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PubMed1987

Effects of heat treatment on the permeability of polyvinyl alcohol films to a hydrophilic solute.

Polyvinyl alcohol (PVA) films may be useful as release-controlling membrane systems. Untreated, they are readily permeable to water and hydrophilic drugs. Because heating has been used to increase crystallinity and thus reduce the solubility and swelling in water of PVA films, we have studied the effects of heat on the permeability of PVA films to a water-soluble drug marker. Heat treatment was varied in the temperature range 100-200 degrees C for 1 h. The effect of time of heating was studied at 100 degrees C for 0.5-160 h. After pre-equilibration with water (heat-treated membranes remained intact, untreated ones dissolved), membrane permeabilities to methylene blue in aqueous solution (37 degrees C) were determined in a rotating diffusion cell. Permeabilities decreased with increased heating times (0.98-0.039 cm X min-1 for 0.5-160 h at 100 degrees C, respectively). Heating in air or N2 produced similar results. Further dramatic decreases in permeability occurred with increasing pretreatment temperatures; membrane permeability fell by a factor of approximately 500 with increasing temperature in the range 100-200 degrees C. There was no evidence of decomposition at temperatures less than or equal to 190 degrees C for 1 h. Results were consistent with literature reports of heat-induced increases in crystallinity. Membranes were simple to prepare and permeability could be controlled without recourse to chemical manipulation.

Diffusion↗
PubMed1987

Effect of bile salts on nasal permeability in vitro.

Nasal mucosa excised from dogs or rabbits was mounted as a flat sheet in an in vitro chamber. The permeability was assessed by measuring the unidirectional flux of the radiolabeled tracer compounds, water, sucrose, polyethylene glycol, and cholecystokinin octapeptide. The permeability coefficients calculated from the fluxes indicate that the nasal mucosa is moderately permeable to water-soluble compounds and compares with ileum or gallbladder. The addition of 0.5% sodium deoxycholate to the mucosal bathing solution caused a rapid, four- to fivefold increase in permeability to sucrose or cholecystokinin octapeptide. The increase in permeability was bidirectional, was not reversed by washing, and was accompanied by histological evidence of extensive loss of the surface epithelial layer. These results indicate that bile salts enhance nasal permeability by removing the epithelial cells, which constitute a major permeability barrier, rather than causing a chemical modification of the mucosal cells. This argues against the use of bile salts to enhance nasal drug absorption in patients.

Animals↗
PubMed1995

Water permeability of isolated cuticular membranes: a structural analysis.

Water permeability of isolated cuticular membranes from mature green and ripe Lycopersicon esculentum Mill, fruits was investigated. The water permeability of ripe tomato cuticles in the H+ form was strongly dependent on pH and increased when the pH of the external solution increased. The water permeability of the cuticles of mature green fruits was higher than that of the ripe fruit cuticles and had a low pH dependence. The isolated fruit cuticles were put in the Na+ form at three different pH levels and their water permeabilities were measured at the respective pH values in the external solution. The water permeability values were related to the nature and exchange capacity of hydroxyl functional groups of the flavonoids naringenin and chalconaringenin present in the ripe tomato cuticles, and to the phenolic acids of both types of cuticles. Whereas the water permeability of the mature green cuticles in the sodium form increased according to their small exchange capacity, the water permeability of ripe tomato cuticles reached a saturation value at high pH. The results indicate that the flavonoids play an important role in the control of water transport across the polymer matrix of these membranes. X-ray diffraction study of the different cuticles confirmed structural changes in the polymer when the isolated cuticles were put in the different homoionic forms. Analysis of the basal spacings confirms a structural model of tomato fruit cuticle with two major hydrophobic interplanar spaces around 1.0 and 0.45 nm wide.

Cell Membrane↗
PubMed1996

Induction of a permeability transition in rat kidney mitochondria by pentachlorobutadienyl cysteine: a beta-lyase-independent process.

