Calcium pyrophosphate-induced pleurisy in rats: a new model of acute inflammation. 1975.
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Acute Disease↗
Biomedical subjects
F Capasso
Publications and source records attributed to F Capasso.
Platelet activating factor potentiates rat paw oedema induced by different phlogogen agents.
Carrageenin oedema is enhanced by the simultaneous injection in the rat paw of platelet activating factor (PAF). The enhancement of carrageenin oedema is observed throughout the time course of the experiments. This enhancement is also present when the oedema-producing agent is dextran, cellulose sulphate, histamine, 5-hydroxytryptamine, bradykinin or prostaglandin E2. Both verapamil and BN 52021 abolished the enhancement induced by PAF without modifying significantly carrageenin oedema. In essential fatty acid deficient (EFAD) rats depleted of kininogen and amines, carrageenin oedema is not modified by PAF. These findings suggest that PAF interacts with other inflammatory mediators regulating the formation of oedema induced by irritants injected locally.
Animals↗
Nitric oxide as a mediator of the laxative action of magnesium sulphate.
1. Magnesium sulphate was studied for its effects on diarrhoea, fluid secretion, gastrointestinal transit and nitric oxide (NO) synthase activity in rats. 2. At a dose of 2 g kg-1 orally magnesium sulphate produced diarrhoea that was delayed in onset and intensity in a dose-related manner by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). This was prevented by the NO precursor, L-arginine and the NO donating compound, isosorbide-5-mononitrate (IMN). 3. Nitric oxide synthase activity was stimulated in gut tissue from rats given magnesium sulphate and this was inhibited by L-NAME. Dexamethasone (1 mg kg-1, i.p.), an inhibitor of inducible NO synthase, had no effect on magnesium sulphate-induced diarrhoea. 4. Magnesium sulphate stimulated fluid and electrolyte accumulation in the intestinal lumen; these effects were prevented by L-NAME but not D-NAME. 5. Gastrointestinal transit of a non-absorbable marker (charcoal suspension) was increased by oral magnesium sulphate from a mean value of 54.1% to 72.9% (P < 0.01), and this was prevented by pretreatment with L-NAME. 6. The results demonstrate that oral magnesium sulphate produces diarrhoea in rats by increasing the accumulation of fluid in the intestinal lumen and enhancing flow from the proximal to distal intestine. The mechanism involves release of NO, probably through stimulation of the constitutive form of NO synthase. Whether or not the effects of magnesium sulphate are due to an osmotic action or an intrinsic effect of the magnesium or sulphate ions cannot be determined from these experiments.
Amino Acid Oxidoreductases↗
Dissociation of castor oil-induced diarrhoea and intestinal mucosal injury in rat: effect of NG-nitro-L-arginine methyl ester.
1. Castor oil (2 ml orally) produced diarrhoea in rats 1-7 h after challenge, which was associated with gross damage to the duodenal and jejunal mucosa. 2. The injury was accompanied by release of acid phosphatase into the gut lumen, indicating cellular injury. 3. Intraperitoneal injection of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 2.5-50 mg kg-1 twice), prevented the diarrhoea. The dose of L-NAME (50 mg kg-1) completely blocked the diarrhoea but increased the release of acid phosphatase and worsened the gross damage. 4. The NO donating compound, isosorbide-5-mononitrate (IMN, 150 mg kg-1 twice) reversed the effects of L-NAME (50 mg kg-1) on castor oil-induced diarrhoea, gross damage and acid phosphatase release. 5. The apparent dissociation of the diarrhoeal and intestinal mucosal damaging effects of castor oil suggest that NO has a protective effect on the rat duodenal and jejunal mucosa, but that NO mediates, in part, the diarrhoea effect of this laxative.
Acid Phosphatase↗
Nitric oxide as a mediator of bisacodyl and phenolphthalein laxative action: induction of nitric oxide synthase.
