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PubMed2005

Efficacy of lower doses of vanadium in restoring altered glucose metabolism and antioxidant status in diabetic rat lenses.

Vanadium compounds are potent in controlling elevated blood glucose levels in experimentally induced diabetes. However the toxicity associated with vanadium limits its role as therapeutic agent for diabetic treatment. A vanadium compound sodium orthovanadate (SOV) was given to alloxan-induced diabetic Wistar rats in lower doses in combination with Trigonella foenum graecum, a well-known hypoglycemic agent used in traditional Indian medicines. The effect of this combination was studied on lens morphology and glucose metabolism in diabetic rats. Lens, an insulin-independent tissue, was found severely affected in diabetes showing visual signs of cataract. Alterations in the activities of glucose metabolizing enzymes (hexokinase, aldose reductase, sorbitol dehydrogenase, glucose-6-phosphate dehydrogenase) and antioxidant enzymes (glutathione peroxidase, glutathione reductase) besides the levels of related metabolites, [sorbitol, fructose, glucose, thiobarbituric acid reactive species (TBARS) and reduced glutathione (GSH)] were observed in the lenses from diabetic rats and diabetic rats treated with insulin (2 IU/day), SOV (0.6 mg/ml), T. f. graecum seed powder (TSP, 5%) and TSP (5%) in combination with lowered dose of vanadium SOV (0.2 mg/ml), for a period of 3 weeks. The activity of the enzymes, hexokinase, aldose reductase and sorbitol dehydrogenase was significantly increased whereas the activity of glucose-6-phosphate dehydrogenase, glutathione peroxidase and glutathione reductase decreased significantly in lenses from 3 week diabetic rats. Significant increase in accumulation of metabolites, sorbitol, fructose, glucose was found in diabetic lenses. TBARS measure of peroxidation increased whereas the levels of antioxidant GSH decreased significantly in diabetic condition. Insulin restored the levels of altered enzyme activities and metabolites almost to control levels. Sodium orthovanadate (0.6 mg/ml) and Trigonella administered separately to diabetic animals could partially reverse the diabetic changes, metabolic and morphological, while vanadate in lowered dose in combination with Trigonella was found to be the most effective in restoring the altered lens metabolism and morphological appearance in diabetes. It may be concluded that vanadate at lowered doses administered in combination with Trigonella was the most effective in controlling the altered glucose metabolism and antioxidant status in diabetic lenses, these being significant factors involved in the development of diabetic complications, that reflects in the reduced lens opacity.

Analysis of Variance↗
PubMed1999

Effects of the soluble guanylyl cyclase activator, YC-1, on vascular tone, cyclic GMP levels and phosphodiesterase activity.

The vasomotor and cyclic GMP-elevating activity of YC-1, a novel NO-independent activator of soluble guanylyl cyclase (sGC), was studied in isolated rabbit aortic rings and compared to that of the NO donor compounds sodium nitroprusside (SNP) and NOC 18. Similarly to SNP and NOC 18, YC-1 (0.3-300 microM) caused a concentration-dependent, endothelium-independent relaxation that was greatly reduced by the sGC inhibitor 1-H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ 10 microM; 59% inhibition of dilation induced by 100 microM YC-1) suggesting the activation of sGC as one mechanism of action. Preincubation with YC-1 (3 and 30 microM) significantly increased the maximal dilator responses mediated by endogenous NO in aortic rings that was released upon exposure to acetylcholine, and enhanced the dilator response to the exogenous NO-donors, SNP and NOC 18, by almost two orders of magnitude. Vasoactivity induced by SNP and YC-1 displayed different kinetics as evidenced by a longlasting inhibition by YC-1 (300 microM) on the phenylephrine (PE)-induced contractile response, which was not fully reversible even after extensive washout (150 min) of YC-1, and was accompanied by a long-lasting elevation of intracellular cyclic GMP content. In contrast, SNP (30 microM) had no effect on the vasoconstrictor potency of PE, and increases in intravascular cyclic GMP levels were readily reversed after washout of this NO donor compound. Surprisingly, YC-1 not only activated sGC, but also affected cyclic GMP metabolism, as it inhibited both cyclic GMP break down in aortic extracts and the activity of phosphodiesterase isoforms 1-5 in vitro. In conclusion, YC-1 caused persistent elevation of intravascular cyclic GMP levels in vivo by activating sGC and inhibiting cyclic GMP break down. Thus, YC-1 is a highly effective vasodilator compound with a prolonged duration of action, and mechanisms that are unprecedented for any previously known sGC activator.

