Biomedical subjects
Publications and source records attributed to T R Hendrix.
This paper describes the purpose and organization of a dedicated center at The Johns Hopkins Medical Institutions for the evaluation of swallowing problems. The multidisciplinary approach outlined will permit a better understanding and more accurate diagnosis of the functional or organic lesions affecting the swallowing mechanisms. Illustrative cases are presented.
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The gastric emptying characteristics of physiological saline (0.9% NaCl) and glucose solutions of three different concentrations (0.05, 0.125, 0.25 g/ml) were examined in order to identify distinctions in the control of the stomach's activity. Saline emptied rapidly and exponentially. Glucose assumed, soon after filling the stomach, a slow and calorie-constant emptying pattern such that 2.13 kcal of glucose were delivered per minute to the duodenum for all three concentrations of glucose. When, by means of a catheter passed beyond the pylorus, glucose was infused into the duodenum in amounts varying from 26.5 to 120 kcal, an inhibition on the gastric emptying of physiological saline of 0.46 min/kcal of intraduodenal glucose was demonstrated. Since 2.13 kcal/min and 0.46 min/kcal are reciprocals, it appeared that in emptying saline, the gastroduodenal system acts as an "open-loop" system passing liquids from the stomach at a rate primarily determined by the volume of gastric contents. With glucose, however, a "closed-loop" system is established that assumes a steady-state balance between the delivery of glucose to the duodenum and the inhibition of this delivery evoked from the duodenum by the glucose that enters it.
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Cholera toxin produces intestinal secretion and elevation of intestinal cyclic AMP. Nicotinic acid has been shown to prevent these responses. The effect of nicotinic acid on cholera toxin-induced secretion could be caused by decreased plasma-to-lumen flux, increased lumen-to-plasma flux, or a combination of both. The purpose of this study was to define the effects of nicotinic acid on net fluid movement and unidirectional sodium fluxes in rabbit jejunal loops exposed to cholera toxin. In the untreated animals receiving no nicotinic acid, the cholera toxin-exposed loops secreted 0.91 ml/cm/4h above the control loops receiving no cholera toxin (p < 0.01). On the other hand, pretreatment with 100 mg/kg nicotinic acid caused a striking decrease in secretion in the cholera toxin loop, so that the cholera toxin loop was not significantly different from the control loop. Unidirectional sodium fluxes in untreated animals showed that cholera toxin caused an increase in the plasma-to-lumen flux and a decrease in the lumen-to-plasma flux. Both effects were abolished by pretreating the animals with nicotinic acid. These studies indicate that nicotinic acid prevents cholera toxin-induced secretion by restoring the unidirectional fluxes to control levels.
We compared the findings from gastric aspiration for blood with the site of gastrointestinal (GI) hemorrhage ultimately identified by endoscopy or angiography in 1,190 patients whose cases were analyzed retrospectively and prospectively during a six-year period. Gastric aspirates were positive for blood in 837 patients. An upper GI site proximal to Treitz' ligament was identified in 93%, and none had a lower GI site. A negative aspirate was found in 353 patients; a lower GI site was identified in 60%, and 1% (three patients) had an upper GI site. In these three patients, hemorrhage occurred in clinical settings suggesting ulcer disease, and bleeding duodenal ulcers were found in all three. All of the other 180 patients with a bleeding duodenal ulcer had a positive gastric aspirate.
Eight patients with intrathoracic esophageal disruptions were managed nonoperatively and without pleural drainage. Criteria for nonoperative treatment included the following: disruption contained in the mediastinum or between the mediastinum and visceral lung pleura; drainage of the cavity back into the esophagus; minimal symptoms; and minimal signs of clinical sepsis. Cause of the esophageal perforation was pneumostatic dilatation (1 patient), vomiting (2), and a leak following esophageal operation (5). Antibiotics were administered intravenously to all patients; hyperalimentation was accomplished intravenously in 5, and nasogastric suction was used in only 1. The cavities contracted and the esophageal leaks sealed in all instances. Time before oral intake was resumed ranged from 7 to 38 days (average, 18 days). Days until discharge ranged from 15 to 52 days (average, 28 days).