Bisacodyl and phenolphthalein are diphenylmethane laxatives that have effects on intestinal water and electrolyte transport and smooth muscle contractility. Nitric oxide (NO) is produced in the intestine, where it stimulates electrolyte secretion and relaxes smooth muscle. Therefore, we studied in rats the effect of these laxatives on diarrhea, fluid transport in vivo, gastrointestinal transit and NO synthase activity in the absence and presence of inhibitors of NO synthesis. Both laxatives (50 mg/kg p.o.) produced diarrhea, which was delayed in onset by 25 mg/kg (i.p.) of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). The L-NAME effect was reversed by the NO donor isosorbide-5-mononitrate (30-120 mg/kg i.p.). L-Arginine (600 and 1500 mg/kg i.p.) prevented the inhibitory effect of L-NAME on diarrhea. The laxatives evoked water and electrolyte secretion and enhanced the transit of a suspension of charcoal through the gastrointestinal tract. This was inhibited by L-NAME but not D-NAME. The inhibitor of inducible NO synthase, dexamethasone (0.03-0.3 mg/kg i.p.), prevented the effects of both laxatives on electrolyte and water transport. Stimulation by these drugs of NO synthase was also inhibited by dexamethasone. The results demonstrate that bisacodyl and phenolphthalein stimulate water and electrolyte secretion, promote transit of intraluminal contents and produce diarrhea in association with enhanced production of NO. Furthermore, it appears that the NO is derived principally from activation of an inducible form of NO synthase.
Amino Acid Oxidoreductases↗
Essential fatty acid-deficient diet modifies PAF levels in stomach and duodenum of endotoxin-treated rats.
Platelet-activating factor (PAF) is thought to play an important role in pathogenesis of endotoxin shock. Here, using essential fatty acid deficient (EFAD) rats, we have evaluated changes in mean arterial blood pressure, PAF levels and damage in both stomach and duodenum following intravenous administration of endotoxin (LPS). In EFAD rats the second phase of LPS-induced hypotension was strongly reduced. Similarly, PAF levels in stomach and duodenum of EFAD rats were also reduced and correlated to the diminished damage. Our study confirms a direct involvement of PAF in LPS-induced gastrointestinal damage.
Animals↗
Nitric oxide and castor oil-induced diarrhea.
The effect of NG-nitro-L-arginine methyl ester (L-NAME) on castor oil-induced diarrhea was studied in control rats and those treated with isosorbide dinitrate or isosorbide-5-mononitrate. Castor oil (2 ml) produced diarrhea that lasted at least 8 h. Pretreatment of the rats with L-NAME (1-25 mg/kg i.p.) 15 min before castor oil did not block the castor oil-induced diarrhea beyond 3 h after challenge but delayed its appearance (P < .05-.001). However, diarrhea was inhibited (P < .01-.001) during the entire 8 h if rats were treated twice with L-NAME (25 mg/kg) (15 min before and 3 h after castor oil). These findings suggest that L-NAME, once administered, loses its activity 3 h after its administration. The nitric oxide synthase substrate, L-arginine (150-600 mg/kg), reversed (P < .05-.01) the inhibitory effect of L-NAME on diarrhea induced by castor oil. This effect is enantiomer-specific because D-arginine (900 mg/kg) was without an effect. These results suggest that castor oil-induced diarrhea in rats involves the L-arginine nitric oxide pathway. This is further supported by the effect of isosorbide dinitrate (0.6-120 mg/kg) and isosorbide-5-mononitrate (0.6-120 mg/kg). When administered to castor oil-treated rats, these two nitric oxide-generating agents prevented in a dose-dependent fashion (P < .01-.001) the inhibitory effect of L-NAME (25 mg/kg).
Animals↗
Suppression of optical absorption by electric-field-induced quantum interference in coupled potential wells.
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Journal Article↗
Inhibitors of nitric oxide synthase enhance rat ileum contractions induced by ricinoleic acid in vitro.
