Back Diffusion of Hydrogen Ions across Gastric Mucosa of Patients with Gastric Ulcer and Rheumatoid Arthritis

Ionic permeability of the gastric mucosa was measured in six patients with an acute exacerbation of severe generalized rheumatoid arthritis receiving either aspirin and prednisone or aspirin and indomethacin as therapy. The results were compared with those in four patients with benign gastric ulcer and nine normal subjects. Compared with controls H⁺ concentration was decreased and Na⁺ concentration increased while corrected H⁺ flux out of the lumen and Na⁺ flux into the lumen were significantly increased in the patient groups, indicating increased mucosal permeability. Abnormality of the gastric mucosal barrier persisted in two patients despite healing of their ulcers. Mucosal permeability of patients with rheumatoid arthritis and gastric ulcer did not differ significantly from one another. One rheumatoid patient with a gastric ulcer showed no difference in mucosal permeability to that of the other rheumatoid patients. These studies suggest that increased H⁺ ion loss contributes to the apparent hyposecretion of acid in patients gastric ulcer; persistence of an abnormal gastric mucosal barrier to H⁺ ions may explain the high recurrence rate of gastric ulcers; and an abnormal gastric mucosal barrier may be a precursor to gastric ulceration in rheumatoid arthritis.     

Regulation of acid secretion and paracellular permeability by F-actin in the bullfrog, Rana catesbeiana

Many studies have implicated F-actin in the regulation of gastric acid secretion using cytochalasin D (CD) to disrupt apical actin filaments in oxyntic cells. However, it is known that CD also affects mucosal permeability by disrupting tight junction structure. Here we investigated the contribution of F-actin to mucosal permeability and acid secretion in the stomach using CD. Stomachs were mounted in Ussing chambers and acid secretion (stimulated or inhibited), transepithelial resistance (TER), mannitol flux, bicarbonate transport, and dual mannitol/sodium fluxes were determined with or without CD. H(+) back diffusion was predicted from its diffusion coefficient. Incubation with CD resulted in a significant reduction in stimulated acid secretion. TER was unchanged in stimulated tissues but significantly reduced in inhibited tissues. Mannitol flux, bicarbonate transport, and H(+)-back diffusion increased significantly with CD. However, the rates of bicarbonate and H(+) flux were not large enough to account for the inhibition of acid secretion. These findings demonstrate that actin filaments regulate paracellular permeability and play an essential role in the regulation of acid secretion in the stomach.     

Adaptative response of Vitis root to anoxia

The effect of anoxia on the energy economy of root cells was studied by measuring heat production, ethanol and ATP production, K(+) fluxes and electrical activity in two Vitis species, V. riparia and V. rupestris, that differ in their tolerance to anoxia. Anoxia triggered a marked decrease of metabolic activity (measured by microcalorimetry) and of ATP levels in both species. In V. riparia after the first 2 h of anoxia, the decrease in the rate of heat production was not associated with a further significant decrease in ATP content, whereas in V. rupestris the ATP level continued to decrease until very low values were reached. The concomitant increase in the rate of ethanol production did not compensate for the decreased aerobic ATP supply. In V. rupestris, anoxia typically led to energy deficit and ATP imbalance, together with the subsequent disruption of ion homeostasis and cell death. In V. riparia, the strong decrease in K(+) membrane permeability together with the fast down-regulation of the electrical signals allowed the cells to avoid severe ion imbalances during prolonged anoxic episodes.     

Prostaglandin E2 aggravates gastric mucosal injury induced by histamine in rats through EP1 receptors

We demonstrated that prostaglandin (PG) E2 aggravates gastric mucosal injury caused by histamine in rats, and investigated using various EP agonists which EP receptor subtype is involved in this phenomenon. Rats were used after 18 hr fasting. Histamine (80 mg/kg) dissolved in 10% gelatin, was given s.c., either alone or in combination with i.v. administration of PGE2 or various EP agonists such as 17-phenyl PGE2 (EP1), butaprost (EP2), sulprostone (EP1/EP3), ONO-NT012 (EP3) and ONO-AE1-329 (EP4). The animals were killed 4 hr later, and the mucosa was examined for lesions. The mucosal permeability was determined using Evans blue (1%). Histamine alone induced few lesions in the gastric mucosa within 4 hr. PGE2 dose-dependently worsened the lesions induced by histamine, the response being inhibited by tripelennamine but not cimetidine. The effect of PGE2 was mimicked by 17-phenyl PGE2 and sulprostone, but not other EP agonists, including EP2, EP3, and EP3/EP4 agonists. The mucosal vascular permeability was slightly increased by histamine, and this response was markedly enhanced by co-administration of 17-phenyl PGE2 as well as PGE2. The mucosal ulcerogenic and vascular permeability responses induced by histamine plus PGE2 were both suppressed by pretreatment with ONO-AE829, the EP1 antagonist. These results suggest that PGE2 aggravates histamine-induced gastric mucosal injury in rats. This action of PGE2 is mediated by EP1 receptors and functionally associated with potentiation of the increased vascular permeability caused by histamine through stimulation of H1-receptors.     

