations in 39 (30.2%) patients. On the basis of histologic examinations-adenocarcinomas dominated (120 patients--93%). The postoperative mortality was 4.65% and five-year survival 12%.

[Simultaneous bezoars in the stomach, ileum and cecum causing acute ileus in a 30-year-old imbecile--case report]. / Súcasný bezoár zalúdka, ilea a céka u 30rocného imbecila pod obrazom akútneho ilea--kazuistika.

Bezoars are concretions of foreign materials in the stomach, small intestine or bowel in people or animals, which impair GIT motility or cause intestinal obstruction. The authors describe an interesting case report of a 30-year-old imbecile with manifestation of simultaneous bezoar of stomach, ileum and caecum and its operative treatment. They describe a short characteristics of this clinical unit, which is reported in the literature only in a few case reports.

[Personal experience with laparoscopic cholecystectomy in acute cholecystitis]. / Nase skúsenosti s laparoskopickou cholecystektómiou pre akútnu cholecystitídu.

Authors refer about their experiences with operations of acute cholecystitis by laparoscopy. They have evaluated retrospectively 1600 cases of laparoscopic cholecystectomies (LCHE) realized in the period from 1994 to 2000. In 302 (18.8%) cases was realized laparoscopic cholecystectomy for acute cholecystitis, which was confirmed by histopathological finding. During the mentioned period a total number of laparoscopic cholecystectomies for acute cholecystitis (n = 302) rise a number of classical cholecystectomies for the same diagnosis (n = 227). Very important role by authors take early dispatching a patient to a department of surgery and early estimation the diagnosis with consecutive laparoscopic treatment. Rates of peroperation, postoperation complications and reoperations in laparoscopic surgery of acute cholecystitis is comparable with elective laparoscopic cholecystectomy.

[Review of revascularization and arterial reconstructive procedures in arteriosclerosis performed at the Hospital in Lucenec]. / Prehl'ad revaskularizacných a rekonstrukcných arteriálnych výkonov pre artériosklerózu v NsP v Lucenci.

The authors present a review of revascularisation and reconstruction operations for arteriosclerosis in a group of 2341 patients (1754 (75%) operations). Direct reconstruction operations were made 825 times (47%), indirect operations--sympathectomy 598 times (34.1%) and endovascular intervention 331 times (18.9%). Intervention vascular radiology significantly changes the indication, the strategy and the tactics of surgical treatment of arteriosclerosis and its complications.

Concentration-dependent effects of tetracaine on excitation-contraction coupling in frog skeletal muscle fibres.

The effects of low (10-100 microM) concentrations of tetracaine on intermembrane charge movement and on the rate of calcium release (Rrel) from the sarcoplasmic reticulum (SR) were studied in cut skeletal muscle fibres of the frog using the voltage clamp technique. The fibres were mounted in a single or double vaseline gap chamber to study the events near the contraction threshold or in a wide membrane potential range. Although the 'hump' component of charge movement (Q gamma) was suppressed to some extent, the voltage dependence and the parameters of the Boltzmann distribution were not modified significantly at tetracaine concentrations below 50 microM. At 50 and 100 microM of tetracaine the midpoint voltage of the Boltzmann distribution was shifted to higher membrane potentials and the steepness was decreased. The total available charge remained the same at all concentrations tested. Using fura-2 to measure calcium transients at 100 microM tetracaine the threshold for calcium release was found to be significantly shifted to more positive membrane potentials. Tetracaine reversibly suppressed both the early inactivating peak and the steady-level of Rrel but the concentration dependence of the effects was markedly different. The inactivation component of calcium release was decreased with a Hill coefficient of approximately 1 and half effective concentration of 11.8 microM while the steady-level was decreased with a Hill coefficient of greater than 2 and a half effective concentration of 47.0 microM. These results favour two sites of action where tetracaine would suppress the calcium release from the SR.

Effects of phlorizin and phloretin on passive and dynamic electrical properties in muscle membrane.

