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Prednisolone and other glucocorticosteroids are used by some peritoneal dialysis patients because of underlying diseases such as peritonitis. Although corticosteroids are potent inhibitors of various processes during inflammation, their influence on the transport properties of peritoneum is little known. Our study investigated the influence of prednisolone (0.001 g/dL) on glucose (1.8 g/dL) and uric acid (0.02 g/dL) transfer across isolated parietal peritoneum taken from the anterior abdominal wall of white Hyplus 59 rabbits and placed inside a modified Ussing-type chamber. Values for transfer from the interstitial (I) to the mesothelial (M) side of membrane (I-->M) and in the opposite direction (M-->I) were calculated using the mathematical model of mass transport and are expressed as a coefficient of diffusive permeability [P (in centimeters per second)]. Four separate series of experiments were done. In the first and second series, we respectively examined glucose transport under control conditions (for 120 minutes) and then before (15-60 minutes) and after (75-120 minutes) introduction of prednisolone on the M side of the membrane. In the third and fourth series, similar studies of uric acid transfer were done. In the control (first and third) series, the stability of bidirectional transport for solute of interest was observed. The values of P +/- standard error of the mean (all x0.0001) for I-->M and M-->I transfer of glucose were, respectively, 2.489 +/- 0.329 cm/s and 2.259 +/- 0.493 cm/s. In the case of uric acid, the transport values were lower and amounted 1.936 +/- 0.324 cm/s and 1.895 +/- 0.596 cm/s for I-->M and M-->I respectively. Application of prednisolone on the M side of membrane lowered bidirectional transfer of glucose across peritoneal membrane by a mean of 73% (p < 0.02) and transport of uric acid by a mean of 19% (p < 0.003). These results show that, in vitro, prednisolone lowers glucose and uric acid transport across the peritoneal membrane, modifying the transfer dynamics of glucose to a greater extent. These observations may have clinical importance, especially in patients with disorders of peritoneal permeability, diabetes, and hyperuricemia.

Glucose or its polymer is usually added to dialysis solution for the development of sufficient ultrafiltration during peritoneal dialysis. The aim of the present study was to determine the influence of glucose and icodextrin on the transport of gentamicin and insulin from the mesothelial to the interstitial side of the peritoneal membrane. Transfer values are expressed as a coefficient of diffusive permeability, P, in centimeters per second. Each of the molecules was tested in 3 series of experiments using rabbit parietal peritoneum, a modified Ussing chamber, and a mathematical model of mass transport. First, transperitoneal transfers of gentamicin (0.040 g/dL) and insulin (0.1 g/dL) were analyzed in control conditions for 120 minutes. Then, transport parameters for gentamicin and insulin were separately determined before (15-60 minutes) and after (75-120 minutes or 75-130 minutes) the application of glucose (1.8 g/dL) or icodextrin (2 g/ dL) on the mesothelial side of the peritoneal membrane. Insulin transport was observed to be stable in the control series. Gentamicin transfer was not stable; its passage declined by 52% (p < 0.01) in the control series. The mean transfer parameters were 7.41 +/- 1.40 cm/s (x0.0001) over 15-30 minutes and 3.21 +/- 0.54 cm/s (x0.0001) over 75-130 minutes. Gentamicin transfer declined less in the series with glucose or icodextrin, by 21% (p < 0.04) and 30% (p < 0.05) respectively, than in the control series. For insulin, the mean P (+ standard error of the mean) was 0.15 +/- 0.02 cm/s (x0.0001) at the first hour of transfer and 0.14 - 0.02 cm/s (x0.0001) at the second. Glucose induced a nonsignificant intensification of insulin transport. Icodextrin increased insulin passage by 107% (p < 0.03). Osmotic and oncotic factors (glucose and icodextrin) both stabilize the transfer of gentamicin across the peritoneal membrane in vitro. Glucose polymer intensifies insulin transport from the mesothelial to the interstitial side of the peritoneum. Similar modifications might be observed in vivo during peritoneal dialysis or continuous intraperitoneal administration of insulin, influencing the efficiency of those treatments.