Permeability of the urinary bladder of the turtle, Pseudemys scripta elegans, to ammonia

1. The permeability of the isolated turtle urinary bladder to ammonia was investigated by varying the ratio of NH3 to NH4+ concentration in the serosal bath and measuring the flux of ammonia into the mucosal bath. 2. The permeability of the turtle bladder to NH3 was in the range of 5.4-6.1 x 10(-3) cm/sec and the permeability of the unstirred layer to NH4+ was in the range of 1.1-2.1 x 10(-5) cm/sec. 3. The flux of ammonia calculated from the permeability of NH3 can account for the decrease in mucosal H+ secretion observed with addition of NH4Cl to the serosal bath.     

Effects of Anoxia on Wheat Seedlings: I. INTERACTION BETWEEN ANOXIA AND OTHER ENVIRONMENTAL FACTORS

Anoxia was imposed on 4–6-d-old, intact wheat seedlings,after the roots had first been exposed for 1 d to O₂ concentrationsbetween 0·016 and 0·06 mol m^–3. Apices ofthe main axis of the seminal roots were considered to have toleratedanoxia if elongation occurred after return from anoxia to air,hereafter called ‘retention of elongation potential’.During anoxia, elongation potential was retained longer in rootsof intact seedlings than in 0–5 mm excised root tips suppliedwith 50 mol m^–3 glucose. In intact seedlings, elongation potential was retained longerat 15°C than at 25°C, and at pH 50 and 60 than at pH40. These differences between treatments were maintained inthe presence of exogenous glucose, and glucose supply prolongedthe retention of elongation potential in all anoxic treatments. Elongation potential was retained much longer at very low 02concentrations (0006 to 00l mol m^–3) than under anoxia;this was established at pH 40. Anoxia inhibited the transport of sugars from the shoots and/orendosperm to the root by 79-97%, as assessed from experimentswith roots of intact plants exposed to anoxia at pH 60 and 15°C. Overall, the results demonstrate: (i) that the occurrence ofadverse effects of anoxia during waterlogging in the field mayinteract with other environmental factors and (ii) that thereare pronounced difficulties integrating data on tolerance toanoxia obtained in different laboratories. Key words: Anoxia, wheat seedlings, pH, temperature     

大鼠浸水应激性胃粘膜损伤机制的研究

本工作观察了室温下单纯束缚加生理盐水,浸水应激加生理盐水,浸水应激加阿托品(0.5mg/kg),浸水应激加酚苄明(10mg/kg),浸水应激加戊巴比妥钠(30mg/kg)5组大鼠的胃粘膜损伤程度,胃酸分泌,胃壁结合粘液分泌和胃运动的变化。结果表明:大鼠浸水应激后胃粘膜损伤严重,胃酸分泌增加,胃壁结合粘液分泌减少,胃运动亢进;预先应用阿托品再浸水应激可显著减轻胃粘膜损伤程度,抑制胃酸分泌和胃运动,但增加胃壁结合粘液的分泌;预先应用应巴比妥钠亦显著减轻胃粘膜损伤程度,抑制胃运动和增加胃壁结合粘液的分泌,但对胃酸分泌无影响;预先应用酚苄明对胃粘膜损伤程度、胃酸分泌、胃壁结合粘液分泌和胃运动均无明显影响。上述结果提示,胃运动亢进、胃壁结合粘液分泌减少及胃酸分泌增加均不同程度地参与了浸水应激性胃粘膜损伤的形成,但在胃运动受到抑制及胃壁结合粘液分泌增加的情况下,仅胃酸的存在不致引起胃粘膜严重损伤。     

Role of bradykinin in gastric vasodilation caused by hypertonic saline and acid back diffusion

