Repetitive ICD discharges during an ambulance ride: an unusual pacemaker-ICD interaction.
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Ambulances↗
Biomedical subjects
T Wang
Publications and source records attributed to T Wang.
The periplasmic nitrate reductase in Pseudomonas sp. strain G-179 catalyzes the first step of denitrification.
Both membrane-bound and periplasmic nitrate reductases have been found in denitrifying bacteria. Yet the role of periplasmic nitrate reductase in denitrification has not been clearly defined. To analyze the function of the periplasmic nitrate reductase in Pseudomonas sp. strain G-179, the nap gene cluster was identified and found to be linked to genes involved in reduction of nitrite and nitric oxide and anaerobic heme biosynthesis. Mutation in the nap region rendered the cells incapable of growing under anaerobic conditions with nitrate as the alternative electron acceptor. No nitrate reduction activity was detected in the Nap- mutant, but that activity could be restored by complementation with the nap region. Unlike the membrane-bound nitrate reductase, the nitrate reduction activity in strain G-179 was not inhibited by a low concentration of azide. Nor could it use NADH as the electron donor to reduce nitrate or use chlorate as the alternative substrate. These results suggest that the periplasmic nitrate reductase in this strain plays a primary role in dissimilatory nitrate reduction.
Bacterial Typing Techniques↗
Sequences between the enhancer and promoter in the long terminal repeat affect murine leukemia virus pathogenicity and replication in the thymus.
We previously showed that the 93-bp region between the enhancer and promoter (named DEN for downstream of enhancer) of the long terminal repeat (LTR) of the MCF13 murine leukemia virus is an important determinant of the ability of this virus to induce thymic lymphoma. In this study we observed that DEN plays a role in the regulation of virus replication in the thymus during the preleukemic period. A NF-kappaB site in the DEN region partially contributes to the effect of DEN on both lymphomagenicity and virus replication. To further study the effects of DEN and the NF-kappaB site on viral pathogenicity during the preleukemic period, we examined replication of wild-type and mutant viruses with a deletion of the NF-kappaB site or the entire DEN region in the thymus. Thymic lymphocytes which were infected with wild-type and mutant viruses were predominantly the CD3(-) CD4(+) CD8(+) and CD3(+) CD4(+) CD8(+) cells. The increase in infection by wild-type virus and both mutant viruses of these two subpopulations during the preleukemic period ranged from 9- to 84-fold, depending upon the time point and virus. The major difference between the wild-type and both mutant viruses was the lower rate and lower level of mutant virus replication in these thymic subpopulations. Significant differences in replication between wild-type and both mutant viruses were seen in the CD3(-) CD4(+) CD8(+) and CD3(-) CD4(-) CD8(-) subpopulations, suggesting that these thymic cell types are important targets for viral transformation.
Animals↗
Hypoxic hypometabolism in the anesthetized turtle, Trachemys scripta.
A hypometabolic response during acute exposure to hypoxia has been measured in both endothermic and ectothermic vertebrates. In the turtle, we determined the metabolic response to normocapnic hypoxia and hypercapnic hypoxia. In addition, we tested the hypothesis that hypoxic hypometabolism was a regulated response that did not depend on O(2) availability. Metabolic, cardiovascular, and blood gas measurements were collected in anesthetized turtles under two conditions: during normocapnic hypoxia [fractional inspired O(2) FI(O(2)) = 0.1 and 0.05] and during hypercapnic hypoxia [FI(O(2)) = 0.1 and 0.05 plus fractional inspired CO(2) (FI(CO(2))) = 0.05]. During normoxia, rate of O(2) consumption (VO(2)) was 0.82 ml. min(-1). kg(-1) and was reduced by nearly 30% at the lowest FI(O(2)). Normocapnic hypoxia of FI(O(2)) = 0.1 had no significant effect on VO(2). The addition of 5% CO(2) to the inspired air did not enhance the effects of hypoxia. Injections of 2,4-dinitrophenol increased VO(2) during hypercapnic hypoxia in some animals to levels greater than those measured during normoxia. We conclude that hypoxia produces a hypometabolic state in anesthetized turtles, and the pharmacological stimulation of VO(2) counteracts the effects of hypoxia on metabolism. The hypoxic hypometabolism in turtles most likely represents a regulated response and does not reflect limited O(2) availability at the cellular level. Finally, we hypothesize that hypoxemia induced by the right-to-left cardiac shunt often associated with diving may trigger the development of a hypometabolic state and therefore contribute to the prolongation of aerobic dive times.