Animals↗
PubMed2002

[Studies on chemotactic behaviors of Strongyloides ratti infective larvae in vitro and migration routes of the larvae in rat head].

For the purpose of clarifying host-finding mechanisms, the infective larvae of Strongyloides ratti were run on an agarose plate which had been placed various attractants around the larvae. They were accumulated at the sites of sodium compounds, serum proteins and albumins. At 20, 30, 40 hours after infection, rats were killed and heads were separated. They were then processed for thin section specimens. Larvae were found in brains, olfactory bulbs and its nerves. These larvae seemed to move along olfactory nerves during descending from the cranial cavity. Another migration study was done by whole body autoradiography after 35S-methionine labeling for clarifying the larval pathway how to invade cranial cavity in the rats. They first crawled under subcutaneous region of rat and then accumulated at the tip of the nose. Next, they began to ascend olfactory nerves. They were in cranial cavity up to 20 hours after infection and then descending same route to nasal cavity. I don't know why they aim the cranial cavity but they had necessity to invade the cranial cavity and stay there for appropriate time to be an adult in the intestine.

Animals↗
PubMed2000

Tyrosine phosphatase inhibitors selectively antagonize beta-adrenergic receptor-dependent regulation of cardiac ion channels.

beta-Adrenergic receptor stimulation regulates the activity of several different cardiac ion channels through an adenylate cyclase/cAMP/protein kinase A-dependent mechanism. Previous work has suggested that basal tyrosine kinase activity attenuates the beta-adrenergic responsiveness of these cardiac ion channels, supporting the idea that tyrosine phosphorylation exerts an inhibitory effect at some point in the common signaling pathway. To determine which element in the beta-adrenergic pathway is regulated by tyrosine kinase activity, we studied the effects of various protein tyrosine phosphatase (PTP) inhibitors on the cAMP-dependent regulation of the L-type Ca(2+) current in guinea pig ventricular myocytes. Three such compounds, sodium orthovanadate, peroxovanadate, and bpV(phen), had no effect on the basal Ca(2+) current, yet each caused a pronounced inhibition of the Ca(2+) current stimulated by the beta-adrenergic receptor agonist isoproterenol. These observations are consistent with the idea that basal tyrosine kinase activity is capable of inhibiting beta-adrenergic responses. However, these PTP inhibitors had no effect on cAMP-dependent stimulation of the Ca(2+) current via activation of adenylate cyclase with forskolin or activation of H(2)-histaminergic receptors with histamine. These results are consistent with the idea that inhibition of PTP activity produces an inhibitory effect involving a tyrosine kinase-dependent mechanism acting selectively at the level of the beta-adrenergic receptor. This signaling mechanism does not seem to be linked to tyrosine kinase activity associated with insulin and insulin-like growth factor receptors, because acute exposure to agonists of these receptors did not inhibit isoproterenol regulation of the Ca(2+) current.

Animals↗
PubMed1997

Role of oxidative stress in the action of vanadium phosphotyrosine phosphatase inhibitors. Redox independent activation of NF-kappaB.

The role of intracellular oxidative stress in the mechanism of action of phosphotyrosine phosphatase (PTP) inhibitors was studied using three vanadium-based compounds. Sodium orthovanadate (Na3VO4), sodium oxodiperoxo(1,10-phenanthroline)vanadate(V) (pV(phen), and bis(maltolato)-oxovanadium(IV) (BMOV) differentially induced oxidative stress in lymphocytes. Treatment with pV(phen), which caused intracellular oxidation, induced strong protein tyrosine phosphorylation compared with Na3VO4 and BMOV. Syk family kinases and the mitogen-activated protein kinase erk2 were rapidly activated by pV(phen) but not by BMOV or Na3VO4. In contrast, both BMOV and pV(phen) strongly activated NF-kappaB. The antioxidant pyrrolidine dithiocarbamate (PDTC) greatly diminished the intracellular oxidation and protein phosphotyrosine accumulation induced by pV(phen). Pretreatment of cells with PDTC reduced and delayed the activation of Syk kinases and erk2. However, NF-kappaB activation by pV(phen) was markedly enhanced in lymphocytes pretreated with PDTC, and another antioxidant, N-acetylcysteine, did not prevent the activation of NF-kappaB by BMOV. These results indicate a role for oxidative stress in the biological effects of some PTP inhibitors, whereas NF-kappaB activation by PTP inhibitors is mediated by mechanisms independent of intracellular redox status.