Our study investigated uric acid transport across isolated parietal peritoneum taken from the anterior abdominal wall of white New Zealand rabbits and placed inside a modified Ussing-type chamber. Values for transfer from the mesothelial to the interstitial side of membrane (M --> I) were calculated using the mathematical model of mass transport and are expressed as a coefficient of diffusive permeability [P (in centimeters per second)]. Four separate series of experiments were done. In the first series, we examined uric acid transfer in control conditions (for 120 minutes). In the second and third series, P was calculated before (15 - 60 minutes) and after introduction of p-cresol (0.005 g/dL) or sodium hyaluronan (0.04 g/dL) on the M side of the membrane. In the fourth series, transfer parameters were measured before (15 - 75 minutes) and after (90 - 150 minutes) application of sodium deoxycholate (0.104 g/dL). The dynamics of transperitoneal transport of uric acid were stable. The values of P +/- standard error of the mean (x0.0001) were 1.936 +/- 0.324 cm/s and 2.078 +/- 0.186 cm/s. Application of p-cresol on the M side of membrane lowered uric acid transport by 10%. Application of sodium hyaluronan produced no change, but application of sodium deoxycholate increased the transfer of uric acid by 155%. These observations may have clinical importance.

Charge factors and reactive carbonyl solutes may change peritoneal structure and the transport properties of peritoneum. The aim of the present study to analyze the influence of polycationic protamine and glucose degradation products on the diffusive permeability (P) of peritoneal membrane for urea in vitro. Values for diffusion from the interstitial (1) to the mesothelial (M) side of the membrane and in opposite direction are expressed as coefficients of diffusive permeability. Four separate series of experiments were conducted. In the first experiment, transperitoneal transfer of urea (20 mg/dL) in control conditions over 120 minutes was analyzed. In the subsequent three experiments, transport parameters were analyzed before (15 - 60 minutes) and after (75 - 120 minutes) the addition of chemical factors (protamine sulfate 5 mg/dL, glyoxal 10 mg/dL, methylglyoxal 1 mg/dL) on the mesothelial side of the peritoneal membrane. Stability of urea transport was observed in the control series (120 minutes). The mean diffusive permeability coefficients (P = standard error of the mean) were 2.293 +/- 0.211 cm/s and 2.621 +/- 0.457 cm/s (x0.0001) for I --> M and M --> I transfer respectively. Protamine and methylglyoxal did not alter transport, but glyoxal lowered urea M --> I transport by 12% (p < 0.01), with a statistically nonsignificant reduction in opposite direction. Similar modifications are observed in vivo during peritoneal dialysis and may influence the efficiency of renal replacement therapy.

This paper specifies the peritoneal dialysis problems as a method of renal replacement therapy in a historical perspective. It pointed out to the dynamic development of peritoneal dialysis in the nineties and distinct slump of the presented treatment form at the turn of XXth and XXIst century, despite substantial progress in the dialysis techniques, effectiveness and biocompatibility of the therapy as well as a detailed evaluation of peritoneal function in vivo and in vitro. It showed descriptions and outline of the peritoneal cavity dating from ancient times, 19th-century animal experiments determining essential laws of peritoneal absorption and removal molecules, as well as the first peritoneal dialysis of a man which took place at the beginning of the 20th-century. The technical problems and peritonitis were the fundamental limitations of this therapy employment in this phase of dialysis development. The application of Tenckhoffs catheter and the technique specified as continuous ambulatory peritoneal dialysis was the invention and at the same time, the turning point which decided about the considerable progress of the described method of dialysis in the nineties. In this period, the analyses concerning failures of the peritoneal transport functions and protection of peritoneum during its long-term use as a dialysis membrane dominated. These studies referred to not absolutely biocompatibility factors of the environment of the peritoneal cavity during peritoneal dialysis. Thence, proposed future directions of analyses include researches concerning components of dialysis solution to assure long-term preservation of peritoneal transport functions and its secretory properties. It is not excluded that experiments of applying the newest achievements of regenerative medicine, in the scope of genetic modification and implantation of mesothelial cells will be continued.

