SummaryWe describe the case of a paraplegic patient who suffered traumatic spinal cord injury at the level of the twelfth thoracic vertebra. Within a short period of time following the injury, urinary (neuropathic bladder) and gastrointestinal (atonic colon) sequelae arose. Treatment with Cisapride (R 51 619,Janssen Pharmaceutica) was undertaken in an attempt to increase colonic motility and to reduce urinary retention. These goals were reached rapidly with a dose of 10 mg q.i.d.; the effect has been maintained for at least 18 months since starting the therapy. Neither clinical examination nor diagnostic tests revealed any abnormalities of cardio-
Plasma protein shedding in the stomach was measured in 23 normal individuals before and after intragastric administration of a 30% solution of ethyl alcohol. Two different methods were used to assess plasma protein shedding. The first technique utilizes [131I]albumin and requires neutralization of the gastric juice. It was used in 12 subjects and failed to demonstrate any increase of plasma protein shedding under the influence of ethanol. The second technique which utilizes [51Cr]chloride was used in 11 subjects. It demonstrated a significant increase of the gastric clearance of plasma protein which reached 2.5 times the control values. The [51Cr]chloride technique does not require prior neutralization of gastric acidity. It is concluded that, in normal man, ethanol administration increases plasma protein shedding in the stomach when it is given in the presence of an acid gastric juice. The effect is not observed when the gastric acidity is neutralized.
The extraction of plasma gastrin during intravenous infusion of exogenous hormone has been measured in the head, gastrointestinal tract, or kidney of dogs submitted to sham surgery, evisceration, or binephrectomy without or with subsequent kidney transplantation. A significant gastrin extraction was demonstrated not only in the kidney, but also in the head and in the gastrointestinal tract; moreover, plasma gastrin extraction in the head and the bowel was considerably reduced by binephrectomy and was brought back to control values after subsequent kidney transplantation. A non-specific effect of surgery and a variation in peripheral blood flow seem to be excluded. Thus a control by the kidney of the peripheral removal of blood gastrin is evidenced, the mechanism of which remains hypothetical.
SUMMARY Serum albumin gastric loss was estimated from the measurement of non-dialysable radioactivity of the gastric juice after intravenous injection of radioiodinated serum albumin (RISA). Immunochemical quantitation of serum albumin was performed in some of the samples.In the control group, the mean gastric clearance of albumin was 1.71 ml per hour with a range of 0.41 to 4.41 ml per hour. This represented a gastric loss of 1.9 gram of albumin per day and 11 % of the daily degradation of albumin. There was no significant change in the gastric albumin loss after stimulating the gastric secretion. No significant difference in the gastric albumin leakage was found between normal subjects and patients with gastric or duodenal ulcer.In pernicious anaemia albumin loss into the stomach was greater (mean: 3-72 ml per hour; SD 1.52 ml) than in the normal group and accounted for the greater albumin fractional catabolic rate. This fact had never been proved before. In both patients with giant rugae of the gastric mucosa the gastric clearance of serum albumin was also increased.It is concluded first that albumin is not secreted by the chief and parietal cells of the mucosa and probably passes through the gastric wall between the cells of the mucosa, perhaps during the exfoliation of the surface epithelial cells, and secondly that the stomach is one of the sites of serum albumin breakdown, a fact that supports the view that the gastrointestinal tract plays a major role in the catabolism of serum albumin.
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