The effects of NG-nitro-L-arginine methyl ester (L-NAME) and NG-monomethyl-L-arginine (L-NMMA), inhibitors of nitric oxide (NO) synthase, were studied on ricinoleic acid-evoked contractions in rat isolated ileum. Ricinoleic acid (10(-5) to 10(-4) M) caused a concentration-dependent contraction. Addition of L-NAME (30-300 microM) or L-NMMA (30-300 microM) to the Tyrode's solution increased in a concentration-dependent fashion the amplitude of the ricinoleic acid-evoked responses. L-Arginine (900 microM), a natural substrate of NO synthase, but not D-arginine (900 microM), counteracted the effect of L-NAME (300 microM). The potentiating effect of L-NAME was also prevented by sodium nitroprusside (0.1-1 microM), a generator of NO. These results provide evidence that endogenous NO may modulate the contraction of rat ileum induced by ricinoleic acid. As the contraction induced by ricinoleic acid is not blocked by tetrodotoxin (0.6 and 6.0 microM) the contractile effect of ricinoleic acid results mainly from a direct action on the smooth muscle.
Amino Acid Oxidoreductases↗
Inhibitors of nitric oxide synthetase prevent castor-oil-induced diarrhoea in the rat.
1. Castor oil (2 ml orally) produced copious diarrhoea in rats 3 h after its administration. 2. Pretreatment (intraperitoneal, i.p.) of rats with the NO synthesis inhibitors NG-nitro-L-arginine methyl ester (L-NAME, 1-25 mg kg-1) and NG-monomethyl-L-arginine (L-NMMA, 2.5-100 mg kg-1) inhibited or prevented castor-oil-induced diarrhoea. L-Arginine (150-600 mg kg-1, i.p.) administered to rats pretreated with L-NAME 10 mg kg-1, drastically reduced the antidiarrhoeal activity of L-NAME in a dose-related manner. D-Arginine (900 mg kg-1) did not modify the protection by L-NAME. 3. Pretreatment (i.p.) of rats with L-NAME (2.5-25 mg kg-1) decreased the intestinal fluid accumulation and Na+ secretion induced by castor oil. L-Arginine (600 mg kg-1) but not D-arginine (900 mg kg-1) counteracted the inhibitory effect of L-NAME (10 mg kg-1). 4. L-NAME (10 and 25 mg kg-1) had no significant effect on the intestinal transit in normal rats or those given castor oil. 5. These results provide evidence that nitric oxide (NO) could play an important role in castor-oil-induced diarrhoea.
Amino Acid Oxidoreductases↗
Increased ex-vivo colonic generation of PAF induced by diphenylmethane stimulant laxatives in rats, mice, guinea-pigs and rabbits.
The effects of in-vivo treatment with bisacodyl, phenolphthalein, picosulphate, sulphosuccinate, mannitol and lactulose laxatives were examined on the ex-vivo formation of platelet-activating factor (PAF) by duodenum and colon of rat, mouse, guinea-pig and rabbit. Bisacodyl (10 mg kg-1), phenolphthalein (20 mg kg-1) and picosulphate (10 mg kg-1), but not sulphosuccinate (40 mg kg-1), mannitol (50 mg kg-1) or lactulose (50 mg kg-1), at doses that all caused laxation, markedly increased PAF in the colon (P < 0.01) but not in the duodenum. Intraluminal release of acid phosphatase was also significantly increased in the colon of rats treated with bisacodyl, phenolphthalein and picosulphate, but not in colons of animals treated with sulphosuccinate, mannitol or lactulose. The data show that enhanced generation of PAF is associated with the colonic damage induced by diphenylmethane laxatives, but do not show whether this is a cause or a consequence of the pathophysiological changes.
Acid Phosphatase↗
Platelet activating factor and the responses of rat isolated stomach strip to prostaglandin E2.
The effect of platelet activating factor (PAF) on contractions evoked by acetylcholine, 5-hydroxytryptamine (5-HT) and prostaglandin E2 (PGE2) was studied in-vitro on rat stomach strip. Addition of PAF to the organ bath increased PGE- but not 5-HT- or acetylcholine-evoked responses. The effect of PAF was unaffected by atropine, methysergide or indomethacin, but prevented by a specific PAF receptor antagonist BN 52021. The data support a specific interaction between PAF and PGE2 on rat stomach strip.
Acetylcholine↗
Inhibition of intestinal motility and secretion by flavonoids in mice and rats: structure-activity relationships.