Hyaluronan (HA), an essential component of peritoneal extracellular matrix, participates in restoring peritoneal integrity and remodeling the peritoneum changed by prolonged peritoneal dialysis and repeated peritonitis episodes. The aim of the present study was to compare urea, creatinine, and uric acid transport across the peritoneal membrane in control conditions and after HA application. Experiments were undertaken using rabbit parietal peritoneum and a modified Ussing-type chamber. Values of the transfer directed from the interstitial to the mesothelial side of the membrane (I --> M) and in the opposite direction (M --> I) were expressed as coefficients of diffusive permeability P. Transperitoneal transport in control conditions (for 120 minutes) and transfer parameters before (15 - 60 minutes) and after HA application (2000 kDa, 0.04 g/dL, 75-120 minutes) were examined. In the control series, stability of bidirectional transport for urea (0.02 g/dL), creatinine (0.1 g/dL), and uric acid (0.02 g/dL) was observed. The values of P +/- standard error of the mean for I --> M and M --> I transfers were respectively 2.293 +/- 0.211 and 2.621 +/- 0.457 for urea, 1.522 +/- 0.102 and 1.865 +/- 0.244 for creatinine, and 1.936 +/- 0.324 and 2.078 +/- 0.186 for uric acid [all x 10(-4) cm/s]. Application of HA reduced bi-directional urea transport by a mean of 12%, but did not change the P for creatinine and uric acid. These results show that in vitro HA modifies the dynamics of transport for certain small solutes.

The aim of the in vitro studies was to examine the effect of sodium deoxycholate, glucose, and methylglyoxal on icodextrin peritoneal transfer. The rabbit peritoneum in a modified Ussing chamber was an experimental model. Transport and morphometric analyses were performed. In the first of them, the icodextrin (7.5 g/dL) diffusion from the mesothelial to the interstitial side of the membrane, expressed as a diffusive permeability coefficient (P), was evaluated in the control stage, after chemical modification of the membrane using sodium deoxycholate (104 mg/dL), after the addition of glucose (1.8 g/dL) and methylglyoxal (1 mg/dL), in the separate experimental series. In the second morphometric studies, the thickness and transverse cross-section surface area of native tissue, in 75 min of experiment and after application of sodium deoxycholate, were investigated. In the control conditions, the rate of glucose polymer passage remained constant. A mean value of P +/- SD was 0.194 +/- 0.126 (x10(-4), cm/s) during 120 min of the study. The transfer of icodextrin was enhanced by 224% after 3 min of incubation of the peritoneum with sodium deoxycholate. The introduction of glucose into the circulating medium with icodextrin caused the increase of P values for glucose polymer by 94% during 60 min. In the same conditions, the usage of methylglyoxal did not change transport parameters. Both thickness and transverse cross-section surface area of the native tissue in 75 min of the study did not differ. It was 4.87 microm and 12.50 x 10(2) microm(2) for the mesothelial layer, and 63.83 microm and 208.10 x 10(2) microm(2) for the whole peritoneal membrane. The application of sodium deoxycholate caused the decrease of mesothelium thickness by 20% but the increase of thickness and transverse cross-section surface area of the peritoneum by 37% in comparison with 75 min of experiment. In conclusion, sodium deoxycholate and glucose, but not methylglyoxal, intensify peritoneal transport of icodextrin in vitro. These modifications are probably connected with the exfoliation of the mesothelium and looseness of the interstitium caused by sodium deoxycholate as well as the physical and metabolic influence of glucose on the peritoneum.

This paper is a review of the literature describing the complexity of the peritoneal membrane structure and functions, mechanisms of the peritoneum failure as a dialyzing membrane and strategies for its protection during prolonged peritoneal dialysis.

