acid-phosphatase and Gastrointestinal-Hemorrhage

Topics: Acid Phosphatase; Adult; Aged; Alkaline Phosphatase; Bone Marrow Cells; Cerebral Hemorrhage; Daunorubicin; Female; Gastrointestinal Hemorrhage; Glucuronidase; Humans; Leukemia; Leukemia, Monocytic, Acute; Leukemia, Myeloid; Leukemia, Myeloid, Acute; Leukocytes; Male; Middle Aged; Monocytes; Muramidase; Naphthol AS D Esterase; Periodic Acid-Schiff Reaction; Peroxidases; Pregnancy; Prognosis; Remission, Spontaneous

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.

Topics: Acid Phosphatase; Animals; Arginine; Castor Oil; Diarrhea; Dose-Response Relationship, Drug; Gastrointestinal Hemorrhage; Intestinal Mucosa; Isosorbide Dinitrate; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Rats; Rats, Wistar; Vasodilator Agents

The ability of prostaglandin E2 (PGE2) and its analogue, 16,16-dimethyl PGE2 (dmPGE2) to protect the rat gastric mucosa from damage has been investigated using the release of enzyme markers as an index of surface cell disruption. These studies have been extended to investigate whether prostanoids can also enhance the rapid repair process which re-establishes epithelial continuity. With low oral doses of PGE2 (100 micrograms kg-1) and dmPGE2 (2.5 micrograms kg-1), the deep necrotic damage induced by intragastric instillation of ethanol was inhibited, yet the mucosal enzyme release (acid phosphatase and lactate dehydrogenase) determined in vitro was unaltered. At higher doses, both prostanoids reduced enzyme release, suggesting some preservation or rapid re-establishment of epithelial cell continuity under these conditions. Studies utilizing the gastric chamber indicated that high doses of dmPGE2 (20-40 micrograms kg-1) reduced the changes in potential difference and potassium efflux following challenge with 50% ethanol, and accelerated the rate of recovery of these parameters. Furthermore, a reduced level of epithelial cell discontinuity was determined by histological techniques. Thus, prostanoids not only protect deeper mucosal cells from necrotic damage by local irritants, but may protect the surface cells at higher doses under some conditions, and may enhance the process of epithelial restitution.

Topics: 16,16-Dimethylprostaglandin E2; Acid Phosphatase; Animals; Dinoprostone; Ethanol; Gastric Mucosa; Gastrointestinal Hemorrhage; In Vitro Techniques; L-Lactate Dehydrogenase; Male; Prostaglandins E; Prostaglandins E, Synthetic; Rats

Gastrointestinal bleeding was the presenting manifestation in four patients without readily apparent prostate cancer. Three of these patients had laboratory evidence of acute disseminated intravascular coagulation (DIC) and one patient had a friable rectal mass. The diagnosis of prostate cancer was made in three patients by employing an immunoperoxidase technique for prostatic acid phosphatase in metastatic foci. Dramatic resolution of DIC occurred in two patients following hormone therapy. Radiation therapy was effective in controlling bleeding in another patient. Two patients are alive with no further bleeding episodes at 8 and 18 months follow-up, respectively. In patients who present with a bleeding diathesis and adenocarcinoma of unknown primary, it is important to consider prostate cancer because of its frequent and prolonged responsiveness to hormonal therapy.

Topics: Acid Phosphatase; Aged; Disseminated Intravascular Coagulation; Gastrointestinal Hemorrhage; Humans; Immunoenzyme Techniques; Male; Middle Aged; Prostatic Neoplasms

The effects of pretreatment with 16,16-dimethyl prostaglandin E2 (dmPGE2) on ethanol-induced colonic damage were studied in the rat. Colonic damage was assessed macroscopically, histologically, and using cytoplasmic (lactate dehydrogenase) and lysosomal (acid phosphatase) enzyme markers of cell disruption. Intrarectal administration of 30% ethanol produced grossly visible regions of hyperemia and hemorrhage. Histologically, the ethanol injury was characterized by complete destruction of the surface epithelium and necrosis extending throughout most of the mucosal layer. When incubated in vitro after challenge with ethanol in vivo, the colons released significantly more acid phosphatase and lactate dehydrogenase than did controls. Intrarectal pretreatment with dmPGE2 caused a dose-dependent reduction in ethanol-induced damage, as measured by all three parameters. A significant (P less than 0.05) reduction of macroscopically visible damage was observed with 0.2 micrograms/kg dmPGE2, while at higher doses (20 micrograms/kg) the histological signs of damage, including that to the colonic epithelium, were reduced or completely prevented. This dose of dmPGE2 also reduced (P less than 0.01) the release of the enzyme-markers to control levels. The possibility that this protection was mediated by increased colonic fluid secretion was studied. Pretreatment with dmPGE2 had no effect on net colonic fluid secretion (measured using the nonabsorbable marker [3H]inulin) or on the absorption of ethanol by the colon. This study demonstrates that intrarectal administration of dmPGE2 can protect the colonic mucosa from damage induced by direct application of a potent topical irritant. With the highest dose of dmPGE2 tested (20 micrograms/kg), protection of the colonic epithelium from ethanol injury was observed.

Topics: Acid Phosphatase; Animals; Colonic Diseases; Ethanol; Gastrointestinal Hemorrhage; Hyperemia; Intestinal Mucosa; L-Lactate Dehydrogenase; Male; Prostaglandins E, Synthetic; Rats; Rats, Inbred Strains

Topics: Acid Phosphatase; Blood Glucose; Blood Viscosity; Carbon Dioxide; Electrolytes; Gastric Acidity Determination; Gastric Juice; Gastrointestinal Hemorrhage; Hematocrit; Humans; Lactates; Male; Military Medicine; Oxygen; Peptic Ulcer; Prospective Studies; Vietnam; Wounds and Injuries