2,4-Dinitrophenol↗
Mechanism of proximal tubule bicarbonate absorption in NHE3 null mice.
NHE3 is the predominant isoform responsible for apical membrane Na(+)/H(+) exchange in the proximal tubule. Deletion of NHE3 by gene targeting results in an NHE3(-/-) mouse with greatly reduced proximal tubule HCO(-)(3) absorption compared with NHE3(+/+) animals (P. J. Schultheis, L. L. Clarke, P. Meneton, M. L. Miller, M. Soleimani, L. R. Gawenis, T. M. Riddle, J. J. Duffy, T. Doetschman, T. Wang, G. Giebisch, P. S. Aronson, J. N. Lorenz, and G. E. Shull. Nature Genet. 19: 282-285, 1998). The purpose of the present study was to evaluate the role of other acidification mechanisms in mediating the remaining component of proximal tubule HCO(-)(3) reabsorption in NHE3(-/-) mice. Proximal tubule transport was studied by in situ microperfusion. Net rates of HCO(-)(3) (J(HCO3)) and fluid absorption (J(v)) were reduced by 54 and 63%, respectively, in NHE3 null mice compared with controls. Addition of 100 microM ethylisopropylamiloride (EIPA) to the luminal perfusate caused significant inhibition of J(HCO3) and J(v) in NHE3(+/+) mice but failed to inhibit J(HCO3) or J(v) in NHE3(-/-) mice, indicating lack of activity of NHE2 or other EIPA-sensitive NHE isoforms in the null mice. Addition of 1 microM bafilomycin caused a similar absolute decrement in J(HCO3) in wild-type and NHE3 null mice, indicating equivalent rates of HCO(-)(3) absorption mediated by H(+)-ATPase. Addition of 10 microM Sch-28080 did not reduce J(HCO3) in either wild-type or NHE3 null mice, indicating lack of detectable H(+)-K(+)-ATPase activity in the proximal tubule. We conclude that, in the absence of NHE3, neither NHE2 nor any other EIPA-sensitive NHE isoform contributes to mediating HCO(-)(3) reabsorption in the proximal tubule. A significant component of HCO(-)(3) reabsorption in the proximal tubule is mediated by bafilomycin-sensitive H(+)-ATPase, but its activity is not significantly upregulated in NHE3 null mice.
Absorption↗
Abstracts of the conference on gastrin
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Journal Article↗
Effect of Am-80, a synthetic derivative of retinoid, on experimental arthritis in mice.
Am-80 is a newly snythesized retinoid with the structure of one aromatic amide among retinobenzoic acids. It exhibits specific biological activities of retinoic acid such as the activation of cellular differentiation and proliferation. We investigated the effect of Am-80 on collagen-induced arthritis (CIA) in mice and the immunopharmacological action on the production of several cytokines in the in vitro and in vivo models. Am-80, at doses of 0.3, 1 and 3 mg/kg, significantly inhibited the severity and development of the arthritis index, progression of foot pad swelling, bone damage and histopathological alterations. Am-80 also inhibited the production of anti-type II collagen (CII) IgG antibody, but did not affect the delayed-type hypersensitivity (DTH) response in arthritic mice. To determine the inhibitory mechanism of Am-80, we studied the effect of Am-80 on the production of cytokines. Am-80 did not affect the production of IFN-gamma by Th1 cells (1E10.H2 cells) and IL-4 by Th2 cells (D10.G4.1 cells), respectively. Am-80 selectively inhibited bacterial lipopolysaccharide (LPS)-induced IL-6, but not TNF-alpha and IL-1beta, production in mice. Moreover Am-80 inhibited IL-1beta induced IL-6 production and IL-6 mRNA expression in human osteoblast-like cells (MG-63). The inhibition of IL-6 production by Am-80 was due to downregulation of the pretranscription or the transcription of IL-6 in MG 63 cells. These findings suggest that the inhibitory effect of Am-80 on CIA is partially by modulating the production of the proinflammatory cytokine, IL-6.