A Ca2+-dependent inner mitochondrial membrane permeability transition is induced by a number of agents, an effect which is thought to cause cytotoxicity. This transition involves formation of a pore allowing the passage of solutes of up to 1500 Da; it is blocked by cyclosporine A and Ca2+ chelating agents. The mitochondrial nephrotoxicant S-(1,2,3,4, 4-pentachlorobutadienyl)-L-cysteine (PCBC) caused collapse of the mitochondrial membrane potential, Ca2+-independent oxidation of pyridine nucleotides and release of accumulated Ca2+ in isolated rat kidney mitochondria, three hallmarks of the permeability transition. These effects were blocked by cyclosporine A and by ethylene glycol bis(beta-aminoethyl ether) tetraacetic acid (EGTA). Furthermore, EGTA was capable of reversing the collapse of the membrane potential. These data indicate that PCBC induced an inner membrane permeability transition. Interestingly, addition of aminoxyacetic acid, a beta-lyase inhibitor, did not prevent the permeability transition, and a nonmetabolizable analog of PCBC, S-(1,2,3,4, 4-pentachlorobutadienyl)-L-alpha-methyl cysteine, induced the permeability transition. Thus PCBC may act to induce the permeability transition through a mechanism that does not require metabolism by a beta-lyase. Since metabolism by a beta-lyase is required for PCBC toxicity, it is not clear that the permeability transition is involved in cysteine conjugate-mediated renal cell injury.

Acetylcysteine↗
PubMed1996

A mitochondrial signal peptide from Neurospora crassa increases the permeability of isolated rat liver mitochondria.

Mitochondria that contain Ca2+ can be induced by a variety of triggering agents and conditions to undergo a permeability transition (PT); the inner membrane becomes nonselectively permeable to small solutes. Mastoparan, an amphipathic peptide from wasp venom, has recently been reported to induce this transition (Pfeiffer et al., 1995, J. Biol. Chem. 270,4923). We have examined the effect on the permeability of isolated rat liver mitochondria of a second amphipathic peptide, the signal sequence of cytochrome oxidase subunit IV from Neurospora crassa (pCoxIV, amino acids 3-22), which targets subunit IV to its mitochondrial location. Permeability increases were visualized via mitochondrial swelling with the following results. (1) pCoxIV (5-100 microM) induced concentration-dependent mitochondrial swelling. Control peptides from the N- and C-termini of the voltage-dependent anion-selective channel had no such effect. (2) Swelling required mitochondrial energization; it was eliminated or halted by the uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone. (3) Peptide-induced swelling was slowed by increasing concentrations of KCl. (4) Swelling was enhanced by inorganic phosphate (<1 mM). (5) Trifluoperazine (50 microM), propranolol (0.5 mM), and dibucaine (0.5 mM) were potent inhibitors of peptide-induced swelling, whereas other inhibitors of the classical PT (cyclosporin A, EGTA, and ADP) inhibited only partially. (6) pCoxIV opened a pore rather than disrupting mitochondrial membrane structure, but 50% inhibition of peptide-induced swelling required polyethylene glycol of molecular weight substantially larger than that needed to inhibit the Ca2+-induced PT to the same extent. In summary, pCoxIV opens a pore in isolated mitochondria. The dependence of pore opening on membrane potential and the inhibition of the peptide-induced permeability increase by increasing salt concentration suggest that this effect of the signal peptide is related to its interactions with mitochondria during protein import. The peptide-induced pore appears, however, to be distinct from both the classical permeability transition pore and the mastoparan-induced permeability increase.

Amino Acid Sequence↗
PubMed2002

The permeability of synthetic fractal aggregates with realistic three-dimensional structure.

The permeability of fractal porous aggregates with realistic three-dimensional structure is investigated theoretically using model aggregates composed of identical spherical primary particles. Synthetic aggregates are generated by several techniques, including a lattice-based method, simulation of aggregation by differential settling and turbulent shear, and the specification of simple cubic structures, resulting in aggregates characterized by the number of primary particles, solid fraction, characteristic radius, and fractal dimension. Stokesian dynamics is used to determine the total hydrodynamic force on and the distribution of velocity within an aggregate exposed to a uniform flow. The aggregate permeability is calculated by comparing these values with the total force and velocity distribution calculated from the Brinkman equation applied locally and to the entire aggregate using permeability expressions from the literature. The relationship between the aggregate permeability and solid fraction is found to be best predicted by permeability expressions based on cylindrical rather than spherical geometrical elements, the latter tending to underestimate the aggregate permeability significantly. The permeability expressions of Jackson and James or Davies provide good estimates of the force on and flow through porous aggregates of known structure. These relationships are used to identify a number of general characteristics of fractal aggregates.

Fractals↗
PubMed2002

Similar permeability responses to nitric oxide synthase inhibitors of venules from three animal species.