We undertook in vitro experiments to examine the importance of mesothelium and interstitium in icodextrin (7.5 g/dL) transport and the change in that transport caused by gentamicin and methylglyoxal. Rabbit peritoneum, a modified Ussing chamber and a mathematical model of mass transport were used. Transfer from the interstitial to mesothelial side of the membrane (I-->M) and in the opposite direction (M-->I), expressed as a diffusive permeability coefficient P, was determined in control series, after chemical modification of the peritoneum by sodium deoxycholate, and after introduction of gentamicin and methylglyoxal. We also investigated the thickness of native tissue 75 minutes into the study and after use of sodium deoxycholate. In the control series, icodextrin I-->M transport increased by 50%, but M-->I transport remained stable [15-60 min vs. 75-120 min. I-->M P, 0.32 +/- 0.04 x 10(-4) cm x s(-1) (standard error of the mean); M-->I P, 0.19 +/- 0.03 x 10(-4) cm x s(-1)]. After application of sodium deoxycholate, I-->M transport was observed to increase by 21% and M-->I by 192% as compared with the 2nd hour of the control series. Gentamicin caused a rise of M-->I transport by 21% without a change of I-->M. We observed no difference in p values (I-->M and M-->I) after application of methylglyoxal. Mean thickness before and 75 minutes into the study was 4.96 +/- 0.28 microm for mesothelium and 62.09 +/- 2.40 microm for the whole peritoneum. Sodium deoxycholate reduced the mesothelium thickness by 20% and increased the peritoneum thickness by 37%. The present study confirms that, in vitro, icodextrin I-->M peritoneal transport changes with time, but M-->I is constant. Asymmetry of glucose polymer diffusion is observed. I-->M predominates over M-->I. Chemical modification of the peritoneum by sodium deoxycholate (I-->M and M-->I directions) and by gentamicin (M-->I direction only), but not by methylglyoxal, intensifies icodextrin transport. Sodium deoxycholate causes exfoliation of the mesothelium and looseness of the interstitium.

In patients with end-stage renal disease on peritoneal dialysis, the peritoneum is effectively utilized as an endogenous semipermeable membrane. Chemical agents may alter the structure of the peritoneum and induce changes in its transfer properties. The purpose of our in vitro study was to compare the influence of sodium hyaluronan (a cytoprotective glycosaminoglycan, 2000 kDa, 40 mg/dL) and sodium deoxycholate (an intense oxidative stress factor, 414 Da, 104 mg/dL) on the transfer of insulin (5.8 kDa, 100 mg/dL) and albumin (68 kDa, 1000 mg/dL) through isolated rabbit parietal peritoneum. We used a mathematical model to calculate the transport rate of solutes from the interstitial to the mesothelial side of peritoneal membrane (I-->M) and in the opposite direction (M-->I) in three separate series of experiments: Control conditions without chemical agents Before (15-60 minutes) and after (75-120 minutes) introduction of sodium hyaluronan into the experimental system Before (15 -75 minutes) and after (90-150 minutes) introduction of sodium deoxycholate into the experimental system The results are expressed as a diffusive permeability coefficient P in centimeters per second. During the 120 minutes of the control stage, the rate of insulin and albumin bidirectional passage remained constant. Values of P +/- standard error of the mean did not correlate with the molecular weight of the compounds and measured 0.145 +/- 0.033 x 0.0001 cm/s and 0.146 +/- 0.022 x 0.0001 cm/s for insulin, and 0.271 +/- 0.056 x 0.0001 cm/s and 0.315 +/- 0.057 x 0.0001 cm/s for albumin in the I-->M and M-->I transport directions respectively. Application of sodium hyaluronan did not change the bidirectional transport of either solute. However sodium deoxycholate caused the values of P to increase by 142% (p < 0.05) for insulin I-->M transfer and by 102% (p < 0.02) for insulin M-->I transport. Albumin passage increased by 193% (p < 0.01) for both transfer directions. We conclude that, in vitro, sodium deoxycholate but not sodium hyaluronan increases the bidirectional peritoneal transport of insulin and albumin. In the case of larger molecular weight solutes, the modification is greater.