Animals↗
Thiopental attenuates hypoxic changes of electrophysiology, biochemistry, and morphology in rat hippocampal slice CA1 pyramidal cells.
BACKGROUND AND PURPOSE: Thiopental has been shown to protect against cerebral ischemic damage; however, it has undesirable side effects. We have examined how thiopental alters histological, physiological, and biochemical changes during and after hypoxia. These experiments should enable the discovery of agents that share some of the beneficial effects of thiopental. METHODS: We made intracellular recordings and measured ATP, sodium, potassium, and calcium concentrations from CA1 pyramidal cells in rat hippocampal slices subjected to 10 minutes of hypoxia with and without 600 micromol/L thiopental. RESULTS: Thiopental delayed the time until complete depolarization (21+/-3 versus 11+/-2 minutes for treated versus untreated slices, respectively) and attenuated the level of depolarization at 10 minutes of hypoxia (-33+/-6 versus -12+/-5 mV). There was improved recovery of the resting potential after 10 minutes of hypoxia in slices treated with thiopental (89% versus 31% recovery). Thiopental attenuated the changes in sodium (140% versus 193% of prehypoxic concentration), potassium (62% versus 46%), and calcium (111% versus 197%) during 10 minutes of hypoxia. There was only a small effect on ATP (18% versus 8%). The percentage of cells showing clear histological damage was decreased by thiopental (45% versus 71%), and thiopental improved protein synthesis after hypoxia (75% versus 20%). CONCLUSIONS: Thiopental attenuates neuronal depolarization, an increase in cellular sodium and calcium concentrations, and a decrease in cellular potassium and ATP concentrations during hypoxia. These effects may explain the reduced histological, protein synthetic, and electrophysiological damage to CA1 pyramidal cells after hypoxia with thiopental.
Action Potentials↗
Daytime pulmonary hemodynamics in patients with obstructive sleep apnea without lung disease.
It is controversial whether obstructive sleep apnea (OSA) causes pulmonary hypertension (PH) in the absence of hypoxemic lung disease. To investigate this further we measured awake pulmonary hemodynamics, pulmonary gas exchange, and small airways function in 32 patients with OSA (apnea- hypopnea index, mean +/- SE, 46.2 +/- 3. 9/h) who had normal screening lung function. Pulmonary artery pressure (Ppa) and cardiac output were measured by Doppler echocardiography at three levels of inspired oxygen (FIO2 0.50, 0.21, and 0.11) and during incremental increases in pulmonary blood flow (10, 20, and 30 microgram/kg/min dobutamine infusions) while breathing 50% oxygen. Eleven patients had PH (mean Ppa >/= 20 mm Hg, Group I). They did not differ from patients without PH (Group II) in lung function, severity of sleep-disordered breathing, age, or body mass. Compared with Group II, Group I patients had increased small airways closure during tidal breathing (FRC-closing capacity: Group I, -0.16 +/- 0.11; Group II, 0.27 +/- 0.09 L; p < 0.05), more ventilation-perfusion inequality (AaPO2: 23.8 +/- 2.8; 19.8 +/- 1.4 mm Hg; p = 0.08), a greater pulmonary artery pressor response to hypoxia (DeltaPpa FIO2, 0.50 to 0.11: 16.4 +/- 1.93; 6.4 +/- 0.77 mm Hg; p < 0.05) and a marked rise in Ppa during increased pulmonary blood flow. We conclude that PH may develop in some patients with OSA without lung disease and that it is associated with small airways closure during tidal breathing and heightened pulmonary pressor responses to hypoxia and during increased pulmonary blood flow. Such changes are consistent with remodeling of the pulmonary vascular bed in affected patients with OSA, seemingly unrelated to severity of sleep-disordered breathing.
