Modulation of salivary secretion by acid infusion in the distal esophagus in humans.

To examine the relationship between esophageal acid exposure and development of salivation and heartburn, 15 healthy subjects underwent perfusion of the distal esophagus with varying concentrations of hydrochloric acid, different-osmolality saline solutions, and deionized water. In five study subjects, hydrochloric acid was infused in the body of the stomach only. During the study, timed samples of whole and parotid saliva were collected and analyzed for flow rate and bicarbonate concentration. Only hydrochloric acid concentrations of 20 mmol/L or greater (pH 1.8 or lower) induced a rapid (within 2 minutes) and significant (P < 0.05) increase in salivation. The hydrochloric acid-induced salivation was associated with significant (P < 0.05) increase in bicarbonate secretion in both parotid and whole saliva samples. Intravenous atropine administration completely inhibited hydrochloric acid-induced salivary secretion in all six subjects. Changes in osmolality of saline solution infused in the esophagus and hydrochloric acid infused in the stomach did not significantly alter parotid and whole saliva flow rates. These data suggest that in humans, rapid salivation in response to esophageal mucosal exposure to intraluminal hydrochloric acid is a pH-dependent and osmolality-independent phenomenon that is most likely mediated by pH-sensitive chemoreceptors located in the esophageal mucosa.

Resolution of inferior vena cava syndrome after embolization of a hepatic adenoma.

A 77-year-old man presented with severe pruritus and massive lower body edema. Computerized axial tomography of the abdomen showed a large hepatic mass compressing the inferior vena cava, and a liver biopsy specimen showed hepatic adenoma. Embolization of vessels feeding the hepatic tumor resulted in complete resolution of pruritus and ascites, and clinical remission has persisted for 1 year following partial obliteration of tumor vasculature. Angiographic ablation of tumor blood supply represents a nonoperative means for inducing clinical remission in patients with symptomatic hepatic adenoma who are at high surgical risk.