The influence of nitric oxide (NO) on microvascular permeability remains unclear. NO synthase (NOS) inhibitors have been reported to increase as well as to decrease permeability in different experimental models and animal species. We tested the hypothesis that NOS inhibitors influence venular permeability differently in amphibians and mammals. Permeability coefficients to albumin (P(alb)(s)) were measured on in situ mesenteric venules of the frog and rat and excised pig coronary venules before and after exposure to NOS inhibitors. Despite individual variability in magnitude of responses, NOS inhibitors resulted in a reduction in P(alb)(s) in each species. Superfusion with 10(-5) M N(G)-monomethyl-l-arginine (l-NMMA) reduced P(alb)(s) of frog mesenteric venules by 42% (from a median of 11.4 x 10(-7) cm s(-1), n = 12, P < 0.01) and by 67% in porcine coronary venules (from 12.5 x 10(-7) cm s(-1), n = 5, P < 0.05). The response was attenuated in rat mesenteric venules; 10(-4) M N(G)-nitro-l-arginine methyl ester (l-NAME) reduced P(alb)(s) by 23% (from 7.6 x 10(-7) cm s(-1), n = 9, P = 0.01). The inactive d-enantiomers of the NOS inhibitors were without effect on P(alb)(s) in each model. In pig venules, perfusion with blood modified the permeability responses to l-NMMA, suggesting that effects of NO on permeability are modified by one or more elements of blood. These data support a role of nitric oxide release on venular permeability to albumin that is conserved among the three animal species.

Albumins↗
PubMed1997

Toxicokinetics of indomethacin-induced intestinal permeability in the rat.

Numerous studies in humans have demonstrated increases in intestinal permeability resulting from the administration of non-steroidal anti-inflammatory drugs (NSAIDs). The increased permeability correlates well with ulceration. The time course of the changes in intestinal permeability, however, has not been studied, which makes comparative studies between different NSAIDs or different formulations of the same drug difficult. In the present study we have administered single doses of indomethacin to examine both the time course and pharmacokinetic/pharmacodynamic relationships of intestinal permeability in rats estimated by following the urinary excretion of [51Cr]-EDTA. The change in intestinal permeability was both time- and dose-dependent. Following both 10 mg kg-1 and 20 mg kg-1 oral doses of indomethacin, there was a rapid rise in intestinal permeability to a maximum level, after at least 12 h post-dose, which is longer than those previously observed for ibuprofen, ketoprofen, flurbiprofen and naproxen. The maximal effect lasted 12 and 36 h following 10 and 20 mg kg-1 doses, respectively. The side-effect-plasma concentration relationship demonstrated a counter-clockwise hysteresis. The relationship between the observed side-effect and the estimated deep effect compartment concentration was, on the other hand, linear. In comparative permeability studies of NSAIDs the time of administration, concentration and drug dependencies should be considered.

Animals↗
PubMed1983

Neurogenic control of blood-brain barrier permeability.

Evidence from several laboratories strongly suggests that brain capillaries play a dynamic role in the regulation of the internal environment of the brain and, further, that these activities are under neuroendocrine control. First, brain capillaries exhibit a number of anatomical and biochemical features unique to membranes known to regulate water and electrolyte permeability. These include tight junctions between endothelial cells, a high mitochondrial content and a unique compliment of intracellular enzymes. Second, brain capillaries appear to be functionally innervated by adrenergic neurons originating in brain. Finally, brain capillaries exhibit several functional characteristics of membranes that dynamically regulate water and electrolyte permeabilities. These include a restricted permeability to water, a prompt and reversible increase in water permeability to transient hyperosmolarity, a prompt and reversible decrease in permeability to increase perfusion pressure, a change in permeability associated with activation of the central as well as peripheral sympathetic nervous system, and an increase in permeability to centrally administered vasopressin as well as angiotensin II.

Animals↗
PubMed1992

The permeability of reconstituted liposomes containing the purified lens fiber cell integral membrane proteins MP20, MP26 and MP70.