Protective vasodilation in response to tissue injury and acid back diffusion is associated with release of bradykinin in the rat stomach. We hypothesized that bradykinin might be involved in mechanisms behind such vasodilation via influence on mast cells and sensory neurons. Acid back diffusion after mucosal barrier disruption with hypertonic saline evoked degranulation of mast cells in the rat stomach wall. Acid back diffusion was also associated with increased luminal release of histamine and gastric blood flow in normal rats, but not in mast cell-deficient rats. Bradykinin (BK(2)) receptor blockade inhibited degranulation of submucosal mast cells in the stomach and attenuated gastric vasodilation both in response to acid back diffusion and after stimulation of sensory neurons with capsaicin. Gastric vasodilation caused by mucosal injury with hypertonic saline alone was associated with degranulation of mucosal mast cells. These events were unaffected by inhibition of prostaglandin synthesis, whereas bradykinin (BK(2)) receptor blockade was associated with abolished vasodilation and inhibition of mucosal mast cell degranulation. We conclude that bradykinin is involved in gastric vasodilation caused by hypertonic injury alone via influence on mast cells, and by acid back diffusion via influence on both sensory neurons and mast cells.     

Mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine

Acid back diffusion into the rat stomach mucosa leads to gastric vasodilation. We hypothesized that histamine, if released from the rat mucosa under such conditions, is mast cell derived and involved in the vasodilator response. Gastric blood flow (GBF) and luminal histamine were measured in an ex vivo chamber. Venous histamine was measured from totally isolated stomachs. Mucosal mast cells (MMC), submucosal connective tissue mast cells (CTMC), and chromogranin A-immunoreactive cells (CgA IR) were assessed morphometrically. After mucosal exposure to 1.5 M NaCl, the mucosa was subjected to saline at pH 5.5 (control) or pH 1.0 (H(+) back diffusion) for 60 min. H(+) back diffusion evoked a marked gastric hyperemia, increase of luminal and venous histamine, and decreased numbers of MMC and CTMC. CgA IR cells were not influenced. Depletion of mast cells with dexamethasone abolished (and stabilization of mast cells with ketotifen attenuated) both hyperemia and histamine release in response to H(+) back diffusion. GBF responses to H(+) back diffusion were attenuated by H(1) and abolished by H(3) but not H(2) receptor blockers. Our data conform to the idea that mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine.     

Evaluation of early gastric mucosal permeability induced by central thyrotropin-releasing hormone administration

Accumulating evidence suggests that central thyrotropin-releasing hormone (TRH) administration induces gastric erosion 4 h after administration through the vagal nerves. However, early changes in the gastric mucosa during these 4 h have not been described. To assess early changes in the gastric mucosa after intracisternal injection of a stable TRH analog, pGlu-His-(3,3'-dimethyl)-ProNH2 (RX-77368), we measured the blood-to-lumen 51Cr-labeled EDTA clearance and examined the effects of vagotomy, atropine, omeprazole, and hydrochloric acid (HCl) on RX-77368-induced mucosal permeability. A cytoprotective dose of RX-77368 (1.5 ng) did not increase mucosal permeability. However, higher doses significantly increased mucosal permeability. Permeability peaked within 20 min and gradually returned to control levels in response to a 15-ng dose (submaximal dose). Increased mucosal permeability was not recovered after a 150-ng dose (ulcerogenic dose). This increase in permeability was inhibited by vagotomy or atropine. Intragastric perfusion with HCl did not change the RX-77368 (15 ng)-induced increase in permeability, but completely inhibited the recovery of permeability after the peak. Pretreatment with omeprazole did not change the RX-77368 (15 ng)-induced increase in permeability, but quickened the recovery of permeability after the peak. These data indicate that the RX-77368-induced increase in permeability is mediated via the vagal-cholinergic pathway and is not a secondary change in RX-77368-induced acid secretion. Inhibited recovery of permeability on exposure to an ulcerogenic RX-77368 dose or on exposure to HCl plus a submaximal dose of RX-77368 may be crucial for the induction of gastric mucosal lesions by central RX-77368 administration.     

