Adrenergic and serotonergic mechanisms alter human gut motor functions. Genotype variation influences phenotype. Our aim was to test the hypothesis that variation in genes that control these functions is associated with gastrointestinal (GI) motor functions in humans with functional GI disorders (FGID). A database of 251 people was assembled by combining genotype data with measurements of gut transit and gastric volumes. Genetic variations evaluated were: alpha(2A) adrenergic (C-1291G), alpha(2C) (Del 332-325), 5-HT transporter (SLC6A4) and GNbeta3 (C825T). We sought associations between motor function or disease groups and genotypes, adjusting for age, gender and body mass index. Among 251 participants, 82 were healthy, 20 with irritable bowel syndrome (IBS) with mixed bowel habit, 49 with constipation-predominant IBS, 67 with diarrhoea-predominant IBS and 33 with functional dyspepsia. For all candidate genes, there was no significant association between motor function and wildtype vs non-wildtype gene status. There were significant interactions between genotype and motility phenotype, specifically GNbeta3 and alpha(2A) and gastric emptying at 4 h. Borderline associations were noted for SCL6A4 and alpha(2A) and postprandial gastric volume, and for alpha(2C) and gastric emptying at 2 h. We conclude that genotype variation may affect gastric motor functions in different FGID phenotypes. However, these candidate genes account for only a limited amount of the variance in gastric function of patients with FGID.
Cardiac output function curves were used to investigate the effects of carbon monoxide on the heart in the conscious dog. Each dog was briefly exposed to 1,500 ppm carbon monoxide through a permanent tracheostomy. Immediately upon attaining either 10%, 20%, or 30% HbCO a rapid infusion of Ringer's lactate was given to test cardiac capabilities. The combined effects of carbon monoxide and infusion produced significant increases in cardiac output, heart rate, mean left ventricular pressure, dP/dt and (dP/dt)/IP. Cardiac output was sufficient to prevent peripheral hypoxia at all HbCO levels; however, there was evidence of impending cardiac depression beginning at 20% HbCO.
The second lumbar vertebra was surgically removed from 10 dogs, and the shortened vertebral column was stabilized by internal fixation with two types of plastic plates. Shortening of the spinal column was usually not associated with detectable loss of function or neurological deficit. Histological lesions, however, included widely disseminated axonal degeneration, gliosis, and atrophy of spinal nerve roots in the surgical area. The spinal cord adapted to shortening of the vertebral column by becoming intrinsically shorter, rather than be being displaced within the spinal canal.
Six groups of rabbits received whole-body x-irradiation of 0, 100, 200, 300, 400 and 500 r, respectively. Counts of total white blood cells were performed regularly until 11 weeks post exposure when radiation-induced leucopenia had disappeared in all groups. At that time, the animals were re-exposed to the same doses and white cells were once more counted throughout 11 weeks. Then followed a third application of the same doses with subsequent observation of white counts. Statistical analysis of data yielded the following results: in the three exposures, radiation-induced leucopenia showed no significant difference with respect to rate of development, maximal degree and rate of disappearance. Therefore, as judged by the white blood cell count, susceptibility to ionizing radiation appeared unaltered by previous exposure to appreciable doses when the interval between exposures was sufficiently long to permit complete hematopoietic recovery.
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