Antioxidants↗
PubMed1999

Nitric oxide suppresses human T lymphocyte proliferation through IFN-gamma-dependent and IFN-gamma-independent induction of apoptosis.

Human normal and malignant T cells cease to proliferate, down-modulate Bcl-2 expression, and undergo apoptosis when cultured in the presence of NO-donor compounds (sodium nitroprusside and NOC12) for 48 h. At 72 h, cells that evade apoptosis start to proliferate again, overexpress both chains of the IFN-gammaR, and thus become susceptible to apoptosis in the presence of IFN-gamma. By contrast, in the presence of IFN-gamma, no apoptosis, but an increase of proliferation was displayed by control cultures of T cells not exposed to NO and not overexpressing IFN-gammaR chains. The NO-induced cell surface overexpression of IFN-gammaR chains did not affect the transduction of IFN-gamma-mediated signals, as shown by the expression of the transcription factor IFN regulatory factor 1 (IRF-1). However, transduction of these signals was quantitatively modified, because IFN-gamma induces enhanced levels of caspase-1 effector death in NO-treated cells. These findings identify NO as one of the environmental factors that critically govern the response of T cells to IFN-gamma. By inducing the overexpression of IFN-gammaR chains, NO decides whether IFN-gamma promotes cell proliferation or the induction of apoptosis.

Apoptosis↗
PubMed1984

Inhibition of carnitine palmitoyltransferase 1 by phenylalkyloxiranecarboxylic acid and its influence on lipolysis and glucose metabolism in isolated, perfused hearts of streptozotocin-diabetic rats.

The metabolic action of the new hypoglycemic compound, sodium-2-(5-[4-phenyl]-pentyl)-oxirane carboxylate (POCA), was studied in isolated perfused hearts of control and streptozotocin-diabetic rats. Perfusion with POCA selectively inhibited the activity of carnitine palmitoyltransferase 1, but had no influence on the activities of carnitine palmitoyltransferase 2, pyruvate dehydrogenase, and triglyceride lipase. Perfusing the hearts of streptozotocin-diabetic rats with POCA (10 mumol/L) reduced myocardial lipolysis and accelerated the rate of pyruvate and lactate outflow as well as pyruvate oxidation. The insulin sensitivity of the diabetic hearts with respect to lactate production and glucose oxidation was restored by perfusion with POCA. In contrast, defective glycogen synthesis in the diabetic hearts was not influenced by POCA. These data suggest that: (1) The insulin resistance of the glucose-perfused diabetic heart results from two different post-insulin-receptor defects. Whereas the disturbances of glucose oxidation are mediated by the excessive metabolism of endogenous triglycerides, the reason for the disturbed glycogen synthesis remains unclear. (2) Since in vitro perfusion with POCA partially restored the insulin sensitivity of the diabetic hearts, insulin-receptor defects should be of minor importance for the insulin resistance of diabetic hearts. (3) Since POCA inhibited carnitine palmitoyltransferase 1 and reduced the rate of lipolysis but had no effect on triglyceride lipase activity, we assume that product inhibition plays an important role in the regulation of myocardial lipolysis. In summary, inhibition of carnitine palmitoyltransferase 1 by POCA is suggested to be a useful approach for restoring insulin sensitivity depressed by an excessive metabolism of lipids.

Acyltransferases↗
PubMed2005

Modified boron neutron capture therapy for malignant gliomas performed using epithermal neutron and two boron compounds with different accumulation mechanisms: an efficacy study based on findings on neuroimages.