Blood Pressure↗
Three novel mutations at serine 314 in the thyroid hormone beta receptor differentially impair ligand binding in the syndrome of resistance to thyroid hormone.
The syndrome of resistance to thyroid hormone is associated with diverse mutations in the ligand-binding domain of the thyroid hormone beta receptor, localizing to three clusters around the hormone binding cavity. Here, we report three novel resistance to thyroid hormone mutations (S314C, S314F, and S314Y), due to different nucleotide substitutions in the same codon, occurring in six separate families. Functional characterization of these mutant receptors showed marked differences in their properties. S314F and S314Y receptor mutants exhibited significant transcriptional impairment in keeping with negligible ligand binding and were potent dominant negative inhibitors of wild-type receptor action. In contrast, the S314C mutant bound ligand with reduced affinity, such that its functional impairment and dominant negative activity manifest at low concentrations of thyroid hormone, but are more reversible at higher T3 concentrations. The degree of functional impairment of mutant receptors in vitro may correlate with the magnitude of thyroid dysfunction in vivo. Modelling these mutations using the crystal structure of thyroid hormone receptor beta shows why ligand binding is perturbed and why the phenylalanine/tyrosine mutations are more deleterious than cysteine.
Adolescent↗
DRB1*04 and DQ alleles: expression of 21-hydroxylase autoantibodies and risk of progression to Addison's disease.
Of 957 patients with type 1 diabetes without known Addison's disease 1.6% (n = 15) were positive for 21-hydroxylase autoantibodies. Among DQ8/DQ2 heterozygous patients, the percentage expressing 21-hydroxylase autoantibodies was 5% (10 of 208) vs. less than 0.5% of patients with neither DQ8 nor DQ2. Three of the diabetic patients found to have 21-hydroxylase autoantibodies on screening were subsequently diagnosed with Addison's disease. Overall, the genotype DQ8/DQ2, consisting of DRB1*0404/DQ8 with DRB1*0301/DQ2, was present in 14 of 21 patients with Addison's disease (8 of 12 with diabetes and 6 of 9 without diabetes or antiislet autoantibodies) vs. 0.7% of the general population (109 of 15,547; P < 10(-6)) and 11% of patients with DM without Addison's disease (62 of 578; P < 10(-6)). Among patients with diabetes with DQ8, Addison's disease was strongly associated with the specific DRB1 subtype, DRB1*0404 (8 of 9 patients from 8 families, in contrast to only 109 of 408 DQ8 DM patients with diabetes without Addison's disease having DRB1*0404; P < 0.001). Among 21-hydroxylase autoantibody-positive DQ8 patients, 80% with DRB1*0404 (12 of 15) had Addison's disease, in contrast to 1 of 10 autoantibody-positive patients with DRB1*0401 or DRB1*0402 (P < 0.001). We conclude that patients with DRB1*0404 and 21-hydroxylase autoantibodies are at high risk for Addison's disease. Patients with DRB1*0401 and DRB1*0402 have more limited progression to Addison's disease despite the presence of 21-hydroxylase autoantibodies.
Addison Disease↗
Fasting remnant lipoprotein cholesterol and triglyceride concentrations are elevated in nondiabetic, insulin-resistant, female volunteers.