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The cholera enterotoxin produces intestinal secretion associated with an elevation of tissue levels of cyclic adenosine 3',5'-monophosphate levels of cyclic adenosine 3',5'-monosphosphate (cAMP). The objectives of this study were to determine whether intestinal secretion and cAMP elevation induced by cholera toxin could be prevented, or once initiated, reversed by nicotinic acid, an agent known to lower tissue levels of cAMP. In rabbits, four jejunal loops were constructed as alternating control (3-ml isotonic electrolyte solution) and cholera toxin (same solution containing 50 mug purified cholera toxin) loops. Net intestinal secretion was determined by measuring fluid accumulation, after which intestinal biopsies were taken for cAMP assay. The animals were pretreated either subcutaneously with 50 mg/kg nicotinic acid in saline 3 h and 1 h before the introduction of cholera toxin, or intraluminally with 200 mg/kg nicotinic acid in Ringer's lactate solution 15 min before the instillation of cholera toxin. Under these conditions, nicotinic acid blocked the cholera toxin-induced secretion and the rise in cAMP measured 3 h after the loops were exposed to cholera toxin. The effect of the nicotinic acid administered within the lumen on net intestinal secretion was studied. Maximal inhibition of net intestinal secretion was achieved with an intraluminally administered dose of nicotinic acid of 100 mg/kg. This dose was chosen for testing the ability of nicotinic acid to reverse the effects of cholera toxin. When nicotinic acid was instilled into a fifth loop constructed distally to the four experimental loops 3 h after exposure of these loops to cholera toxin, both intestinal secretion and elevation of cAMP were reversed. These results suggest that nicotinic acid can prevent and reverse the secretory effects of cholera toxin and may have a role in the therapy of cholera and other cAMP-associated diarrheal diseases.
The velocity of the front face of a liquid saline bolus ejected from the pharynx into the esophagus was measured by recording changes of luminal electrical impedance with three sets of electrodes in 9 subjects. At a site 26 cm from the incisors, the mean velocity of the front face of the bolus increased from 10 to 70 cm sec-1 as the volume swallowed was raised from 5 to 30 ml. The velocity of the front face of the bolus was greater 26 cm from the incisors than it was 32 cm from the incisors.
Esophageal, fundal, antral, and duodenal mucosal biopsies from 10 patients with heartburn were compared with biopsies from 18 patients with dyspepsia but without heartburn or radiographic or endoscopic evidence of peptic ulcer disease, gastric retention, or esophageal stricture. There was a highly significnt correlation between heartburn and antral gastritis and duodentitis (P less than 0.01). It is suggested that histologic reflux changes are determined by the severity of reflux and reparative potential of the esophageal mucosa. Heartburn, on the other hand, is more related to the nature of the refluxed fluid. The fluid most likely to induce heartburn is one containing duodenal fluid, which is also believed to be an important cause of antral gastritis.
The etiology of recurrent aspiration pneumonitis after the successful repair of esophageal atresia has not been defined. In order to explain this occurrence, we performed esophageal manometric examinations on eight patients who had undergone repair of EA and tracheoesophageal fistula. Two patients who had had recurrent pneumonia had subnormal pressure of the lower esophageal sphincter; they also had a history of severe regurgitation, and a barium esophagram demonstrated free gastroesophageal reflux. The LES incompetence in these patients was apparently corrected by administration of bethanechol.
Diagnosis of esophageal reflux often can be made on the basis of the characteristic symptoms of heartburn and regurgitation. When the picture is not so typical, acid reflux testing and esophageal biopsy appear to be the best indicators of esophageal reflux. Medical management is directed toward preventing reflux, neutralizing refluxed gastric contents, and enhancing clearance of refluxed material. Antacids are a mainstay of therapy, along with restrictions on diet and certain types of activity. If conservative therapy fails to control symptoms and stricture is likely to develop, surgery may be indicated.