OBJECT: To improve the effectiveness of boron neutron capture therapy (BNCT) for malignant gliomas, the authors used epithermal rather than thermal neutrons for deep penetration and two boron compounds-sodium borocaptate (BSH) and boronophenylalanine (BPA)-with different accumulation mechanisms to increase the boron level in tumors while compensating for each other's faults. METHODS: Thirteen patients, 10 of whom harbored a glioblastoma multiforme (GBM), one a gliosarcoma, one an anaplastic astrocytoma, and one an anaplastic oligoastrocytoma, were treated using this modified BNCT between January 2002 and December 2003. Postoperatively, neuroimaging revealed that only one patient with a GBM had no lesion enhancement postoperatively. The patients underwent 18F-BPA positron emission tomography, if available, to assess the accumulation and distribution of BPA before neutron radiotherapy. The neutron fluence rate was estimated using the Simulation Environments for Radiotherapy Applications dose-planning system before irradiation. The patients' volume assessments were performed using magnetic resonance (MR) imaging or computerized tomography (CT) scanning. Improvements in the disease as seen on neuroimages were assessed between 2 and 7 days after irradiation to determine the initial effects of BNCT; its maximal effects were also analyzed on serial neuroimages. The mean tumor volume before BNCT was 42.3 cm3. Regardless of the pre-BNCT tumor volume, in every patient harboring an assessable lesion, improvements on MR or CT images were recognized both at the initial assessment (range of volume reduction rate 17.4-71%, mean rate 46.4%) and at follow-up assessments (range of volume reduction rates 30.3-87.6%, mean rate 58.5%). More than 50% of the contrast-enhanced lesions disappeared in eight of the 12 patients during the follow-up period. CONCLUSIONS: This modified BNCT produced a good improvement in malignant gliomas, as seen on neuroimages.

Adult↗
PubMed1975

Renal metastases simulating Kaposi sarcoma. Radionuclide scanning, an aid in diagnosis and treatment planning.

A case of renal cutaneous metastases simulated Kaposi sarcoma and the condition was misdiagnosed as Kaposi sarcoma. A new technique was employed using the isotope technetium 99m as the compound sodium pertechnetate Tc 99m for the diagnosis and evaluation of the extent of Kaposi sarcoma. The failure to demonstrate a positive isotope scan in our case was a clue to the incorrect diagnosis of Kaposi sarcoma.

Aged↗
PubMed1996

Kinetic analysis of the reaction between d(TTGGCCAA) and [Pt(NH3)3(H2O)]2+ by enzymatic degradation of the products and ESI and MALDI mass spectrometries.

The kinetics of the reaction between the octanucleotide d(TTGGCCAA) in the single-stranded form in pure water and the platinum complex [Pt(NH3)3(H2O)]2+ was investigated by electrospray ionization and matrix-assisted laser desorption/ionization (MALDI) mass spectrometries coupled with enzymatic degradation of the adducts. These methods led to the determination of specific rate constants of platination. The global rate constant characteristic of the formation of adducts on each 5'- or 3'-guanine were measured by electrospray ionization analysis. The ratios between the 5'- and 3'-adducts were determined from enzymatic degradation of the final reaction mixture and MALDI analysis. The platination in water is approximately eight times faster than in 0.1 M NaClO4. The selectivity of platination is a factor of 2 in favor of the 5'-guanine, and similar to that observed for the reaction between d(CTGGCTCA) and [Pt(NH3)3(H2O)]2+ in 0.1 M NaClO4.

DNA Adducts↗
PubMed1994

Functional coupling of a Ca2+/calmodulin-dependent nitric oxide synthase and a soluble guanylyl cyclase in vertebrate photoreceptor cells.

Electrophysiological recordings on retinal rod cells, horizontal cells and on-bipolar cells indicate that exogenous nitric oxide (NO) has neuromodulatory effects in the vertebrate retina. We report here endogenous NO formation in mammalian photoreceptor cells. Photoreceptor NO synthase resembled the neuronal NOS type I from mammalian brain. NOS activity utilized the substrate L-arginine (Km = 4 microM) and the cofactors NADPH, FAD, FMN and tetrahydrobiopterin. The activity showed a complete dependence on the free calcium concentration ([Ca2+]) and was mediated by calmodulin. NO synthase activity was sufficient to activate an endogenous soluble guanylyl cyclase that copurified in photoreceptor preparations. This functional coupling was strictly controlled by the free [Ca2+] (EC50 = 0.84 microM). Activation of the soluble guanylyl cyclase by endogenous NO was up to 100% of the maximal activation of this enzyme observed with the exogenous NO donor compound sodium nitroprusside. This NO/cGMP pathway was predominantly localized in inner and not in outer segments of photoreceptors. Immunocytochemically, we localized NO synthase type I mainly in the ellipsoid region of the inner segments and a soluble guanylyl cyclase in cell bodies of cone photoreceptor cells. We conclude that in photoreceptors endogenous NO is functionally coupled to a soluble guanylyl cyclase and suggest that it has a neuromodulatory role in visual transduction and in synaptic transmission in the outer retina.

