The Effect of Endotoxin on Canine Jejunal Motility and Transit

Changes in Intestinal Transit and Absorption during Endotoxemia Are Dose Dependent

“…However, larger doses (100 g/kg) increased the duration of the MMC interval 10-fold. We have recently demonstrated that lipopolysaccharide causes rapid jejunal transit in both rat [5,6] and canine [7] models of endotoxemia. In rats, endotoxin accelerates small intestinal transit associated with increases in the inducible and constitutive forms of nitric oxide (NO) synthase [5,6].…”

“…The rapid intestinal transit during endotoxemia is normalized with infusions of competitive inhibitors of NO synthase or infusions of oxyhemoglobin, which bind NO after it is produced. In dogs, endotoxin also causes rapid intestinal transit, which may be due to changes in contractile propagation of single pressure waves [7]. Also, canine jejunal absorption of water, electrolytes, and glucose is temporarily impaired following a single, sublethal dose of endotoxin [8].…”

Lipopolysaccharide Induces Cell Death in Cultured Porcine Myenteric Neurons

“…Experimental studies have shown that LPS causes delayed gastric emptying (6,7), intestinal dysmotility (7,8) and sphincteric dysfunction (9), thus unravelling its interaction with enteric nerves. The precise mechanisms behind these acute LPS-induced motor effects are, however, as yet largely unknown.…”

Intestinal expressions of eNOSmRNA and iNOSmRNA in rats with acute liver failure

“…Hemoglobin attenuated the effect of endotoxin on intestinal motor function. Synthetic hemoglobins currently being a test as blood substitutes may be of therapeutic value in treating intestinal dysfunction complicated with sepsis [37][38][39][40][41] . However, the gene expression increase of iNOAmRNA in the intest inal tract produced a large amount of NO, slowed intestinal transit, promoted intestinal bacteria overgrowth during endotoxemia, and reacted with superoide (O 2 -) to form peroxynitrite anion (ONOO respiration and intestinal mucosal barrier dysfunction, prolonged the exposure of cells to large amounts of NO may inhibit cell respiration, cause maldistribution of regional blood flow and cell damage, increase gut permeability; but inhibition of cNOS can decrease dramatically the blood flow of intestine, increase the damage of enteric hemorrhage by induction of LPS, even small dosage of LPS could cause enteric hemorrhage.…”