Recent studies pointed out advantages of high-molecular hyaluronic acid (HA) application into dialysis fluids. This molecule is an essential component of peritoneal extracellular matrix. The compound shows antiadhesive properties and participates in restoring of peritoneal integrality and remodeling of peritoneum, which have been changed by prolonged peritoneal dialysis and returning incidents of peritonitis. Influence of HA on transperitoneal transport of large and small molecules is recognized in a little range. The aim of presented studies in vitro was qualification of hyaluronan influence on transport dynamics of the selected macromolecules (albumin 1 g/dL, icodextrin 7.5 g/dL and insulin 0.1 g/dL). Values of the transfer, directed from the interstitial to the mesothelial side of membrane (I-->M) and in the opposite direction (M-->I) were expressed as coefficient of diffusive permeability P [cm/s]. In the case of each macromolecule, two separate research series of the experiments were done. In the first one transperitoneal transport in the control conditions (120 min) was analyzed, and in the secondtransfer parameters before (15-60 min) and after hyaluronan (0.04 g/dL) application on the mesothelial side of peritoneal membrane (75-120 min) were examined. Stability of albumin and insulin transport (in the case of the both transfer directions) and icodextin passage (only M-->I direction) was observed in the presented studies when we compare the first and the second hours of the experiments. In the opposite direction (I-->M) it was showed an increase of its transport with time by about 50%. The mean values of P +/- SEM amounted to 0,271 +/- 0,056 [x10(-4); cm/s] and 0,315 +/- 0,057 [x10(-4); cm/s] for albumin and 0,145 +/- 0,033 [x10(-4); cm/s] and 0,146 +/- 0,022 [x10(-4); cm/s] for insulin, respectively in the case of I-->M and M-->I directions and 0,194 +/- 0,035 [x10(-4); cm/s] for icodextrin transfer directed from the mesothelial to the interstitial side of membrane. In the opposite direction (I-->M) values of P coefficient amounted to: 0,280 +/- 0,038 [x10(-4); cm/s] in the first experimental hour, and 0,394 +/- 0,046 [x10(-4); cm/s] in the second one. It was observed also asymmetry of glucose polymer passage with I-->M transfer domination. Hyaluronan eliminated this asymmetry. After use this compound the transport parameters of icodextrin were stable for the both I-->M and M-->I directions. Hyaluronan did not change values of diffusive permeability coefficients P in the case of bidirectional transfer of albumin and insulin. The obtained results show, that values of macromolecules transfer across peritoneum in vitro don't depend on their molecular weight and isoelectric points. Dynamics of albumin and insulin transperitoneal passage is stable. Icodextrin transport, directed from the interstitial to the mesothelial side of membrane, predominates transfer in the opposite direction. Hyaluronan modifies dynamics of transperitoneal icodextrin passage, but doesn't influence on permeability of the membrane in the case of albumin and insulin.

We performed in vitro experiments with the isolated rabbit parietal peritoneum to evaluate the importance of fluid stirring intensification and of chemical modification of mesothelium and interstitium to the peritoneal transport of glucose and icodextrin. We used a mathematical model of mass transport to calculate the diffusive permeability coefficient, P, in centimeters per second. In control conditions (intact tissue; stirring rate: 11 mL/min), the rate of glucose (2.0 g/dL) transfer remained constant, and no differences were observed for transport from the interstitial to the mesothelial (I-->M) side of the membrane or in the opposite direction (M-->I). The value of P (+/- standard error of the mean) was 2.731 +/- 0.472 x 10(-4) cm/s. In contrast, the icodextrin (7.5 g/dL) I-->M transport rate was higher than that for M-->I (P: 0.319 +/- 0.038 x 10(-4) cm/s and 0.194 +/- 0.035 x 10(-4) cm/s respectively). Dynamics of the icodextrin M-->I transfer were constant, but I-->M increased by 50% over time. The intensification of the stirring rate increased the value of P at varying rates: the increase was greater for icodextrin than for glucose, and greater for the I-->M transport direction than for the M-->I direction for both solutes. Chemical modification (by 2.5 mmol/L sodium deoxycholate) increased glucose and icodextrin I-->M transfer a mean of 41% and 81% respectively, but increased M-->I transfer by 70% and 224% respectively. The dynamics of glucose and icodextrin peritoneal transfer in vitro are different: glucose diffusion is constant, but I-->M icodextrin transfer increases over time and is greater than M-->I transfer Fluid stirring intensification and chemical injury to the peritoneum enhance diffusion of glucose and icodextrin. Glucose and icodextrin M-->I transfer but not I-->M transfer is restricted more by tissue barriers than by stagnant fluid layers.