Amino Acid Oxidoreductases↗
PubMed2004

Effects of MgO-CaO-P2O5-Na2O-based additives on mechanical and biological properties of hydroxyapatite.

In this research, we improved densification, hardness, and compression strength of synthetic hydroxyapatite (HAp) ceramics by introducing small quantities of MgO-CaO-P(2)O(5)-Na(2)O-based sintering additives. Biological properties of HAp were not altered by this procedure. Phase analyses were performed by using a Philips Xpert fully automated diffractometer with Co K-alpha radiation to understand the influence of additives on phase purity in the final products. All compositions were characterized at green and sintered densities to understand the influence of additives on densification. Some of the compositions showed >40% increase in Vickers microhardness compared with pure HAp processed under the same conditions. Improvement in compression strength was also detected in some compositions. In vitro biological testing used a modified human osteoblast cell line to test biocompatibility, cell attachment, and cell proliferation. All these compositions were nontoxic and biocompatible. Our results indicate that MgO-CaO-P(2)O(5)-Na(2)O-based sintering additives can be used to improve both mechanical and biological properties of HAp ceramics.

Biocompatible Materials↗
PubMed2002

In vitro evaluation of the permeation enhancing effect of polycarbophil-cysteine conjugates on the cornea of rabbits.

It was the aim of this study to investigate the permeation enhancing effect of thiolated polycarbophil on the cornea of rabbits in vitro. The proposed reaction mechanism involves the opening of the tight junctions in the corneal epithelium. The modification of polycarbophil was achieved via covalent attachment of L-cysteine mediated by a carbodiimide. Transcorneal permeation studies were performed in Ussing-type diffusion chambers. As model compounds, sodium fluorescein, as a marker for paracellular transport, and dexamethasone phosphate were used. To evaluate potential corneal damage the corneal hydration level of each cornea was determined. Polycarbophil-cysteine was found to increase the permeation of sodium fluorescein 2.2-fold and that of dexamethasone phosphate 2.4-fold in comparison to the unmodified polymer. The concentration of dexamethasone in the acceptor medium was 1.5-fold increased. As evidenced by the corneal hydration level, polycarbophil-cysteine did not damage the corneal tissues. Therefore, polycarbophil-cysteine conjugates seem to be promising excipients for ocular drug delivery systems where they might be used as safe permeation enhancers.

Acrylic Resins↗
PubMed1994

Induction of a heat shock response (HSP 72) in rat embryos exposed to selected chemical teratogens.

A monoclonal antibody to the 72 kD heat shock protein (HSP 72), Western blot analysis and 2-D gel electrophoresis/autoradiography were used to determine whether selected chemical teratogens induced the synthesis and accumulation of HSP 72 in postimplantation rat embryos exposed in vitro. The chemical teratogens studied include N-Acetoxy-2-acetylaminofluorene (N-Ac-AAF), cadmium chloride (CAD), cyclophosphamide (CP), sodium arsenite (AS), and sodium salicylate (SAL). Exposures to test chemicals were selected that produced obvious embryotoxicity characterized by abnormal development and growth retardation. Of the five chemical teratogens studied, AS and SAL induced the synthesis and accumulation of HSP 72 in day 10 rat embryos. The kinetics of HSP 72 accumulation, however, differed between AS- and SAL-treated embryos. Maximal levels of HSP 72 were observed 24 hours after AS exposure and 10 hours after SAL exposure. N-Ac-AAF, CD, and CP induced obvious embryotoxicity; however, none of these chemical teratogens induced HSP 72 at any of the timepoints assayed. Although only a small sample of chemical teratogens was studied, our results suggest that the heat shock response, characterized by the synthesis and accumulation of HSP 72, is not a general biomarker for chemical teratogens.

Abnormalities, Drug-Induced↗
PubMed1998

Release of two peripheral proteins from chloroplast thylakoid membranes in the presence of a Hofmeister series of chaotropic anions.