A number of lens fiber cell integral membrane proteins have been localized to junctional regions where they have been proposed to play a role in either mediating or controlling cell-to-cell communication. We have examined the effect of three lens fiber cell membrane proteins, MP20, MP26 and MP70, on the permeability properties of unilamellar phospholipid liposomes. This approach has been previously used to examine the channel-forming properties of MP26. Liposome permeability was determined by measuring the effect of Co2+ on the quenching of the fluorescence of N-4-nitrobenzo-2-oxa-1,3 diazole phosphatidyl ethanolamine (NBD-PE)-containing liposomes as described previously by Scaglione and Rintoul (Invest. Ophthalmol. Vis. Sci. 30:961-966, 1989). The effect of all three proteins on liposome permeability was similar. Permeability was dependent on the protein/phospholipid ratio and was not significantly affected by agents known to modify gap junctional permeability in vivo. Glycophorin A, a non-channel-forming integral membrane protein derived from erythrocytes, was also shown to increase the permeability of unilamellar phospholipid liposomes. The ability of a non-channel membrane protein to increase Co2+ quenching of NBD-PE-containing liposomes (presumably in a nonspecific manner) indicates that reports describing the permeability of lens membrane protein-containing liposomes should be interpreted with caution in terms of their relationship to cell-to-cell communication.

Animals↗
PubMed1987

Cation permeability of the blood-brain barrier in streptozotocin-diabetic rats.

Decreased sodium permeability across the blood-brain barrier occurs in streptozotocin-treated rats after 2 weeks of diabetes. To establish whether this is a phenomenon specific for cations, the blood-brain barrier permeability for sodium, potassium and calcium was studied with an arterial integral uptake technique. Experiments were performed in control rats and, after two weeks after diabetes induction, in untreated streptozotocin-diabetic rats and in insulin-treated streptozotocin rats. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 35% (5.2 +/- 1.7 vs 3.4 +/- 1.1 10(-5).cm3.s-1.g-1) and potassium permeability by 39% (19.8 +/- 5.7 vs 12.1 +/- 3.9 10(-5).cm3.s-1.g-1), whereas no differences in calcium permeability occurred. Insulin treatment was associated with an increase in the blood-brain barrier permeability to sodium (4.8 +/- 1.0 10(-5).cm3.s-1.g-1) as compared to untreated diabetes (3.4 +/- 1.1 10(-5).cm3.s-1.g-1). It is concluded that the observed changes in sodium and potassium permeability cannot be caused by electrostatic membrane changes. More specific abnormalities of the transport of sodium and potassium across the blood-brain barrier are likely to occur; disturbances in the sodium-potassium-pump activity could account for such alterations.

Animals↗
PubMed1981

The effect of prostaglandin E2 and ADH on diffusional water permeability in collecting duct of an isolated rat papilla.

The effect of prostaglandin on diffusional water permeability has been studied in collecting ducts in an isolated rat papilla. PGE2 increased water permeability. The effect was significant at a concentration of 10(-8) mol 1(-1) and was maximal with a concentration of 10(-6) mol 1(-1). The maximal increment of 0.94 +/- 0.10 (SEM) micron s-1 was approximately half that produced by maximal stimulation with antidiuretic hormone (2.18 +/- 0.12 micron s-1). A concentration of 10(-8) mol 1(-1) produced an increase in basal water permeability and 24 mu unit ml-1 ADH, which without PGE2 present gave a similar increase, had no incremental effect. ADH 100 mu unit ml-1 increased permeability to a value similar to that observed in the absence of PGE2. Thus PGE2 and ADH both increase water permeability but the increments are not additive. Indomethacin in a concentration that inhibited prostaglandin production altered the response of the collecting duct to ADH. The dose response curve was shifted to the left and the maximal increase in water permeability and the lowest dose at which a response occurred took place at concentrations less than 1/2 those required in its absence. Prostaglandins influence the action of ADH and it is likely that in life they regulate and modulate the change in water permeability induced by anti-diuretic hormone.

Animals↗
PubMed1995

Influence of topical cyclosporine A and dissolvent on corneal epithelium permeability of fluorescein.

The corneal stroma is the major barrier to penetration for the lipophilic Cyclosporine A (CsA) molecule and prevents the use of the common ophthalmic solvents. At present, corn oil, castor oil and olive oil are the three most commonly used vehicles. The aim of this study was to determine the effect that topically applied CsA dissolved in different oils has on corneal epithelial permeability measured by fluorophotometry. Forty healthy volunteers, with absence of ocular or systemic disease and not receiving topical or systemic drugs were enrolled. Measurements were taken before and 45 min after the instillation of 40 microliters of a 2% aqueous solution of sodium fluorescein without preservatives. Basal corneal permeability and the permeability 24 h after the instillation of 2% CsA-olive oil, olive oil alone, 2% CsA-castor oil, castor oil alone, 2% CsA-corn oil and corn oil alone, were calculated. To prepare the topical 2% CsA, a Sandimmun oral solution (Sandoz, Basel, Switzerland) was employed under sterile conditions. We found that epithelial permeability 24 h after the instillation of any CsA formulations or solvents increased more than 6.62 times (p <0.001). No differences in corneal permeability values were found between any of the CsA formulations and the vehicles. We conclude that oils used to dissolve CsA are mainly responsible for the increased corneal epithelial permeability. No differences were found in the effects of the tested solvents on corneal epithelial permeability.