This study was initiated to test the hypothesis that plasma concentrations of remnant lipoproteins would be higher after an overnight fast in insulin-resistant compared to insulin-sensitive volunteers. Forty-three healthy nonobese women were studied, divided into insulin-resistant (n = 21) and insulin-sensitive (n = 22) groups on the basis of their steady state plasma glucose (SSPG) concentration at the end of a 180-min infusion of octreotide acetate, insulin, and glucose. Under these conditions, steady state plasma insulin concentrations are similar in all subjects (approximately 60 microU/mL), and the higher the SSPG concentrations, the more insulin resistant the individual. By selection, mean (+/-SEM) SSPG concentrations were significantly higher (P < 0.001) in the insulin-resistant group (210 +/- 7 vs. 78 +/- 3 mg/dL). In addition, the insulin-resistant group had higher triglycerides (198 +/- 27 vs. 101 +/- 12 mg/dL; P < 0.005) and lower high density lipoprotein cholesterol (48 +/- 4 vs. 60 +/- 4 mg/dL; P < 0.05) concentrations. Finally, insulin resistance was associated with higher remnant lipoprotein particle concentrations of cholesterol (7.2 +/- 0.8 vs. 4.4 +/- 0.3; P < 0.005) and triglycerides (22.2 +/- 3.4 vs. 8.5 +/- 1.0; P < 0.001). All of these differences were seen despite the fact that the two groups were similar in terms of age and body mass index. These results identify additional abnormalities in lipoprotein metabolism that may contribute to the increased risk of coronary heart disease seen in insulin-resistant, nondiabetic subjects (syndrome X).
Blood Glucose↗
Cardiorespiratory responses of the toad (Bufo marinus) to hypoxia at two different temperatures.
Central vascular blood flows and ventilation were measured in conscious toads (Bufo marinus) at 15 and 25 degrees C. The animals were exposed to hypoxia (Fi(O)(sum)=0.10 and 0.05, where Fi(O)(sum) is the fractional oxygen concentration of inspired air) at both temperatures. In addition, the cardiorespiratory responses to hypercapnia (Fi(CO)(sum)=0.05) and atropine injection (5 mg kg(-)(1); 7.4 micromol kg(-)(1)) were studied at 25 degrees C. At 25 degrees C, systemic blood flow ( q_dot (sys)) exceeded pulmocutaneous blood flow ( q_dot (pc)), indicating a large net right-to-left shunt ( q_dot (pc)/ q_dot (sys) was 0.39). q_dot (pc)/ q_dot (sys) was reduced significantly to 0.22 at 15 degrees C. At both temperatures, q_dot (pc) increased significantly during hypoxia (from 26.2 to 50.8 ml min(-)(1 )kg(-)(1) at 25 degrees C and from 11. 2 to 18.9 ml min(-)(1 )kg(-)(1) at 15 degrees C), whereas q_dot (sys) changed little (from 77.2 to 66.2 ml min(-)(1 )kg(-)(1) at 25 degrees C and from 54.3 to 50.1 ml min(-)(1 )kg(-)(1) at 15 degrees C). As a result, the net right-to-left shunt was greatly reduced, while total cardiac output remained almost unaffected. The ventilatory response was more pronounced during hypercapnia but, since q_dot (pc) and q_dot (sys) were affected similarly, there was no change in the shunt pattern. In undisturbed toads at 25 degrees C, atropine injection increased q_dot (pc) and eliminated the net right-to-left shunt. This is consistent with the known vagal innervation of the pulmonary artery. The present study shows that the cardiac right-to-left shunt that prevails in undisturbed and resting toads is reduced with increased temperature and during hypoxia. These findings are consistent with the general view that the cardiac right-to-left shunt is regulated and reduced whenever oxygen delivery is compromised or metabolic rate is increased.
Animals↗
Physiological saline is not a biocompatible peritoneal dialysis solution.