Temporal relationship between neurotransmitter release and ion flux during spreading depression and anoxia

Brain ion homeostasis is severely perturbed during spreading depression of Leao and during anoxia. The ionic composition of the extracellular space changes abruptly and approaches the intracellular concentrations owing to an increase in cell permeability. In spreading depression, synchronous transmitter efflux caused by a depolarization of the presynaptic terminals has been implicated as a possible mechanism that would explain the concomitant movement of ions. Anoxia, having many features in common with spreading depression, may follow the same mechanism. We have measured the concentrations of extracellular potassium with ion-selective microelectrodes and dopamine by in vivo voltammetry with carbon fiber microelectrodes during spreading depression and anoxia to compare the temporal relationship between the release of dopamine and ion movements in the striatum. There is a pronounced release of dopamine during both spreading depression and anoxia. In spreading depression, the sharp increase of potassium concentration that follows an initial smaller and slower increase of potassium is accompanied by the release of dopamine. In anoxia, the dopamine release clearly precedes the fast rise of extracellular potassium concentration. We conclude that in striatum, there is a pronounced dopamine release during spreading depression and anoxia, but that the relationships between ionic changes and transmitter release for these two phenomena are different and probably reflect different mechanisms.     

Chloride flux in bilayer membranes: chloride permeability in aqueous dispersions of single-walled, bilayer vesicles.

Aqueous dispersions of phosphatidylcholine vesicles were utilized to determine bilayer permeability to 36-Cl as a function of pH and temperature. These dispersions were comprised of single-walled vesicles, homogeneous in size, prepared by sonication of purified egg phosphatidylcholine under argon followed by fractionation on a molecular sieve. Permeability constants calculated from the inward flux of 36-Cl and the geometric parameters of these vesicles proved to be dependent on both pH and temperature. Analysis of these dependences leads to the conclusion that 36-Cl permeation in the presence of KCl is due principally to a carrier mediated exchange process involving a phospholipid-HCL complex. Net permeation by H-36-Cl may make a small contribution to the 36-Cl flux, however, studies carried out at very low chloride concentrations show that this flux is much smaller than the exchange flux. Thus chloride permeability for the exchange process is 1.5 times 10- minus 11 cmsec- minus 1 while the corresponding coefficient for the net flux of H-36-Cl is 1.0 times 10- minus 12 cm sec- minus 1 at pH 7. The activation energy for the 36-Cl exchange flux was found to be 19 plus or minus 2 kcal/mol. This value is similar to that obtained for the transbilayer "flip-flop" of phosphatidylcholine molecules in a similar system (Kornberg and McConnell, 1971). This correspondence together with the fact that the experimentally determined flux of 36-Cl agrees well with that calculated from the "flip-flop" parameters, strongly suggests that the flux of 36-Cl and "flip-flop" of phosphatidylcholine may be the same process.     

EEG evaluation of humaneness of asphyxia and decapitation euthanasia of the laboratory rat.

The relative humaneness of asphyxia and decapitation was objectively evaluated in rats by EEG monitoring. EEG activation (low voltage, fast activity) was considered to indicate discomfort, pain, and affective responses to euthansia. Such activation was present 37.3 plus or minus 7.5 sec after asphyxia and 13.6 plus or minus 4,6 sec after decapitation. Decapitation was also characterized by an immediate large, and relatively long-lasting, ultra-slow voltage, detected by non-polarizable scalp electrodes. Isoelectric activity (death) occurred 69.4 plus or minus 9.9 sec after onset of asphyxia and 27.2 plus or minus 4.4 sec after decapitation.     

Hydrogen ion diffusion in dog gastric mucus glycoprotein: effect of associated lipids and covalently bound fatty acids

The effect of neutral lipids, glycolipids and phospholipids associated with dog gastric mucus glycoprotein, and that of covalently bound fatty acids on the ability of glycoprotein to retard the diffusion of hydrogen ion was investigated. Purified mucus glycoprotein in its native form, placed between equimolar (0.155M) solutions of HCl and NaCl in a specially designed two-compartment chamber, caused a 90% reduction in permeability to hydrogen ion when compared with a layer of NaCl. Extraction of associated lipids lead to a 68% increase in permeability of the glycoprotein to hydrogen ion, while removal of the covalently bound fatty acids increased further the diffusion rate by 6%. Reassociation of the delipidated glycoprotein with its neutral lipids reduced the permeability to hydrogen ion by 34%, an 11% reduction was obtained with glycolipids, and 23% with phospholipids. Since neutral lipids account for 47% of the glycoprotein lipids, glycolipids 41.1% and phospholipids 11.9%, the quantitative decrease in permeability of the delipidated glycoprotein following its reassociation with phospholipids is 2.7 times greater than that of neutral lipids and 7.3 times greater than that of glycolipids.     

