Biliary motility: postnatal changes in guinea pigs.

Intravital microscopy, a new in vivo technique, documented age-dependent changes in choledochoduodenal junction motility in male guinea pigs. In the guinea pig, the choledochoduodenal junction served as a pump that actively emptied its luminal contents into the duodenum. In the neonates (less than or equal to 1 wk old), this choledochoduodenal junction pump was not fully developed. Unlike the older guinea pigs, some neonates had an incompetent sphincter ductus choledochi (SDC) allowing retrograde flow of bile during ampullary contractions. While fasting, neonates had decreased frequency of SDC (1.2 +/- 0.4 contractions/min) and ampullary (0.1 +/- 0.1 contractions/min) contractions as compared to juveniles (4-6 wk old) (SDC = 6.4 +/- 1.0; ampulla = 1.2 +/- 0.2 contractions/min) and adults (greater than 1 yr old) (SDC = 6.7 +/- 1.6; 0.8 +/- 0.2 contractions/min). Following a meal (Ensure), unlike older guinea pigs, the neonate did not have a significant increased duration and decreased frequency of SDC contractions. Altered neonatal SDC motility correlated with an incompletely developed SDC including decreased muscle mass and mucosal thickness. By 4 wk of age, choledochoduodenal junction motility was similar to that of the adult. These developmental alterations in junctional motility and structure may affect the flow of bile into the duodenum contributing to physiologic cholestasis and decreased intraduodenal bile acids seen in neonates.

Noncholecystokinin peptides in human serum which cause gallbladder contraction.

In fasting human serum, cholecystokinin (CCK) is not the principal substance which causes in vitro rabbit gallbladder contraction. Removal of CCK by affinity chromatography from fasting sera from 8 healthy adults reduced bioactivity only by 18 +/- 4% (SEM). Unlike CCK, the bioactivity of serum was enhanced by 30 to 57% rather than destroyed by pronase and chymotrypsin respectively and was not inhibited by dibutyryl cGMP. Reduction of serum bioactivity by carboxypeptidase Y indicated that the bioactive substances in serum are peptides. On Sephadex G-50, bioactive substances eluted in positions different from any known form of CCK. Thus, the principal substances in fasting human serum causing in vitro gallbladder contraction are not CCK but are most likely small peptides which act at receptors different from the receptors for CCK.

Increased [125I]trypsin-binding in serum from cystic fibrosis patients.

The capacities of normal and cystic fibrosis (CF) sera to bind to exogenous human [125I]trypsin were compared. Sera from eight older CF patients bound significantly more exogenous human [125I]trypsin than did sera from eight normal subjects (p less than 0.001). Disregarding the increased trypsin-binding (TB) of CF sera, serum immunoreactive trypsinogen (SIRT) levels were not detectable in these eight older CF patients. However, when SIRT levels were corrected for TB, four CF patients had normal SIRT concentrations and four had low but detectable SIRT levels. As compared to five normal newborns' sera, serum from a newborn with CF had normal TB and the SIRT levels were very high. In conclusion, increased TB in CF serum lowers results of SIRT assays. Therefore, unless SIRT levels are corrected for TB, results obtained from currently available SIRT kits may be invalid.