The effects of phlorizin and phloretin on the cable properties were investigated in frog sartorius muscle by conventional cable analysis. Actions of phloretin on voltage-dependent ionic conductances were also studied by analysis of the phase plane trajectories. Both drugs evoked a significant decrease in specific membrane resistance (Rm) in chloride-containing Ringer's solution. The linear membrane capacitance increased by about 30%. On the contrary, in the presence of the non-penetrating anion, glutamate, a slight increase in Rm was induced by phlorizin. It is suggested that these drugs may increase the chloride conductance in the muscle membrane. Under the effect of phloretin the resting membrane potential remained unchanged but the amplitude of the action potential was lowered and the rate of repolarization was significantly reduced. The rate of depolarization during the "foot" of the action potential and the conduction velocity calculated from the rate constant of depolarization decreased. The maximum Na conductance was not altered by phloretin but K conductance was reduced. The time constant (tau K) reflecting the kinetic properties of K conductance was increased about seven-fold. It is suggested that great importance may be attributed to the dipole properties of these drugs in the actions presented above.

Chloride-dependence of the actions of phlorizin on frog skeletal muscle membrane.

The effects of phlorizin on the membrane potential changes induced by cevadine were compared in the presence and absence of external chloride anions in frog skeletal muscle. The action of the drug on 24Na-efflux was also studied in chloride-free medium. In accordance with previous results, it was found that phlorizin reduced the frequency of the membrane potential oscillation (1 mmol/l) or fully inhibited the rhythmic activity (2 mmol/l) in the presence of chloride anions. Replacing the total chloride content of bathing fluid with non-penetrating anions (glutamate, isethionate or sulphate) the inhibitory action of phlorizin on the membrane potential oscillation failed to appear while it reappeared rapidly if the chloride ions were partially restored in the incubating medium. The membrane potential changes evoked by changing the chloride concentration of Ringer solution at constant [K]0 were more expressed in the presence of phlorizin. The action of phlorizin on 24Na-transport proved to be a chloride-independent phenomenon. This finding indicates that the inhibitory effect of phlorizin on Na-transport processes may not be the reason of its blocking action on membrane potential oscillation. Furthermore, it suggests that failure of the drug to inhibit the membrane potential oscillation in the absence of chloride anions may not be accounted for the lack of phlorizin-binding under those circumstances. It is therefore assumed that the increase in chloride conductance may play a causal role in the inhibitory effect of phlorizin on membrane potential oscillation.

Inhibition of sodium for sodium exchange by phlorizin in frog sartorius muscle.

The effects of phlorizin (2 X 10(-3) mol X l-1) on the Na transport of frog (Rana esculenta) sartorius muscle were investigated in glucose-free medium. Phlorizin decreased the rate coefficient of 24Na efflux by about 40%. The degree of inhibition was comparable to that caused by ouabain (10(-4) mol X l-1). Phlorizin could evoke a further reduction in the 24Na efflux also in the presence of ouabain. The intracellular Na content of the phlorizin-treated muscles remained unchanged, in contrast to a 60% increase induced by ouabain. 42K uptake was not affected by phlorizin. Data indicate that the ouabain-sensitive Na-K pump was not involved in the action of phlorizin. At the same time, phlorizin failed to alter the residual 24Na efflux measured in Li-Ringer solution containing ouabain. When Na: Na exchange was restored by replacing Na into the washout solution in the presence of ouabain, the increase of 24Na efflux was significantly diminished by phlorizin. Phlorizin reduced the 24Na uptake into a compartment with a half time of 6 min by about 40% without affecting the intracellular compartment. The results suggest that phlorizin inhibits the ouabain-insensitive Na: Na exchange in a superficial Na compartment.

Cevadine-induced changes of membrane potential and sodium transport of muscle membrane in a chloride-free solution.

