Chemiluminescence assay of mucosal reactive oxygen metabolites in inflammatory bowel disease.

Previous studies suggesting increased reactive oxygen metabolite (ROM) production in inflammatory bowel disease have been restricted to peripheral blood and isolated intestinal phagocytes. In the current study, chemiluminescence and the effect of various scavengers, enzymes, and enzyme inhibitors were used to show that ROMs account for the increased production of oxidants by colorectal mucosal biopsy specimens in inflammatory bowel disease. Luminol-amplified chemiluminescence was increased in active ulcerative colitis [macroscopic grade 1: 25 photons.mg-1.min.10(-3) (median), 8-47 (95% confidence intervals), n = 40; grade 2: 89, 65-156, n = 30; grade 3: 247, 133-562, n = 13] and Crohn's disease [mild: 9, 3-84, n = 6; severe: 105, 25-789 (range), n = 5] compared with normal-looking mucosa (ulcerative colitis: 0.8, 0.4-1.4, n = 22, P less than 0.01; Crohn's disease: 0.8, 0.1-2, n = 6, P less than 0.05) and controls (0.6, 0.04-1.4, n = 52, P less than 0.01). In ulcerative colitis, luminol chemiluminescence correlated with microscopic inflammation (Spearman's p = 0.74, P = 0.0001) and was decreased by sodium azide (-89%, P less than 0.05), taurine (-31%, P less than 0.05), catalase (-23%, P less than 0.05), and dimethyl sulfoxide (-29%, P less than 0.05). Superoxide dismutase and oxypurinol decreased lucigenin chemiluminescence in ulcerative colitis by -63% (P less than 0.05) and -27% (P less than 0.05), respectively. Luminol chemiluminescence correlated with lucigenin chemiluminescence (Spearman's rho = 0.72, P = 0.003). These results suggest that neutrophil-derived oxidants (superoxide, hydrogen peroxide, hydroxyl radical, and hypochlorite) are generated in colorectal mucosa in active inflammatory bowel disease and support the hypothesis that production of such metabolites by neutrophils is of major pathogenetic importance.

Impaired memory registration and speed of reasoning caused by low body temperature.

Volunteers' body core temperatures were lowered by immersion in water at 15 degrees C. Aspects of cognitive function were subsequently tested after rewarming had been started in water at 41 degrees C when their skin was warm and they felt comfortable but their body core temperature remained low. Memory registration was found to be impaired progressively when core temperature fell from about 36.7 degrees C; at core temperatures of 34-35 degrees C the impairment caused loss of approximately 70% of data that could normally be retained. However, recall of previously learned data was not impaired at these core temperatures. On a two-digit calculation test, speed of performance was impaired by about 50% at a core temperature of 34-35 degrees C, but provided enough time was available, accuracy of performance was not reduced.

Restoration of thermoregulatory response to body cooling by cooling hands and feet.

Deep body temperature fell progressively by 0.5-1.4 degrees C during 3-h immersions in 29 degrees C water. Both in unacclimatized volunteers and, to a lesser degree, in divers in cold-water training, cooling the hands and feet for 1 h in 12 degrees C water during such immersion caused sensation of cold, shivering, and rise in metabolic rate; it caused body temperature to rise in unacclimatized subjects and halted its fall in divers. Tissue conductances generally fell a little in divers but rose in unacclimatized subjects, probably because of muscle blood flow associated with the greater shivering in the latter. Soaking the skin for 4 h produced no major changes in cutaneous thermal sensation assessed in the forearm, though with seawater it sometimes reduced cold sensation and with distilled water sometimes reduced warm sensation, a little. It is concluded that uniform skin temperature of 29 degrees C often induces insufficient heat-gain reflexes to maintain body temperature and that cooling of the extremities can restore adequate thermoregulatory response.