In the present study, we compared the influence of icodextrin (2 g/dL) on uric acid (20 mg/dL) and albumin (1 g/dL) transfer through isolated rabbit parietal peritoneum. In separate series of experiments, we used a mathematical model to calculate the transport rate of solutes from the interstitial to the mesothelial side of peritoneal membrane (I --> M) and in the opposite direction (M --> I) before and after introduction of glucose polymer. In control conditions, the rates of uric acid and albumin passage across the rabbit peritoneum remained constant. Mean values [x +/- standard error of the mean (SEM)] of the diffusive permeability coefficient P were 1.936 +/- 0.324 (I --> M) and 2.078 +/- 0.186 (M --> I) for uric acid and 0.341 +/- 0.066 (I --> M) and 0.389 +/- 0.084 (M --> I) for albumin (all x10(-4) cm/s), respectively. The introduction of glucose polymer into the experimental system did not alter the I --> M transport of either solute; but, in the opposite direction, it caused a 17% decline in the P for uric acid (p < 0.05), and an increase of 77% in the same parameter for albumin (p < 0.03). Hence, I --> M transfer dominated M --> I transfer of uric acid (p < 0.04). In contrast, in albumin transport, M --> I was higher than I --> M (p < 0.02). We conclude that, in vitro, icodextrin modifies the diffusive permeability of the peritoneum and induces transport asymmetry for some small and large solutes.

The effect of fluid mixing intensification, damage of mesothelial cells, gentamicin, and icodextrin on the diffusive glucose transport across the peritoneal membrane were evaluated in in vitro studies. A mathematical model of mass transport was used to calculate the diffusive permeability, expressed as a diffusive permeability coefficient (P). In the control conditions, the rate of glucose transfer from the interstitial to the mesothelial side of membrane (I-->M) and in the opposite direction (M-->I) remained constant, and the P value at mean was 2,731 +/- 1,493 x 10-4 (cm x s-1). The change of the stirring rate from 5.5 to 11 ml/min increased P values by about 74% for transport direction I-->M and 58% for M-->I, and the change from 11 to 22 ml/min enhanced P at mean by about 42% for both directions. The damage of the mesothelial layer, using sodium deoxycholate (2.5 mmol/L; 103.6 mg%), increased the glucose transfer from the interstitial to the mesothelial side of the peritoneum by 41% and to the opposite direction by 70%. Addition of icodextrin to the glucose solution increased glucose bidirectional transport at mean by about 14% for I-->M and 24% for M-->I. Furthermore, gentamicin did not change the I-->M transfer, but diminished M-->I transport by about 12%. In conclusion, the reduction of unstirred fluid layers at the mesothelium and the interstitium-fluid interfaces, removal of mesothelium, and addition of icodextrin increased the diffusive glucose transport in vitro; unstirred fluid layers restricted glucose transfer (I-->M) more than the mesothelium; and peritoneal glucose transport, directed from the mesothelial to the interstitial side of the peritoneum, decreased slightly after the addition of gentamicin.

Unlabelled: The effect of mixing fluid intensification, damage of mesothelial cells and gentamicin on the diffusive glucose transport across the peritoneal membrane were evaluated in the presented in vitro studies. A mathematical model of the mass transport was used to calculate the diffusive permeability, expressed as a diffusive permeability coefficient P [cm x s-1], for the investigated specimens. In the control conditions glucose transfer from the interstitial to the mesothelial side of membrane (I-->M) and in the opposite direction (M-->I) remained constant and P value at mean was 2.731 +/- 1.493 [cm x s-1 x 10(-4)]. The change of the stirring rate from 5.5 to 11 mL/min increased P values by about 74% for transport direction I-->M and 58% for M-->I, but change from 11 to 22 mL/min enhanced P at mean by about 42% for the both direction. The damage of the mesothelial layer, using of sodium deoxycholate (2.5 mmol/L; 103.6 mg%), increased the glucose transfer from the interstitial to the mesothelial side of the peritoneum by 41% and to the opposite direction by 57%. Furthermore, gentamicin did not change the I-->M transfer, but diminished M-->I transport by about 12%., In Conclusion: 1. The reducing of unstirred fluid layer at the mesothelium and interstitium--fluid interface and the mesothelium damage increase the diffusive glucose transport in vitro; 2. The unstirred fluid layer restricts glucose transfer more than tissue barrier (mesothelium); 3. The peritoneal glucose transport, directed from the mesothelial to the interstitial side of the peritoneum (but not transfer to the opposite direction), decreases slightly after gentamicin introduction.