Intraperitoneal administration of some flavonoids (apigenin, flavone, kaempferol, morin, myricetin, naringin and rutin; 12.5-50 mg kg-1) significantly (P < 0.05-0.01) reduced small (28-69%) and large (83-134%) intestinal transit in mice. Other flavonoids (naringenin, silibinin, silymarin and taxifolin, 100-200 mg kg-1) reduced (23-41%; P < 0.05-0.01) intestinal transit at doses of 100-200 mg kg-1 while hesperitin, catechin and phloridzin (up to 200 mg kg-1) had no effect. This effect was antagonized by yohimbine (87-96%) and phentolamine (87-91%) but not by prazosin, propranolol, atropine, hexamethonium, mepyramine, cyproheptadine and naloxone. Yohimbine (92-96%) also antagonized the inhibitory effect of flavonols (12.5-50 mg kg-1) (P < 0.05-0.01) on intraluminal accumulation of fluid and diarrhoea induced by castor oil. By contrast, verapamil potentiated the flavonol effect. It is suggested that these effects, influenced by the structure of the molecules, are mediated by alpha 2-adrenergic receptors and calcium.
Animals↗
Effect of senna is not mediated by platelet-activating factor.
The effect of in vivo treatment with senna was examined on the ex vivo formation of platelet-activating factor (PAF) by small and large intestine of rat, mouse and guinea pig. A single or a prolonged oral administration of senna (60-240 mg/kg) to animals did not increase intestinal PAF content. Nor did senna increase the intraluminal release of acid phosphatase. A similar result was obtained in the colonic tissue of rat perfused in vitro with rhein (1-500 micrograms/ml) or rhein anthrone (1-500 micrograms/ml). In contrast, a single oral administration of phenolphthalein (20 mg/kg), bile salts (20 mg/kg) or magnesium sulfate (30 mg/kg) to rats increased intestinal PAF content. Magnesium sulfate also increased the intraluminal release of acid phosphatase. Colonic tissue of rats perfused in vitro with calcium ionophore A23187 (10 micrograms/ml) formed large amounts of PAF and acid phosphatase. PAF stimulates intestinal motility and secretion and mediates gut damage while acid phosphatase is a marker of cellular damage. Therefore, our data suggest that senna is well tolerated in animals and PAF does not mediate senna-induced laxation.
Acid Phosphatase↗
Chaotic quantum phenomena without classical counterpart.
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Journal Article↗
Giant, triply resonant, third-order nonlinear susceptibility chi 3 omega (3) in coupled quantum wells.
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Journal Article↗
Time course of PAF formation by gastrointestinal tissue in rats after castor oil challenge.
When castor oil was administered by gavage to rats, the duodenum and jejunum, but not the stomach, produced large amounts of platelet activating factor 3-7 h after oil challenge with a peak at 3 h. Intraluminal release of acid phosphatase was also markedly increased in the duodenum and jejunum of castor oil-treated rats, especially 3-5 h after oil challenge. No increase was observed in the stomach. There was a correlation between elevated release of acid phosphatase and intestinal hyperaemia.
Acid Phosphatase↗
Effects of senna and its active compounds rhein and rhein-anthrone on PAF formation by rat colon.
A single or a prolonged oral administration of senna (60 mg kg-1) to rats did not increase either colonic PAF (platelet activating factor) content or intraluminal release of acid phosphatase. A similar result was observed in the colonic tissue of rats perfused in-vitro with rhein (1-300 micrograms mL-1) or rhein-anthrone (1-300 micrograms mL-1). A single or prolonged administration of castor oil (2 mL) to rats increased both colonic PAF content and intraluminal release of acid phosphatase. Colonic tissue of rats perfused in-vitro with calcium ionophore A23187 (1 and 10 micrograms mL-1) formed large amounts of PAF and acid phosphatase. Since PAF can mediate intestinal damage and acid phosphatase is a marker of cellular injury, we conclude that senna and its derivatives, rhein and rhein-anthrone, are well tolerated in rats.
Animals↗