Nine healthy human volunteers underwent colonic perfusion and recording of the intraluminal pressure simultaneously in the right, transverse, and left colon. Isotonic saline was infused into the caecum at various flow rates from 10 to 30 ml per min. During colonic perfusions, pressure waves were simple and distorted only by respiratory artifacts. Their amplitude was large (10 to 44 cm of H2O), of long duration (8 to 68 sec), and of low frequency (0.2 to 1.8 wave per min). The frequency of the waves was very stable and this stability was uninfluenced by the site of recording and the rate of perfusion. A pressure wave in the right colon was always followed within 3 sec by a wave in the transverse and left colon. The frequency and amplitude of the waves increased in all subjects and at all rates of perfusion from right to left colon (P less than 0.001). The wave frequency increased with the perfusion flow rate (P less than 0.001). The relationship between the perfusion flow rate and the waves amplitude was curvilinear (P less than 0.01). It is concluded that in the human colon perfused in situ there is a gradient of motility preventing aboral propulsion. This study suggests that during perfusion, liquids are trapped in the right colon. Data on transport of water and electrolytes, obtained from whole colon perfusion, may in fact reflect events occurring in the proximal part of the large bowel.

Although the irritable bowel syndrome has been characterized as an abnormality in colonic motor activity occurring in response to certain stimuli, the etiology of this abnormality is unclear. The purpose of this study was to compare colonic myoelectric and motor activity in normal subjects and in patients with the irritable bowel syndrome. Myoelectric activity was recorded using a bipolar electrode clipped to the mucosa of the rectal and rectosigmoid areas. Basic electrical rhythm (BER), spike potential activity, and intraluminal pressure were recorded in both groups. Two types of BER were observed. The major component of the BER had a frequency of approximately 6 cycles per min, whereas the minor component had a frequency of approximately 3 cycles per min. Although both types of BER were recorded in the two groups, thitable bowel syndrome. The 3 cycles per min activity was present as 44.1 +/- 1.3% of the total BER in the irritable bowel syndrome, as compared with 10.0 +/- 1.6% in the normal group (P less than 0.001). Basal spike potential and motor activity were similiar in both groups. Because it had been demonstrated previously that colonic responsiveness to certain stimuli was increased during the slower frequency BER, it is suggested that the abnormalities in colonic motor response reported in the irritable bowel syndrome may be related to this difference in colonic BER.

The histopathological changes that occur in the jejunal mucosa of humans infected with the Norwalk or Hawaii agent of acute infectious nonbacterial gastroenteritis ("viral" gastroenteritis) have ben well characterized. The pathogenesis of diarrhea in this syndrome remains unknown; however, recent reports have suggested a possible role for the adenylate cyclase system. In this combined paper, two groups of investigators working independently and employing slightly different techniques report that: (1) there is marked interindividual variation in the apparent specific activity of adenylate cyclase in human jejunal biopsy tissue; (2) such variation can be minimized by expressing enzyme activity as a fraction of maximal that can be stimulated by 10(-2) M sodium fluoride; and (3) adenylate cyclase activity in jejunal mucosa is not increased during diarrhea or illness in human viral gastroenteritis, therefore suggesting no role for the adenylate cyclase system in the pathogenesis of diarrhea in this common clinical entity.

A case of disseminated herpes simplex infection is reported in a 31-year-old renal transplant recipient. The patient presented with a unique clinical syndrome: high fever, severe sore throat with buccal and pharyngeal ulcerations, fulminant hepatitis, thrombocytopenia, and leukopenia. The patient died from hepatic failure, disseminated intravascular coagulopathy, and upper gastrointestinal bleeding. The diagnosis was made by positive herpes simplex virus culture from the throat, and was confirmed at autopsy by typical Cowdry's type A intranuclear inclusions in hepatocytes with positive herpes simplex virus culture from the liver. Review of the literature reveals that other reported cases have had very similar clinical findings, making disseminated herpes simplex infection with fulminant hepatitis a recognizable syndrome.

15-Methyl PGE2 and 16,16-dimethyl PGE2 were found (1) to be 40 and 100 times, respectively, more potent than PGE2 after intravenous administration in inhibiting histamine-stimulated gastric secretion in dogs with a denervated (Heidenhain) gastric pouch, (2) to be active orally and intrajejunally, whereas PGE2 was inactive, and (3) to exert antisecretory activity for longer duration than PGE2. 16,16-Dimethyl PGE2 was about 2.5 times more potent than 15-methyl PGE2. Volume, acid concentration, and output, and pepsin output (but not concentration) were reduced in a dose-dependent manner. In the rat, 16,16-dimethyl PGE2 also inhibited gastric secretion and prevented the formation of ulcers produced by various methods: gastric ulcers (Shay, and steroid induced) and duodenal ulcers (secretogogue induced). In this species, 1l816-dimethyl PGE2 was 2 to 50 times more potent than PGE2, depending on the endpoint, and was active orally. These prostaglandins appear to inhibit gastric acid secretion by acting directly on the parietal cells, and making these unresponsive to most stimulants. Vomiting was a side effect of the prostaglandin analogues in the dog, but almost exclusively when these were given orally. After intravenous or intrajejunal administration at doses inhibiting gastric secretion by 80%, vomiting was seen only once. These results suggest that 15-methyl PGE2 and 16,16-dimethyl PGE2 may be of value in the treatment of peptic ulcer.