Administration, Topical↗
PubMed1991

[Intestinal permeability in patients with acquired immunodeficiency syndrome (AIDS)].

Intestinal permeability has been assessed as a parameter of the small intestinal barrier function in 33 patients with AIDS (WR 6), in 25 healthy volunteers, 32 patients with Crohn's disease, 18 patients with ulcerative colitis and in 12 patients with untreated coeliac disease. Permeability was measured by means of the 5 hour urinary excretion of lactulose and rhamnose after administration of these sugars (1 g rhamnose, 10 g lactulose) which allowed to calculate the urinary lactulose/rhamnose--ratio (L/R-r) as an index of intestinal permeability. Compared to the controls (L/R-r = 0.014 +/- 0.010) patients with AIDS had significantly increased lactulose/rhamnose--ratios (0.189 +/- 0.164; p less than 0.01) indicating abnormal permeation both of lactulose and rhamnose. This alteration of intestinal permeability was more pronounced than the significant increase of the L/R-r in the patients with either Crohn's disease or coeliac disease. However, intestinal permeability was not altered in the patients with ulcerative colitis. Among the patients with AIDS, the most abnormal permeability ratios were observed in two subjects with intestinal cryptosporidiosis. This investigation demonstrates by means of the "double sugar ratio", that intestinal permeability in patients with AIDS is highly abnormal, the impairment being even more abnormal than in patients with other small intestinal disease.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Diacylglycerol downregulates junctional membrane permeability. TMB-8 blocks this effect.

We tested the question whether junctional cell-to-cell communication is regulated by the diacylglycerol branch of the phosphoinositide transmembrane signal pathway. Cultured epithelial rat liver cells were treated with the synthetic diacylglycerol 1-oleoyl-2-acetyl glycerol, while their junctional permeability was probed with the microinjected 443-dalton fluorescent tracer Lucifer Yellow. The treatment reduced junctional permeability (without affecting Lucifer permeability of nonjunctional cell membrane). The effect was dose dependent, with a threshold of about 25 micrograms diacylglycerol/ml in sparse cultures and about 50 micrograms/ml in confluent cultures. The reduction of junctional permeability began within 3 min of diacylglycerol application, peaked within 20 min, and reversed spontaneously within 90 min. The phorbol ester TPA mimicked the diacylglycerol effect, but the (spontaneous) reversal was slower. We propose that cell-to-cell communication is under dual physiological control: an up-regulatory one, as exerted by the cyclic AMP signal route (Loewenstein, W.R., 1985, Biochem. Soc. Symp. London, 50: 43-58), and a downregulatory one, by the diacylglycerol signal route. TMB-8 (54-70 microM)--a blocker of intracellular Ca2+ mobilization--impeded the diacylglycerol action on junctional permeability. It prevented the effect of low diacylglycerol doses completely and it markedly reduced the effect of high doses. (It also counteracted the effect of TPA.) Ca2+ thus emerges as a possible candidate for a role in the junctional downregulation by the diacylglycerol signal route. We tentatively advance two models. In one, leaning closely on the Calcium Hypothesis of cell-to-cell channel regulation (Loewenstein, W.R., 1966, Ann. N.Y. Acad. Sci. 137:441-472), Ca2+ mediates the action of the route on the channel. In the other, Ca2+ acts farther removed from the channel, on protein kinase C. Calmidazolium (5-10 microM)--an inhibitor of calmodulinactivated proteins--did not prevent the diacylglycerol-induced reduction of junctional permeability. Nor did sodium orthovanadate (25 or 50 microM)--an inhibitor of tyrosyl phosphatase--prevent the reversal of diacylglycerol-induced (or TPA-induced) reduction of junctional permeability.

Animals↗
PubMed1986

Vascular permeability changes by proteinase inhibitors in carrageenin-induced inflammation in rats.