Inhibition of posthemorrhagic transfusion-induced gastric injury by a long-acting superoxide dismutase derivative

Although oxygen-free radicals have been postulated to play an important role in the pathogenesis of gastric mucosal injury induced by posthemorrhagic blood transfusion, direct evidence supporting this hypothesis is lacking. Superoxide dismutase (SOD) has been shown to inhibit oxygen toxicity in vitro in various types of cell injury. However, in some cases, oxidative tissue injury cannot be decreased efficiency predominantly due to its rapid elimination by renal glomerular filtration. To overcome such frustrating situations, we have synthesized a SOD derivative that circulates bound to albumin with a half-life of 6 hr. When blood was withdrawn from the rat (22 ml/kg) for 30 min followed by transfusion of the extracted blood, marked gastric mucosal lesions occurred within 30 min after transfusion. Intravenously injected SOD derivative markedly decreased gastric mucosal injury. Kinetic analysis using 125I-labeled albumin revealed that the vascular permeability of the stomach increased significantly after transfusion by a SOD derivative inhibitable mechanism. Thus, superoxide radical and/or its metabolite(s) play a critical role in the pathogenesis of posthemorrhagic transfusion-induced gastric injury.     

Urea permeability of human red cells

The rate of unidirectional [14C]urea efflux from human red cells was determined in the self-exchange and net efflux modes with the continuous flow tube method. Self-exchange flux was saturable and followed simple Michaelis-Menten kinetics. At 38 degrees C the maximal self-exchange flux was 1.3 X 10(-7) mol cm-2 s-1, and the urea concentration for half-maximal flux, K1/2, was 396 mM. At 25 degrees C the maximal self-exchange flux decreased to 8.2 X 10(-8) mol cm-2 s-1, and K1/2 to 334 mM. The concentration-dependent urea permeability coefficient was 3 X 10(-4) cm s-1 at 1 mM and 8 X 10(-5) cm s-1 at 800 mM (25 degrees C). The latter value is consonant with previous volumetric determinations of urea permeability. Urea transport was inhibited competitively by thiourea; the half-inhibition constant, Ki, was 17 mM at 38 degrees C and 13 mM at 25 degrees C. Treatment with 1 mM p-chloromercuribenzosulfonate inhibited urea permeability by 92%. Phloretin reduced urea permeability further (greater than 97%) to a "ground" permeability of approximately 10(-6) cm s-1 (25 degrees C). This residual permeability is probably due to urea permeating the hydrophobic core of the membrane by simple diffusion. The apparent activation energy, EA, of urea transport after maximal inhibition was 59 kJ mol-1, whereas in control cells EA was 34 kJ mol-1 at 1 M and 12 kJ mol-1 at 1 mM urea. In net efflux experiments with no extracellular urea, the permeability coefficient remained constantly high, independent of a variation of intracellular urea between 1 and 500 mM, which indicates that the urea transport system is asymmetric. It is concluded that urea permeability above the ground permeability is due to facilitate diffusion and not to diffusion through nonspecific leak pathways as suggested previously.     

Carbohydrate metabolism in the central nervous system of the megalobulimus oblongus snail during anoxia exposure and post-anoxia recovery

The effects of anoxic exposure and the post-anoxia aerobic recovery period on carbohydrate metabolism in the central nervous system (CNS) of the land snail Megalobulimus oblongus, an anoxia-tolerant land gastropod, were studied. The snails were exposed to anoxia for periods of 1.5, 3, 6, 12, 18, or 24 hr. In order to study the post-anoxia recovery phase, snails exposed to a 3-hr period of anoxia were returned to aerobic conditions for 1.5, 3, 6, or 15 hr. Glycogen and glucose concentrations in the CNS, hemolymph glucose concentration, and glycogen phosphorylase (active form, GPa) activity in the CNS were analyzed. Anoxia does not significantly affect the concentration of CNS glucose but induces hyperglycemia and a reduction of CNS GPa activity. The glycogen concentration was decreased at 12 hr of anoxia; however, by 18 and 24 hr in anoxia, the glycogen content was not significantly different from basal control values. During the post-anoxia period, the reduction in GPa activity and the increased hemolymph glucose concentration induced by anoxia returned to control values. These results suggest that the CNS of M. oblongus may use hemolymph glucose to fulfill the metabolic demands during anoxia. However, the hypothesis of tissue metabolic arrest cannot be excluded.     

