Unilateral tumid lupus erythematosus.

Few cases of inflammatory blaschkolinear dermatoses have been described. We report a case of blaschkolinear cutaneous tumid lupus erythematous and discuss the potential association between cutaneous genetic mosaicism, Blaschko lines and lupus susceptibility.

Effect of endotoxin on canine colonic motility and transit.

Diarrhea is a common problem in patients who have episodes of sepsis and are being fed enterally. Endotoxemia results in gastrointestinal motor dysfunction characterized by slowed gastric emptying and rapid intestinal transit; however, the effect of endotoxin on colonic motility is unknown. The aim of our study was to determine the effects of a single sublethal dose of endotoxin on colonic motility and transit. Seven dogs underwent construction of a 50 cm colonic Thiry-Vella fistula. Five manometry catheters were sewn into the colonic lumen at 8 cm intervals along the fistula. Following recovery, the fistula was perfused with an isotonic solution at 2.9 ml/min, and fasting and postprandial colonic motility was determined. Liquid transit was assessed by bolus of a nonabsorbable marker instilled into the proximal end of the Thiry-Vella fistula. Recordings of gastrointestinal contractile activity were made digitally to determine contractile frequencies and motility indexes. Following completion of the baseline studies, each dog was given a single dose of E. coli lipopolysaccharide, 200 microgram/kg intravenously, and studies were repeated daily for the next 3 days. Endotoxin doubled the fasting colonic contractile frequency on postendotoxin day 1 and also increased motility indexes on that same day. Fasting motility indexes and contractile activity were decreased on postendotoxin days 2 and 3. The postprandial frequency of contractions and motility indexes were decreased on postendotoxin day 3. Fasting colonic liquid transit was rapid on postendotoxin day 1, whereas postprandial liquid transit was rapid on both postendotoxin days 1 and 2. Endotoxin temporarily speeds liquid transit and increases both the frequency and strength of colonic contractions. These effects may contribute to the diarrhea that occurs during episodes of sepsis.

Endotoxin temporarily impairs canine colonic absorption of water and sodium.

Diarrhea is a common manifestation of sepsis. We hypothesized that endotoxin may impair colonic absorption of water and electrolytes, an effect which may be related to altered liquid transit in the colon. Five dogs underwent construction of 50-cm colonic Thiry-Vella fistulas (TVF). Following recovery, absorption studies were performed by perfusing the TVF with an isotonic solution at 2.9 ml/min containing polyethylene glycol (5 g/L). Fasting and postprandial colonic absorption of water, electrolytes, and glucose were determined. Liquid transit was assessed by bolus of a nonabsorbable marker (PSP) instilled into the proximal end of the TVF. Following completion of the baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide 200 micrograms/kg i.v. and the studies were repeated daily for the next 3 days. Following endotoxin bolus, colonic absorption of water and sodium were decreased during fasting, while postprandial colonic absorption of water was also decreased. Colonic absorption of water and sodium returned to baseline values on postendotoxin day 2. Colonic secretion of potassium was decreased on postendotoxin days 1 and 3 in both the fasting and the fed periods. Fasting and postprandial liquid transit was also rapid on postendotoxin day 1, which correlated with the decreased absorption seen on that day. Liquid transit returned to baseline values on postendotoxin day 2. We conclude that endotoxin temporarily impairs postprandial colonic absorption, which may be due to the rapid liquid transit that occurs. These effects may contribute to the diarrhea seen during and after septic episodes.

Gastrointestinal transit during endotoxemia: the role of nitric oxide.

We hypothesized that the disrupted gastrointestinal transit that occurs during endotoxemia is mediated by nitric oxide (NO) and that the inhibition of NO synthesis will normalize intestinal transit and gastric emptying. To determine the effects of endotoxin and steroids on the activity of gastrointestinal smooth muscle NO synthase, rats underwent placement of an intravenous (iv) line and then were given Escherichia coli lipopolysaccharide (LPS) 10 mg/kg/iv; LPS, 10 mg/kg/iv + dexamethasone, 3 mg/kg/iv; or saline. The activity of nitric oxide synthase in the stomach, small intestine, and colon were determined by measuring the conversion of L-[3H]arginine to L-[3H]citrulline. To determine intestinal transit and gastric emptying, gavage feedings of nonabsorbable liquid markers were given and rats divided into eight groups: 0.9% NaCl, 1 ml/hr x 5 hr (control); LPS, 10 mg/kg/iv; LPS + N-omega-nitro-L-arginine methyl ester (L-NAME), 10 mg/kg/hr x 5 hr; LPS + N-omega-nitro-D-arginine methyl ester (D-NAME), 10 mg/kg/hr x 5 hr; LPS + L-arginine, 100 mg/kg/hr x 5 hr; LPS + L+NAME + L-arginine; LPS + N-omega-nitro-L-arginine (L-NNA) 10 mg/kg/hr; or LPS + L-NNA + L-arginine. LPS increased the enzymatic activity of both the constitutive and the inducible forms of NO synthase in the small intestine and fundus of the stomach. The acceleration of intestinal transit produced by endotoxemia was reversed with both L-NAME and L-NNA but not with D-NAME. Endotoxemia slowed gastric emptying but this effect was not reversed with either L-NAME or L-NNA. We conclude that NO plays a major role in mediating the rapid intestinal transit during endotoxemia.