UNLABELLED: We have previously demonstrated that daily exposure to dialysis fluid results in significantly increased peritoneal lymphatic flow. In this study, we investigated if daily intraperitoneal infusion of saline (isotonic, glucose free) could cause similar changes. METHODS: Sixteen male SD rats received daily infusion (i.p.) of 20 ml saline for ten days (Saline group). Twenty-four hours after the last infusion, a 4 hour dwell study using 25 ml 3.86% glucose dialysis solution with frequent dialysate and blood sampling was done in each rat as well as in rats which did not receive daily infusion (Control, n=8). Radiolabeled human albumin (RISA) was added to the solution as an intraperitoneal volume marker. Radioactivity, glucose, urea, sodium, and potassium were measured for each sample. In a separate study, the RISA absorption to peritoneal tissue was also determined. RESULTS: The net ultrafiltration was significantly decreased in the daily infusion group (p<0.05). However, the apparent volume at 3 minutes of the dwell was markedly increased; this was due to a significant increase in the RISA binding (1.5-12.0% in the Saline group vs. 0.45-1.12% in the Control group) to peritoneal tissues as assessed by measurement of RISA recovery at 3 min of the dwell. This resulted in a significant overestimation both of the intraperitoneal volume (IPV) at 3 min and the (apparent) fluid absorption rate (as estimated by the transport of RISA out of peritoneal cavity): 0.087+/-0.026 ml/min in the Saline group vs. 0.052+/-0.007 ml/min in the Control group, p<0.001. The direct lymphatic flow as estimated by the clearance of RISA to plasma (which should not be affected by the RISA binding) also increased markedly (0.021+/-0.005 ml/min in the Saline group vs. 0.008+/-0.001 ml/min in the control group). There was no significant difference in the D/P values for small solutes (urea, sodium, potassium, urate) and D/D0 for glucose between the two groups. CONCLUSIONS: 1) Daily infusion of physiological saline into peritoneal cavity may increase the peritoneal lymphatic flow; 2) The significant (apparent) increase in IPV shortly after infusion may suggest increased RISA binding to peritoneal tissues (which may be related to the damage of the tissues, and results in overestimation of the peritoneal fluid absorption rate); 3) Saline is not a biocompatible peritoneal dialysis solution, and should therefore not be used as a control or flush solution.
Absorption↗
[Comparison of hypervariable region gene of hepatitis C virus between an individual infected persistently and an individual recovered from infection].
OBJECTIVE: To explore the law of recovery from HCV infection. METHODS: Amplifiying, sequenceing and analyzing the gene of hypervariable region from an individual infected persistently and an individual recovered from infection. RESULTS: One base insertion (two clones, 10%) in the person recovered other than that infected persistently, but there is no difference between them in percentage of mumation, diversity of quasispecies and genetic distance among clones. CONCLUSION: The range of genetic variation at one time point did not seem to have obvious relationship with the HCV persistent infection or recovery from HCV infection. This study gave basic information for searching the relation of genetic variation and clinical status, and designing HCV vaccine.
Base Sequence↗
Alterations in water and solute transport with time on peritoneal dialysis.
Peritoneal ultrafiltration capacity and small-solute transport characteristics seem to be relatively stable in most patients treated with PD for up to 3 years. However, in patients treated with PD for 4 years or more, there is a tendency towards increasing diffusive transport for small solutes as well as a tendency towards decreasing net UF, whereas the peritoneal protein clearances seem to be reduced or stable. Loss of UFC is a well-known complication during long-term PD treatment, and the risk for loss of UFC may be as high as 50% after 6 years on PD. Several different mechanisms of UFC loss have been reported. In particular, the most common mechanism for loss of UFC is increased diffusive transport resulting in rapid glucose absorption and thus rapid loss of the osmotic driving force. Also reported as causes of UFC loss have been: reduced efficiency of the osmotic agent (perhaps owing to decreased transcellular water transport); loss of peritoneal surface area with slow solute transport owing to fibrosis and the formation of adhesions (during the late stage of sclerosing peritonitis); and increased peritoneal fluid absorption. In individual patients, a combination of several mechanisms may be involved in the apparent UFC failure.
Animals↗
Intraperitoneal addition of hyaluronan improves peritoneal dialysis efficiency.
