bismuth-tripotassium-dicitrate and Necrosis

Clostridium perfringens-associated necrotic enteritis causes significant economic losses. The objective of this study was to evaluate the effect of bismuth citrate, lactose, and organic acid on the development of necrotic enteritis in broilers. The first study was a dose response that evaluated bismuth citrate at 50, 100, or 200 ppm on bacterial intestinal colonization and lesion development associated with our C. perfringens challenge model. The second study evaluated bismuth citrate, lactose, and citric acid on intestinal pH and lesion development. For the third study, we determined if lactose would enhance the efficacy of bismuth citrate against intestinal colonization and lesion development associated with C. perfringens. In study 1, intestinal lesion scores at the 50, 100, and 200 ppm bismuth citrate treatment level were reduced (P < or = 0.05) when compared with the birds fed 0 ppm bismuth citrate. Intestinal C. perfringens colonization of the 100 and 200 ppm bismuth citrate treatment group was significantly reduced when compared with birds fed 0 ppm bismuth citrate. In study 2, we found no significant differences in lesion development, after C. perfringens challenge, between birds fed 100 ppm bismuth citrate or fed a combination of 100 ppm bismuth citrate with dietary lactose or citric acid relative to the controls. The intestinal pH of birds fed 100 ppm bismuth citrate or fed a combination of 100 ppm bismuth citrate with dietary lactose or citric acid was not significantly reduced when compared with the controls. However, a significant reduction in pH was observed in birds fed a combination of 100 ppm bismuth citrate and lactose relative to the negative controls. In study 3, a decrease (P < or = 0.05) in intestinal lesion scores occurred in birds fed lactose with 100 ppm bismuth citrate, compared with the positive controls. There were no significant differences in intestinal bacterial colonization. These preliminary data suggest that bismuth citrate may reduce intestinal lesion development and C. perfringens colonization in broilers infected with necrotic enteritis.

Topics: Animals; Chickens; Citric Acid; Clostridium Infections; Clostridium perfringens; Drug Therapy, Combination; Enteritis; Female; Lactic Acid; Male; Necrosis; Organometallic Compounds; Poultry Diseases

Bismuth induced nephrotoxicity has been reported to occur after acute overdoses of Bi-containing therapeutic drugs. We studied the development of bismuth induced nephropathy and bismuth biokinetics in rats. Bismuth nephropathy was induced in 33 young adult female Wistar rats weighing ca. 175 g by feeding them a single overdose of colloidal bismuth subcitrate containing 3.0 mmol Bi/kg at (t = 0). Control animals (n = 7) were fed the vehicle only. The animals were sacrificed after 1-48 h. Plasma creatinine increased from 51 +/- 6 micromol/l at t = 0 to 550 +/- 250 micromol/l after 48 h in the experimental group. The S3 segment of the proximal tubule showed epithelial cell vacuolation after 1 h and necrosis after 3 h. Cells of the S1/S2 segment demonstrated vacuolation after 6 h and necrosis after 12 h. Biokinetics of bismuth in blood could best be described with a one-compartment model characterized by an absorption half-life of 0.32 h and an elimination halflife of 16 h. The peak concentration of about 7.0 mg Bi/l was reached after 2 h. In conclusion, cells of the S3 segment of the proximal tubule necrotized first after an oral colloidal bismuth subcitrate overdose and biokinetics of Bi in blood was best described by a one-compartment model.

Topics: Absorption; Animals; Anti-Ulcer Agents; Bismuth; Blood Glucose; Creatinine; Epithelial Cells; Female; Half-Life; Kidney Tubules, Proximal; Necrosis; Organometallic Compounds; Rats; Rats, Wistar; Toxicity Tests, Acute; Vacuoles

Prostaglandin E2 (PGE2), colloidal bismuth subcitrate (CBS), and sucralfate (SUC) are known to protect the gastric mucosa from ethanol injury. The proposed central role for the microcirculation in gastric mucosal defense and as a site for the expression of the protective effects of these agents was investigated in the rat stomach. Animals were pretreated with either PGE2, CBS, or SUC. Control rats were given normal saline. After allowing 15 min for expression of the pretreatment, ethanol was administered as a 10%, 25%, 50%, or 100% solution to groups of rats with normally perfused stomach and to other groups of rats in whom the stomach was made ischemic by cross-clamping the supracoeliac aorta immediately prior to the instillation of ethanol. The extent of gastric mucosal damage was measured using quantitative histological techniques and expressed as a percentage of surface area and volume of mucosa damaged. In the presence of ischemia, the extent of damage by ethanol was markedly increased, with total destruction of the mucosa by the 50% and 100% solutions. With 25% ethanol, the volume of mucosal damage was increased from 0.5% in the normally perfused stomach to 53.5% with ischemia. When 10% ethanol was instilled into the ischemic stomach, only 0.8% of the volume of the mucosa was damaged, which was not different from the volume of mucosa damaged after the ischemic stomach was exposed to normal saline alone (1.0%). Pretreatment with PGE2, CBS, or SUC did not significantly change the extent of damage seen with exposure of the ischemic stomach to 25% or 50% ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Antacids; Dinoprostone; Ethanol; Gastric Mucosa; Ischemia; Male; Microcirculation; Necrosis; Organometallic Compounds; Rats; Sucralfate

In groups of white Wistar rats, the cytoprotective effect induced by TDB on the gastric mucosa against the ethanol injury, was studied; where macroscopic protection and histologic cytoprotection in gastric corpus was found, and no in antrum mucosa. The cytoprotective mechanism give by TDB, were studied by the test of Indomethacin, Cl2Hg, Domperidone, Chlorpromazine and Acetazolamide, where each drug was given as pretreatment. Was conclude that TDB give gastric cytoprotection by the mechanism of the nonprotein sulfhydryl, by to be one peripheral agonist of the neuronal dopamine receptors, by increase of endogenous prostaglandin, by little increment of cAMP and no participate the gastric bicarbonate secretion.

Topics: Acetazolamide; Animals; Chlorpromazine; Domperidone; Ethanol; Female; Gastric Mucosa; Indomethacin; Male; Mercuric Chloride; Necrosis; Organometallic Compounds; Rats; Rats, Inbred Strains