Because disadvantages are inherent in the conventional station pull-through technique (SPT) currently used for recording lower esophageal sphincter pressure (LESP), a more suitable recording method is needed. In study, we evaluated a rapid pull-through technique (RPT) for recording LESP and compared the results with those obtained by SPT. The RPT features rapid withdrawal of recording sensors across the LES during a 10- to 20-sec interval of suspended respiration. This method avoids recording "artifact" caused by respiratory LES motion and provides precise end points for scoring and measurement. In 12 normal subjects, LESP measured by RPT (24.3 plus or minus 0.5 mm Hg) was comparable, but significantly greater, than LESP measured by SPT (21.1 plus or minus 9.1 mm Hg). Analysis of LESP scores for the two recording methods revealed that both intraobserver and interobserver error were substantially less for RPT than SPT (P less than or equal to 0.01). Further correlation of LESP between studies was greater for the RPT than the SPT recording method. We conclude that RPT represents a convenient method for recording LESP which is easier to perform and yields more reproducible values than LESP recording by SPT.

It is now well documented that a characteristic mucosal lesion of the proximal small intestine is present in acute nonbacterial gastroenteritis. To determine whether a gastric mucosal lesion also accompanies this illness, stool filtrate containing Norwalk agent was given orally to 15 volunteers after base line biopsies of gastric fundal and/or antral mucosa had been obtained. Gastric fundal and/or antral biopsies were then obtained serially between 24 and 168 hr after administration of the inoculum. Nine volunteers developed symptoms of gastroenteritis. gastric biopsies from those with normal base line fundal and/or antral biopsies remained normal during and after clinical illness. Those volunteers who had mild to moderate gastritis in their base line biopsies showed persistence but no progression of the lesion during illness. In 4 of the volunteers who became ill, intestinal biopsies were available and showed the typical gastroenteritis lesion. These results indicate that acute infectious nonbacterial gastroenteritis induced by Norwalk agent is not associated with histologically detectable gastric mucosal lesion.

Intraarterial vasopressin has been reported to be effective in the treatment of massive upper gastrointestinal hemorrhage. A prospective, controlled clinical trial comparing conventional treatment with conventional therapy plus intraarterial vasopressin was undertaken. Sixty episodes of upper gastrointestinal hemorrhage were evaluated during a 40-month period; 32 received conventional and 28 conventional plus vasopressin therapy. The two groups of patients were similar in type and severity of their bleeding lesions and in their underlying diseases. Vasopressin was more effective in controlling hemorrhage from nonvariceal lesions (P less than 0.05) and from varices (P less than 0.01) than conventional therapy. Transfusion requirements were significantly reduced in those patients who received vasopressin. Paradoxically, survival was not affected by vasopressin administration. The failure of cessation of hemorrhage to improve survival is thought to be due to the degree of advancement of the underlying disease, to the torrential nature of the hemorrhage, to the frequency of recurrent hemorrhage, and to the use of intraarterial vasopressin in some patients in the conventional treatment group in whom conventional therapy had failed.

The incidence of peptic ulcer is increased in cirrhosis and is widely believed to be even greater in cirrhotic patients with portacaval anastomosis (PCA). Two prospective, controlled investigations of prophylactic PCA were evaluated to compare the frequency of peptic ulcer in two groups of cirrhotic patients with similar clinical and laboratory manifestations of cirrhosis randomly selected to be an unoperated Control Group (60 patients) or to have PCA (Shunt Group, 48 patients). In addition, nonrandomized groups of cirrhotic patients, 77 of whom were excluded from the randomized study and 44 of whom had therapeutic PCA, were studied. A diagnosis of chronic peptic ulcer was based on the demonstration of an ulcer crater by X-ray, endoscopy, surgery, or autopsy. Prior to inclusion in these studies, approximately 10% of patients had had peptic ulcer. After inclusion, during a mean follow-up period of 45 months, 12% of both the Control and Shunt Groups developed peptic ulcers. The frequency of complications of peptic ulcer, of recurrence of peptic ulcer, or of acute or symptomatic (unproved) ulcer were similar in both groups. Ulcers tended to develop later in shunted than in unshunted patients. Similar data were obtained from three of four other controlled investigations of PCA. This investigation does not find an increased occurrence of peptic ulcer after PCA. The frequency of ulcer in cirrhosis appears to increase with the duration of the disease independent of the presence or absence of PCA.