Role of extrinsic innervation in carbohydrate-induced ileal modulation of pancreatic secretion and upper gut function.

Previously we showed that carbohydrate (CHO) in the ileum slowed gastric emptying and increased pancreatic amylase secretion relative to that of other enzymes. Our aim here was to determine if extrinsic innervation of the jejunoileum participates in the CHO-induced ileal modulation of postprandial upper gut function. Six dogs were studied before and 2-3 weeks after in situ neural isolation of the jejunoileum (complete extrinsic denervation). Gastric emptying (GE) and pancreatic amylase secretion were quantitated for 4 h after a 300-ml meal containing 3H-PEH (liquid marker) and 99mTc sulfur colloid cooked with eggs (solid marker). Coincident with feeding, we started a distal ileal infusion of 150 mM NaCl or 40 mg.min-1 CHO. Extrinsic denervation abolished the slowing of GE of liquids and solids and the augmented increase in amylase and trypsin in relation to solid emptying seen in the neurally intact dogs prior to denervation. Denervation also abolished the decrease in total pancreatic exocrine secretion in response to ileal CHO. Increases in plasma concentrations of peptide YY (PYY) were correlated temporally with decreased GE of solids and increased exocrine secretion during ileal CHO in neurally intact dogs, but no increases in PYY release occurred after extrinsic denervation. Extrinsic denervation of the jejunoileum abolished the effect of ileal CHO on GE of liquids and solids, the decrease in total amylase secretion during ileal CHO, and the relative increase in enzyme secretion expressed as total enzyme output per percentage solid marker emptied. Extrinsic innervation of the jejunoileum mediates ileal modulation of GE and the relationship of amylase secretion to GE of solids. The mechanism of this effect may be via neurally mediated release of PYY.

Restrictive ventricular septal defect: how small is too small to close?

Historically, indications for ventricular septal defect closure have included congestive heart failure, pulmonary hypertension, aortic insufficiency with or without aortic valve prolapse, and prior bacterial endocarditis. However, controversy exists as to how the lifetime risk of an isolated, nonoperated restrictive ventricular septal defect compares with the risk of surgical closure in an asymptomatic child. Between 1980 and 1991, cardiac catheterization and elective ventricular septal defect closure (age > 1 year, pulmonary to systemic flow ratio < 2.0) were performed in 141 patients aged 1 to 23 years (mean age, 6.1 +/- 4.7 years). Mean systolic pulmonary artery pressure was 26.9 +/- 13.0 mm Hg, and mean pulmonary to systemic flow ratio was 1.6 +/- 0.3. Aortic valve prolapse was present in 63 patients (45%), aortic insufficiency was present in 25 (18%), and 5 (3.5%) had prior bacterial endocarditis. There were no early or late deaths or major morbidity. No patient required a ventriculotomy to accomplish ventricular septal defect closure. Mean postoperative intensive care unit stay was 1.3 +/- 0.9 days, and mean hospital stay was 5.5 +/- 1.9 days. There were no instances of permanent complete atrioventricular dissociation, reoperations for bleeding, postoperative wound infections, or reoperations for residual or recurrent ventricular septal defect. These improved results justify a reevaluation of historic indications for ventricular septal defect closure.(ABSTRACT TRUNCATED AT 250 WORDS)