Cevadine-induced changes in membrane potential, sodium transport, intracellular Na, K, and water content were investigated in sartorius muscles incubated in chloride-free (glutamate) Ringer. Cevadine sensitivity of muscles incubated in glutamate Ringer was about five times greater than that of muscles incubated in normal Ringer. Therefore, even 0.005 mmol/l cevadine could induce depolarization and membrane potential oscillations. The membrane potential oscillations were recorded much longer from muscles incubated in chloride-free Ringer (even in the 15th hour of treatment) than in normal Ringer. Depolarization and membrane potential oscillations reversed more slowly in cevadine-free glutamate Ringer than in alkaloid-free normal Ringer. The rhythmic activity could be recorded even in the 10th-15th hour of incubation in cevadine-free glutamate Ringer. Cevadine increased the 24Na uptake of muscles incubated in glutamate Ringer by an average of 230%. In comparison, the cevadine-induced increase of 24Na uptake of muscles incubated in normal Ringer was approximately 350%. In the presence of cevadine the 24Na loss of muscles incubated either in glutamate or in normal Ringer increased to the same degree, i.e. three times. The increase of 24Na loss developed faster in glutamate Ringer than in the presence of chloride. The water content of muscles incubated in cevadine containing, chloride-free (glutamate) Ringer did not increase significantly. Muscles incubated in normal Ringer with cevadine showed a 42.7% increase of water content in 2 hours. Intracellular Na content and Na concentration increased by about 60% during a 2-hour-treatment with cevadine in a chloride-free environment. At the same time, cevadine treatment increased the intracellular Na content and Na concentration of muscles incubated in normal Ringer by about 160% and 80%, respectively. The cevadine-induced decrease of intracellular K content and concentration of muscles incubated in glutamate Ringer was 5% and 10%, respectively, in 2 hours. On the other hand, the decrease of intracellular K concentration in muscles incubated in cevadine-containing normal Ringer occasionally reached 30% due to the increase of water content of the muscles. The cevadine-induced increase of the wet weight of muscles incubated in normal Ringer was practically irreversible. It was not possible to eliminate the increase of wet weight even by washout lasting for 10-15 hours.

Effect of phlorizin on the changes of membrane potential, water, Na and K transport induced by cevadine in frog muscle.

The effect of phlorizin on the parameters of cevadine induced membrane potential oscillation and the development of the potential changes were investigated in frog (Rana esculenta) sartorius muscles. The action of phlorizin on Na transport, water and cation contents of cevadine-treated muscles were also studied. On the effect of phlorizin applied at a concentration of 1 mmol/1 the frequency of the membrane potential oscillation evoked by cevadine decreased by about half, parallel with an about four-fold increase in the duration of the resting period and the prepotential. Phlorizin, applied at a concentration of 2 mmol/l on the neural part of the muscle before cevadine treatment, delayed the development of depolarization evoked by cevadine. In the cevadine-pretreated muscles the enhanced 24Na-uptake was not reduced by 2 mmol/l phlorizin. 2 mmol/l phlorizin, applied during the radioactivity washout period, diminished reversibly the rate coefficient for 24Na loss by 49% in 120 min. The 24Na-efflux increasing effect of cevadine, which is characteristic otherwise, was prevented by phlorizin. This action was also reversible. The intracellular water, Na, and K contents of muscles were not altered significantly by 2 mmol/l phlorizin even in 3 hours. Under the effect of cevadine the characteristic gain in intracellular water, Na content and [Na]i developed despite phlorizin treatment, but the changes mentioned above evolved more slowly. In the phlorizin-pretreated muscles the K-content decreasing effect of cevadine failed to come about. In the muscles pretreated with phlorizin the [K]i was reduced by cevadine at a proportional degree to water-uptake.

Effect of phlorizin on the action potential and voltage-dependent ionic conductances in frog skeletal muscle.

The effects of phlorizin on the action potential and voltage-dependent ionic conductances were investigated in frog (Rana esculenta) sartorius muscles. In order to study the ionic currents, phase plane trajectories of the action potentials were analysed. As a consequence of lowering the overshoot by 19%, the amplitude of the action potential was decreased on the effect of phlorizin applied at a concentration of 2 mmol/l. The maximum rate of rise of the action potential (V +max) was reduced on the average by 23%. The maximum rate of fall of the spike potential (V -max) was also diminished by about 25% and the repolarization was prolonged consequently. Due to phlorizin treatment the early negative after-potential was significantly lowered or was not noticeable at all. Analysing the phase plane trajectories of the action potentials the peak inward (Na) current was found to be decreased by about 16% despite the unchanged maximum Na conductance. At the Na equilibrium potential a 9.2 mV shift towards negative direction was observed. Both the peak outward (K) current and the maximum outward (K) conductance were reduced by 25 and 29%, resp. tau K, the time constant reflecting the kinetic properties of K conductance was increased by 36%. Phlorizin treatment prevented the repetitive activity induced by cevadine. The inhibiting actions of phlorizin on fast ionic currents developed also in cevadine-treated muscles. All of the effects of phlorizin were reversible. The presented data show that phlorizin, the well-known inhibitor of phosphorylase and a competitive antagonist of sugar uptake, is also capable of modifying the electrical properties of the frog skeletal muscle membrane.