The dynamics of bidirectional glucose transport across parietal peritoneum from anterior abdominal wall or diaphragm and small-bowel mesentery was analyzed. The mean transport values, expressed as transport coefficients, of intact peritoneum amounted 2.61; 0.18; 5.43 (10(-4) x cm x S-1), respectively. The chemical destruction of the mesothelium (2.5 mmol/l sodium deoxycholate) increased transperitoneal glucose transport across the investigated tissues. However, the intensification of transfer was different. Removal of the diaphragm pleural mesothelium caused greater increase of bidirectional glucose transport than the peritoneal mesothelium. Furthermore, the mean values of transport coefficient after peritoneal mesothelium damage were higher in relation to mesentery than to the peritoneum isolated from anterior abdominal wall and diaphragm. The obtained results suggest topographic heterogeneity of peritoneal membrane which refer to the mesothelium and submesothelial layers.

The changes of peritoneal absorption and excretion of urea, uric acid and gentamicin caused by glucose or mannitol have been analysed. These modification were differentiated, depended on the type of transported molecule, used osmotic agent and time of its activity as well as transfer direction. For example, glucose caused the increase of uric acid absorption and the decrease of urea excretion by about 40%. In contrast, mannitol didn't change the uric acid transport, but lowered the bidirectional transfer of urea. The mean values of gentamicin transport diminished after application of glucose or mannitol. This lowering was smaller in comparison with isoosmolar conditions. The reasons of above modifications are complex. It supposes that in vitro the direct physical action of hyperosmolality, metabolic activity of glucose and membrane effect of gentamicin balanced the solvent drag process. Furthermore, the heterogenecity of glucose and mannitol influence on the transperitoneal compounds transport are related to the transport rates (mechanism) of the examined osmotic agents and/or their metabolic activity.

The changes of the transperitoneal molecules transport caused by glucose and dynamics of its transport have been determined in the case of undamaged tissue and the membrane with injured mesothelium in the in vitro studies. In the intact glucose induced increase of peritoneal uric acid absorption (40%) and lowering of urea and gentamicin excretion (25-40%). Glucose in the dialysis fluid lowered uric acid absorption and urea excretion (20-40%) in denuded animal peritoneum. The transperitoneal glucose transport remained constant at 2.61 x 10(-4) x cm x s-1. The mesothelium destruction caused an increase (32%) of mean values of absorption and excretion of this compound. The obtained results suggest that modifications of transport functions of the peritoneum caused by glucose depend rather on direct action of hypertonicity and metabolic effects of glucose than of the osmotic gradient. Furthermore, these changes may contribute to the rapid transperitoneal transport of glucose which increase after the destruction of the mesothelium.

It was shown elsewhere that in a peritoneally dialyzed woman with pulmonary tuberculosis, oral treatment with rifampicin and pyrazinamide (11 and 25 mg/kg/day, respectively) caused a decrease in the peritoneal transport of sodium, potassium, urea, uric acid, protein, and ultrafiltration rate by 48% to 75% compared to the pretreatment values. Pyrazinoic acid (PA), a metabolite of pyrazinamide, may account for these changes, because rifampicin was also previously used in this patient without peritoneal function impairment. Thus in the present study the influence of PA on the human peritoneum is examined using the modified Ussing-type chamber. PA (1 mg/dL) was introduced into the medium on the interstitial side of the membrane. After the introduction of PA, uric acid transfer from the interstitial to the mesothelial side decreased by about 50%. There were no significant changes in the urea and albumin transfer rates. In conclusion, PA induces changes in uric acid transfer acting directly on mesothelial cells, whereas a decrease in the peritoneal transfer of other solutes may be caused by a decrease in convective transfer rates due to impaired ultrafiltration.