Gallbladder symptoms

Gallbladder Function

The gallbladder concentrates and stores bile secreted by the liver during the fasting state and delivers bile into the duodenum in response to a meal. Since the usual capacity of the gallbladder as a reservoir is only about 30 to 60 mL, the remarkable absorptive capacity of the gallbladder accounts for its ability to store much of the 600 mL of bile produced each day. The gallbladder mucosa has the greatest absorptive capacity per unit area of any structure in the body. Bile is usually concentrated 5- to 10-fold by the absorption of water and electrolytes leading to a marked change in bile composition.

Active sodium chloride transport by the gallbladder epithelium is the driving force for the concentration of bile. Water is passively absorbed in response to the osmotic force generated by solute absorption. The concentration of bile may affect the solubility of two important components of gallstones: calcium and cholesterol. Although the gallbladder mucosa absorbs calcium, this process is not nearly as efficient as for sodium or water, leading to greater relative increase in calcium concentration. As the gallbladder bile becomes concentrated, several changes occur in the functional capacity of the cholesterol solubility system . The solubility in the micellar fraction is increased, but the stability of phospholipid-cholesterol vesicles is greatly decreased. Because cholesterol crystal precipitation occurs preferentially by vesicular rather than micellar mechanisms, the net effect of concentrating bile is an increased tendency for cholesterol nucleation.

The gallbladder lining cell secretes at least two important products into the gallbladder lumen: glycoproteins and hydrogen ions. Secretion of mucus glycoprotein occurs primarily from the glands of the gallbladder neck and cystic duct. The resultant mucin gel is believed to constitute an important part of the unstirred layer (diffusion-resistant barrier) that separates the gallbladder cell membrane from the luminal bile. This mucus barrier may be very important in protecting the gallbladder epithelium from the strong detergent effect of the highly concentrated bile salts found in the gallbladder. However, considerable evidence also suggests that mucin glycoproteins play a role as a pronucleating agent for cholesterol crystallization. The transport of hydrogen ions by the gallbladder epithelium leads to a decrease in gallbladder bile pH through a sodium-exchange mechanism. Acidification of bile promotes calcium solubility, thereby preventing its precipitation as calcium salts. The gallbladder's normal acidification process lowers the pH of entering hepatic bile from 7.5 to 7.8 down to 7.1 to 7.3.

The gallbladder fills from the continuous production of bile by the liver against the force of a contracted sphincter of Oddi. As the pressure within the common bile duct exceeds that within the gallbladder lumen, bile enters the gallbladder by retrograde flow through the cystic duct, wherein it is rapidly concentrated. Periods of filling are punctuated by brief episodes of partial emptying (∼10%-15% of its volume) of concentrated gallbladder bile that are coordinated through the duodenum of phase III of the migrating myoelectric complex (MMC).

Following a meal, the gallbladder contracts in response to both a vagally mediated cephalic phase of activity and the release of cholecystokinin (CCK), the major regulatory hormone of gallbladder function. In the next 60 to 120 minutes, about 50% to 70% of gallbladder bile is steadily emptied into the intestinal tract. CCK is localized to the proximal small intestine, especially the duodenal epithelial cells, where its release is stimulated by intraluminal fat, amino acids, and gastric acid and inhibited by bile. In addition to stimulating gallbladder contractions, CCK also acts to functionally inhibit the normal phasic motor activity of the sphincter of Oddi. Gallbladder refilling then occurs gradually over the next 60 to 90 minutes.