Effects of physostigmine on the voltage dependent ionic conductances of skeletal muscle fibres.

The voltage dependent ionic conductances were studied by analysing the phase plane trajectories of action potentials evoked by electrical stimulation of the sartorius muscles of the frog (Rana esculenta). The delayed outward potassium current was measured also under voltage clamp conditions on muscle fibres of either the frog (Rana esculenta) or Xenopus laevis. On analysing the effect of physostigmine decreasing the peak amplitude, the rate of both the rising and falling phases of the action potentials, it was revealed that the alkaloid at a concentration of 1 mmol/l reduced significantly both the delayed potassium conductance and the outward ionic current values during the action potentials. The inhibition of sodium conductance and inward ionic current was less expressed. The maximum value of delayed potassium conductance measured under voltage clamp conditions was decreased by 1 mmol/l physostigmine. The time constant determined from the development of delayed potassium conductance was increased at a given membrane potential. The voltage vs. n relationship describing the membrane potential dependence of the delayed rectifier was not influenced by physostigmine. It has been concluded that physostigmine changes the time course of the action potentials by decreasing the value of both voltage dependent ionic conductances and by slowing down their kinetics. It is discussed that results obtained from the phase plane analysis of complex pharmacological effects can only be accepted with some restrictions.

Membrane potential dependence of potential oscillation induced by cevadine in striated muscle.

The dependence of the membrane potential oscillation induced by cevadine on the actual transmembrane potential was studied in the frog sartorius muscle. 1. If the membrane potential oscillation is recorded for hours, its amplitude is seen to decrease slowly and smoothly and the membrane potential measured during the resting period among the waves of oscillation also decreases simultaneously. This means that the depolarization increases. 2. The increase of depolarization results not only in a decrease in the amplitude of the oscillation but the oscillation ceases between -40 and -55 mV as well. 3. The phenomenon reappears if the membrane is partially repolarized on a cevadine treated muscle fibre on which the membrane potential oscillation has already ceased as a consequence of the relatively marked depolarization. 4. Changing the membrane potential either to a value more positive than -40 mV, or to one more negative than -90 mV the developed oscillation activity may reversibly be suspended. 5. According to the above results, the amplitude of the membrane potential oscillation depends on the actual membrane potential. If other factors which may influence the oscillation parameters are unchanged, the relationship between the oscillation amplitude and the membrane potential can be characterized by a linear equation. In these cases there is a close correlation between the measured values and the calculated ones.

Analysis of the sensitizing effect of veratrum alkaloids to potassium on frog muscle.

1. The sensitizing effect of veratrum alkaloids to potassium is not specific. Reducing the concentration of chloride in Ringer's solution, or treating the muscle with nicotine in a concentration close to threshold after pretreatment with subliminal concentration of cevadine result in a marked mechanical response of the muscle. However, cevadine does not alter the sensitivity of the muscle to caffeine. On the basis of these observations it has been suggested that veratrum alkaloids sensitize the muscle membrane essentially to depolarizing processes. 2. Cevadine, 0.01 mM, fails to depolarize the muscle membrane but increases the depolarizing effect of 10 mM potassium. The depolarizing effect of a reduction of the concentration of chloride from 120 mM to 30 mM is also increased in cevadine pretreated muscle. Cevadine pretreatment increases the depolarizing effect of nicotine, too. 3. The above sensitizing effects are unanimously Na-dependent. Accordingly there is no mechanical response and increased depolarization in muscles equilibrated in sodium-free (choline) Ringer's solution before the cevadine treatment. 4. On the basis of the present data it is suggested that the membrane, when sensitized by veratrum alkaloids, can be triggered by different depolarizing processes and the depolarization increases as the result of increased Na permeability. The increased depolarization at the threshold level becomes sufficient for the automatic regenerative processes of the action potential to develop which activate the contractile elements. However, the mechanical response is a prolonged contraction rather than a contracture, its long period being the result of a very slow repolarization caused by the well-known inhibitory effect of veratrum alkaloids on Na inactivation.