The dissociation of two peripheral spinach (Spinacia oleracea L.) thylakoid membrane proteins, coupling factor CF1 and ferredoxin-NADP+-oxidoreductase, in the presence of chaotropic sodium salts has been investigated, using monospecific antibodies against the proteins as probes. Release of both proteins followed the Hofmeister series of anions (Cl- < NO3- < Br- < I- < SCN-). In mixtures, the different salts had an additive effect. In addition, there were also qualitative differences in the action of the anions, such that NaI and NaSCN led to a different concentration and time dependence of the dissociation of the peripheral proteins from thylakoids. An analysis of the temperature dependence of protein release showed that the more chaotropic ions reduced the activation energy required for the dissociation of the proteins from their binding sites on the membrane. The addition of sugars (glucose, sucrose, or trehalose) reduced the amount of protein released from the membranes in the presence of NaI or NaSCN.

Binding Sites↗
PubMed2000

Influence of sodium ion dynamics on the 23Na quadrupolar interaction in sodalite: a high-temperature 23Na MAS NMR study.

High-temperature 33Na MAS NMR experiments up to 873 K for a number of different sodalites (Na8[AlSiO4]6(NO3)2, Na8[AlSiO4]6(NO2)2, Na8[AlSiO4]6I2, Na7.9[AlSiO4]6(SCN)7.9 x 0.5H2O, Na8[AlGeO4]6(NO3)2, and Na7[AlSiO4]6(H3O2) x 4H2O) were carried out. The spectra of the first five sodalites consist of a quadrupolar MAS pattern with different quadrupolar coupling constants. The quadrupolar interaction for the thiocyanate sodalite, the nitrate aluminosilicate, and germanate sodalite decreases strongly passing a coalescence state on heating, while the quadrupolar interaction of the iodide and nitrite sample shows nearly no change. The basic hydrosodalite shows an asymmetric lineshape at room temperature and, between 350 and 370 K, a second line due to the evaporation of cage-water emerges. The linewidth increases with rising temperature. The temperature dependence of the quadrupolar interaction seems to be a function of the sodalite beta-cage expansion. Two conceivable jump mechanisms are proposed for a tetrahedral two-site jump between occupied and unoccupied tetrahedral sites.

Magnetic Resonance Spectroscopy↗
PubMed1984

Energy dispersive X-ray analysis of tissue gold after silver amplification by physical development.

Rats were treated intraperitoneally with the gold-containing compounds sodium aurothiomalate (Myocrisin), sodium aurothiosulfate (Sanocrysin), and aurothioglucose. Using stem energy dispersive X-ray analysis, gold and silver were shown to be located at the same point in lysosomes of proximal tubular cells of the kidney, in hepatocytes and in macrophages of lymph glands, spleen and liver. This result indicates that, after exposure to ultraviolet radiation, chemically bound tissue gold is transformed to metallic gold that subsequently can catalyze the reduction of silver ions to silver when subjected to physical development, i.e. exposed to a photographic developer containing silver ions in addition to the reducing molecules.

Animals↗
PubMed1994

Protection against necrotizing agents-induced gastric lesions in rats. Unrelated to inhibition of gastric motility.

Effects of necrotizing agents, blockers of gastric motility, and mild irritants on gastric mucosa and gastric motility were investigated in conscious rats. Gastric motor activity was recorded using a miniature balloon placed in the glandular part of the stomach, which was connected to a pressure transducer and polygraph. Necrotizing agents, such as 96% ethanol, 0.6 N hydrochloric acid, 0.2 N sodium hydroxide, or 4 M sodium chloride, were given intragastrically through a fistula on the forestomach. One milliliter of these agents produced hemorrhagic bandlike lesions in the corpus mucosa along the long axis of the stomach with the occurrence of a complete inhibition of gastric motility (smooth muscle relaxation). Blockers of gastric motility alone, such as subcutaneous papaverine HCl (50 mg/kg), and intraperitoneal verapamil (20 mg/kg), or mild irritants (1 ml/rat, orally) such as 20% ethanol or 1 M NaCl, which by themselves suppressed gastric motility, have no effect on gastric mucosa and on the inhibited gastric motility induced by necrotizing agents. Bandlike lesions were significantly prevented by pretreatment with 20% ethanol or 1 M NaCl but not with papaverine HCl or verapamil administered 30 min before necrotizing agents. The gastroprotection offered by 20% ethanol or 1 M NaCl was significantly diminished by pretreatment with subcutaneous indomethacin (30 mg/kg), but the inhibited gastric motility was not reversed by indomethacin. These results indicate that it seems unlikely that gastric contractile activity would play a major role in the development and prevention of gastric lesions after the administration of necrotizing agents.

Animals↗