A total of 306 individuals from South Vietnam were studied: 61 had a diagnosis of primary liver cancer (38 had a tissue diagnosis, and 23 had a clinical diagnosis and a positive alpha-fetoprotein); 9 had viral hepatitis; 101 were hospitalized patients (60 with various other forms of liver disease and 41 without liver disease); 94 were blood donors; 29 were drug users, and 12 were medical students. Alpha-fetoprotein was present in 45 of 61 (74%) of those with a diagnois of primary liver cancer (PLC) and in none of the other patients. Using immunoelectroosmophoresis, hepatitis BS antigen (HBSAg) was found no more frequently in those with PLC than in the other groups studied. In contrast, using a radioimmunoassay technique HBSAg was present 3 to 8 times as frequently in the PLC patients as in other subjects without viral hepatitis. There was a close relationship between the presence of alpha-fetoprotein and HBSAg in the patients with PLC. Malaria seropositivity rates were no different in the PLC groups than the other groups. It appears that in South Vietnam PLC is associated with an increased frequency of HBSAg.

Immunological reactivity in alcoholic hepatitis has bben attributed to alcoholic hyalin, the histological hallmark of this disease. A purified isolate of alcoholic hyalin with electron microscopic, biochemical, and serological characteristics documented previously was added to lymphocytes from healthy subjects and patients with alcoholic hepatitis or other hepatic disorders. Production of migration inhibition factor (MIF) in response to this material was used as an index to lymphocyte reactivity. MIF was significantly increased in lymphocytes obtained from patients with alcoholic hepatis, as compared to the healthy controls (P less than 0.001), and persons with other liver diseases (P less than 0.005). These observations indicate that immunological hyperreactivity to alcoholic hyalin occurs in patients with alcoholic hepatitis; such activity may be of key importance in the pathogenesis or sequelae (or both) of this disease.

From 1 to 5% of patients can be expected to develop recurrent ulceration following current surgical therapy for peptic ulcer disease. The development of recurrent ulcer frequently reflects an inadequacy of the initial procedure. The nature of the inadequacy is often difficult to delineate because of alterations in anatomy and physiology and the lack of accurate diagnostic procedures. Incomplete vagotomy and inadequate gastric resection account for the vast majority of surgical deficiencies. Gastrinoma, retained gastric antrum, and hyperparathyroidism are the most frequently encountered endocrine causes. A thorough evaluation must include gastrointestinal X-rays, fiberoptic endoscopy, multiple serum calcium and gastrin determinations, and provocative testing. Medical management of recurrent ulcer fails in the vast majority of cases. Reoperation is successful in about 70% of cases and has a mortality rate of 4%. Recurrent ulcer after simple gastroenterostomy is best treated by gastric resection or vagotomy and resection. After initial adequate gastric resection, vagotomy alone usually suffices. Antrectomy and, if necessary, re-vagotomy should be done for recurrent ulcer after vagotomy and drainage. Re-vagotomy alone is usually effective therapy for recurrent ulcer after initial vagotomy and resection. Non-acid reducing operations should not be done, as they result in high mortality and high second recurrence rates.

Evidence is present that a common pathway for hepatic injury by a variety of agents may result from impairment of the liver's ability to detoxify bacterial endotoxins from the gastrointestinal tract. Many factors may structurally, metabolically, or hormonally alter the normal liver's ability to render innocuous the small amounts of lipopolysaccharide ordinarily presented to it. This impairment may accentuate existing hepatic damage by allowing toxic levels of endotoxin to develop in the liver tissue, and by allowing endotoxin entry into the systemic circulation, may also lead to extrahepatic effects. Studies are cited that: (1) support a role for intraintestinal endotoxin in the development of experimental cirrhosis. (2) demonstrate how liver injury alters endotoxin detoxification, (3) examine the role of intestinal production and absorption of bacterial lipopolysaccharides in liver disease, and (4) point to a role for endotoxemia in extrahepatic manifestations of liver injury as well. Studies are also reviewed that suggest possible mechanisms for modifying endotoxicity in hepatic damage.

Low residue, chemically defined diets containing all essential nutrients in a readily assimilated form, require minimal digestion and are almost entirely absorbed in the upper gastrointestinal tract. Within the past decade, these diets have been reported to provide nutritional support in a variety of clinical situations. The chemically defined diets presently available commercially differ in several respects. In order to provide optimal nutritional care utilizing chemically defined diets, the physician should compare the diet formulas and make the most appropriate choice for each individual patient. A comparative nutritional analysis of the currently available chemically defined diets is given.

Tumoral secretions and pathophysiology of diarrhea were studied in 1 patient with pancreatic cholera. High concentrations of vasoactive intestinal peptide were found in both systemic blood and tumoral extracts, together with increased plasma levels of calcitonin and protaglandins E and Falpha. Gastric inhibitory peptide and gastrointestinal and pancreatic hormones were absent from the tumor, except for small amounts of glucagon, and their blood levels were normal. Decreased basal but normal pentagastrin-stimulated gastric acid secretion, normal basal and secretin-stimulated pancreatic secretion, increased volume of gallbladder bile with high bicarbonate, and low bile salt concentrations were observed, but the electrolyte content and flow rate of fluid passing the duodenojejunal junction were within normal limits. Small intestine was found to be the origin of the water and electrolyte fasting losses. Jejunum was the site of bicarbonate secretion. Jejunal glucose and leucine-stimulated water and sodium transports were also strikingly decreased, whereas the absorption rates of the sugar and amino acid were normal. Colon reabsorbed high amounts of water and sodium but increased potassium losses. Biological effects of vasoactive intestinal peptide may explain most of the patient's upper digestive secretion abnormalities and small intestinal function impairments, whereas secondary aldosteronism might explain the modified colonic function.