BACKGROUND: It has been shown that hyaluronan (HA) can decrease peritoneal fluid absorption. It is not known, however, how various molecular weights and various concentrations of hyaluronan affect peritoneal fluid absorption rate. METHODS: A study of 4-hour dwells, with frequent dialysate and blood sampling, was performed in male Sprague-Dawley rats (6-7 rats in each group) with 131I albumin as an intraperitoneal volume marker. Each rat was infused intraperitoneally with 25 mL of 1.5% glucose solution alone or 1.5% glucose solution containing hyaluronan at various molecular weights (MW-85 kD, 280 kD, 500 kD, and 4 MD) or containing hyaluronan of MW 500 kD at various concentrations (0.01%, 0.05%, 0.1%, 0.5%). Two additional groups were infused with 40 mL of 1.36% glucose dialysate alone or 1.36% glucose dialysate with 0.01% hyaluronan (MW 500 kD) to test the effect of hyaluronan when high dialysate fill volume was used. RESULTS: Addition of 0.01% hyaluronan significantly decreased peritoneal fluid absorption rate (K(E)) (by 22%, p < 0.01). The decrease was more marked with hyaluronan at high MW or high concentration, or with high dialysate fill volume. The net ultrafiltration tended to be higher in all hyaluronan groups compared to their control groups except in the 4 MD group; this difference was mainly due to a lower K(E) in all the hyaluronan groups. The direct lymphatic flow was significantly decreased in the 0.5% HA group. The transcapillary ultrafiltration rate (Qu) was significantly lower in the 4 MD group as compared to the control group. No difference in Qu was found between the other groups as compared to their control groups. CONCLUSIONS: (1) Intraperitoneal addition of hyaluronan may increase net peritoneal fluid removal, mainly because hyaluronan decreases peritoneal fluid absorption rate. The decrease was more marked when high dialysate fill volume was used, indicating that intraperitoneal addition of hyaluronan can prevent the decreased net ultrafiltration caused by an increase in dialysate fill volume. (2) The decrease in peritoneal fluid absorption rate may be both MW-dependent and concentration-dependent: that is, a higher MW as well as a higher concentration of hyaluronan result in a more marked decrease in peritoneal fluid absorption rate. (3) Low concentrations of high MW hyaluronan may also decrease Qu. However, Qu did not decrease when high concentrations of hyaluronan were used despite a significant decrease in peritoneal fluid absorption rate.
Absorption↗
A simple and fast method to estimate peritoneal membrane transport characteristics using dialysate sodium concentration.
BACKGROUND: The peritoneal equilibration test (PET) is widely used to classify a patient's peritoneal transport characteristics. However, PET is laborious and the prediction of fluid removal based on PET is generally poor. It is believed that osmosis by glucose occurs partially through transcellular water channels, resulting in sieving of sodium and decrease of dialysate sodium concentration when using hypertonic glucose dialysate. OBJECTIVE: In this study, we investigated the possibility of using dialysate sodium concentration to classify the patient's peritoneal transport characteristics. METHODS: A 6-hour dwell study with frequent dialysate and plasma sampling was performed in 46 patients using 2 L of 3.86% glucose dialysate with 131I-albumin as an intraperitoneal volume (IPV) marker. The peritoneal transport of sodium, creatinine, glucose, and fluid was evaluated. RESULTS: The dialysate sodium concentration at 240 min (D(Na240)) significantly correlated with D/P creatinine (r = 0.76, p < 0.001) and D/D0 glucose (r = -0.83, p < 0.001) at 240 min of the dwell (better than dialysate sodium concentration at any other time of the dwell). DNa240 also significantly correlated with IPV at 240 min of the dwell (r = -0.61, p < 0.001)(better than D/P creatinine and D/D0 glucose). There were significant correlations between D(Na240) and the sodium-sieving coefficient (r = 0.71, p < 0.001) and the diffusive mass transfer coefficient for sodium (r = 0.50, p < 0.001). When using D(Na240) to divide the patients into four groups, as in the PET method, no significant difference was found between the two methods. CONCLUSION: Using 3.86% glucose solution, D(Na240) can be used instead of D/P creatinine to classify patients into different transport groups. D(Na240) provides a better prediction of peritoneal fluid transport and reflects both the diffusive and convective transport properties of the membrane. As only one dialysate sample (and no blood sample) is needed, D(Na240) may offer important clinical advantages compared with PET.
Biological Transport↗