The effect of proteinase inhibitors such as TLCK, TPCK and leupeptin on vascular permeability was investigated in the carrageenin-air-pouch inflammation in rats. When each inhibitor was injected into the air-pouch immediately after carrageenin injection, TLCK, TPCK and leupeptin caused a rapid and significant increase in vascular permeability. The TLCK- and TPCK-induced increase declined gradually, whereas leupeptin inhibited the vascular permeability after the temporary increase. When the inhibitors were injected 5 h after carrageenin injection, TLCK and TPCK increased the vascular permeability, whereas leupeptin was without effect. Cyproheptadine, an anti-histamine and antiserotonin drug, inhibited the leupeptin-induced temporary increase, but failed to inhibit the TLCK- and TPCK-induced increase in vascular permeability. These results suggest that the leupeptin-induced increase in vascular permeability was mediated by histamine and serotonin, while TLCK and TPCK may increase vascular permeability as a result of a direct action on endothelial cells.

Animals↗
PubMed1981

Cell junction and cycle AMP: III. Promotion of junctional membrane permeability and junctional membrane particles in a junction-deficient cell type.

The cyclic nucleotide effect on junction was studied in C1-1D cells, a mouse cancer cell type that fails to make permeable junctions in ordinary confluent culture. Upon administration of cyclic AMP, dibutyryl cyclic AMP, dibutyryl cyclic AMP plus caffeine (db-cAMP-caffeine), or cholera toxin (an adenylate cyclase activator), the cells acquired permeable junctions; they became electrically coupled and transferred fluorescent tracer molecules among each other - a transfer exhibiting the molecular size limit of permeation of normal cell-to-cell channels. The effect took several hours to develop. With the db-cAMP-caffeine treatment, junctional permeability emerged within two hours in one-fifth of the cell population, and within the next few hours in the entire population. This development was not prevented by the cytokinesis inhibitor cytochalasin B. Permeable junctions formed also in two other conditions where the cell-endogenous cyclic AMP level may be expected to increase: serum starvation and low cell density. After three weeks of starving, the cells of serum, a junctional permeability arose in confluent cultures, which on feeding with serum disappeared within two to three days. At low cell density, namely below confluency, the cells made permeable junctions, unstarved. In cultures of rather uniform density, the frequency of permeable junctions was inversely related to the average density, over the subconfluent range; at densities of about 1 X 10(4) cells/cm2, where the cells had few mutual contacts, 80% of the pairs presumed to be in contact were electrically coupled. In cultures with adjoining territories of high (confluent) and low cell density, there was coupling only in the last, and in this low-density state the cells were also capable of coupling with other mammalian cell types (mouse 3T3-BalbC and human Lesch-Nyhan cells).

Animals↗
PubMed1992

The effect of prednisolone on substance P-induced vascular permeability in mice.

The effect of prednisolone on the substance P (SP)-induced vascular permeability increase in male ddY, WBB6 F1(-)+/+ (control) and WBB6 F1-W/WV (no mast cell in skin or internal organs) mice was investigated. 1) SP (1-10,000 pg/site) increased vascular permeability in ddY, WBB6 F1(-)+/+ and WBB6 F1-W/WV mice ears. 2) SP (100 pg/site)-induced vascular permeability was inhibited by prednisolone (10 mg/kg) administered intraperitoneally 3 to 12 hours prior to the elicitation of the reaction in ddY mice. When dexamethasone at a dose of 1 mg/kg was administered intraperitoneally 2 to 24 hours prior to the elicitation of the reaction, significant inhibition was observed. When prednisolone was administered intraperitoneally 8 hours prior to the elicitation of the reaction, the SP-induced capillary permeability increase in both ddY and WBB6 F1-W/WV mice was clearly inhibited by the drug at doses of 5 and 10 mg/kg. 3) Diphenhydramine (1 and 10 mg/kg) inhibited SP-induced vascular reaction in ddY mice but not in WBB6 F1-W/WV mice. 4) Atropine (10 mg/kg) inhibited SP-induced vascular reaction in both ddY and WBB6 F1-W/WV mice. But acetylcholine did not cause an increase of vascular permeability in ddY and WBB6 F1-W/WV mice ears. 5) Prednisolone (5 mg/kg) inhibited histamine- and serotonin-induced vascular permeability in ddY and WBB6 F1-W/WV mice ears. 6) Prednisolone (5 and 10 mg/kg) inhibited the SP-induced histamine release from ddY mice peritoneal mast cells. These results suggest that the vascular effect of SP is mediated by both mast cell dependent (release of histamine from mast cells) and mast cell independent mechanisms. Prednisolone inhibits the SP-induced vascular permeability mediated by both mechanisms in mice.

Animals↗