Tributyltin-mediated exchange diffusion of halides in lipid bilayers

This paper describes the effect of tributyltin (TBT) on the inorganic anion permeability of lipid bilayers. When this compound is added in micromolar concentrations to one or both sides of a phosphatidyl ethanolamine (PE) membrane formed in 0.1 M NaCl or KCl (pH 7), there is no change in the electrical conductance. Under these circumstances, the Cl self-exchange flux measured with 36Cl (MCl) increases from a value of approximately 10(-12) mol.cm-2.s-1, to approximately 10(-8) mol.cm-2.s-1. It was further found that the relation between chloride flux and [TBT] and [Cl] can be described as: MCl = B[TBT] [Cl]. When chloride was replaced by an equimolar concentration of different univalent anions in the trans compartment, the heteroexchange flux of chloride followed the sequence: I greater than Br greater than Cl greater than F greater than NO3. Under all experimental conditions tested, the chloride flux was always more than 10(3) times the maximum flux predicted from the value of the membrane conductance, and at least 100 times higher than the expected fluxes of ion pairs (TBT-Cl) diffusing across the unstirred layers. Thus, the mechanism by which tributyltin increases anion permeability in bilayers seems to be that of an obligatory exchange diffusion, with the reaction between tributyltin and the halides occurring at the membrane surface. Measurements of interfacial potentials indicate that tributyltin chloride lowers the positive intrinsic dipole potential of PE membranes by approximately 70 mV (at a TBT concentration of 30 microM) without substantial alteration of other parameters of the bilayer. The estimated adsorption coefficient of TBT-Cl was found to be 3 x 10(-4) cm.     

Mechanism of the cerebrocortical vasodilatation during anoxia.

The possible role of cerebrocortical ion homeostasis, NAD/NADH redox state and of cortical oxygen tension was investigated in the initiation of hypoxic cortical vasodilatation. In addition, changes in cerebrocortical extracellular concentrations of Na+, K+, and Cl- during anoxia were studied. The results were as follows. a) The cerebrocortical reflectance decrease, e.g. cerebral vasodilatation, lagged behind the cortical pO2 decrease by 1-2 sec, but preceded the decrease of arterial blood pressure and ECoG as well as the extracellular Na+, K+, Cl- increases by 20-30 sec. Since the cortical pO2 decreased first and the ion changes lagged behind the onset of vasodilatation by 20-30 sec, it is suggested that the CBF increase in hypoxia is mediated via the cortical pO2 decrease. b) A significant NAD reduction was already present after 20 sec. of nitrogen breathing. Since the ECoG and MABP decreased, and K+ activity increased much later than this, it is presumed that the NAD reduction during the first 30-40 sec of anoxia indicates an increased rate of glycolysis, but not mitochondrial hypoxia. c) In the predepolarization phase a 17% K+, 4% Na+, 5% Cl- increase is probably the result of a reduction of the extracellular spaces caused by water movement and by the migration of Na+ and Cl- from the extracellular to the intracellular space. The large K+, Na+, Cl- changes during terminal depolarization can be interpreted as a result of the failure of the membrane bound Na+ -K+ pump and of the altered ion permeability of the cell membranes.     

Role of carbohydrates in the viscosity and permeability of gastric mucin to hydrogen ion

The effect of carbohydrate removal on the viscosity of gastric mucin and its ability to impede the diffusion of hydrogen ion was investigated. The mucin, purified from dog gastric mucus, was subjected to partial or extensive deglycosylation with specific exoglycosidases and then used in the measurements. The obtained results revealed that removal of peripheral fucose or N-acetylglucosamine caused in each case only about 5% reduction of the glyco-protein viscosity. An 18% drop in the viscosity, however, occurred following removal of sialic acid, while extensive deglycosylation (removal of 86% carbohydrate) reduced the glycoprotein viscosity by 40%. The ability of mucin to retard the diffusion of hydrogen ion increased by 7% following removal of fucose or N-acetylgalactosamine, a 28% increase was obtained following removal of sialic acid, while the permeability to hydrogen ion of the extensively deglycosylated glycoprotein decreased by 42%. The results suggest that carbohydrates contribute significantly to the viscoelastic and permselective properties of gastric mucin.