ABSTRACT
Knowledge of the anterolateral abdominal wall anatomy is crucial for a surgical approach to the abdominal cavity and for reconstructive surgery of abdominal wall defects. Furthermore it can help the surgeon ensure optimal surgical results by avoiding anatomical complications. This overview presents the surgical relevant anatomy and emphasizes surgical principles and pitfalls in abdominal wall surgery.
Subject(s)
Abdominal Wall/anatomy & histology , Abdominal Wall/surgery , Abdominal Wound Closure Techniques , Abdominal Muscles/anatomy & histology , Abdominal Muscles/surgery , Humans , Incisional Hernia/etiology , Incisional Hernia/prevention & control , Incisional Hernia/surgery , Postoperative Complications/etiology , Postoperative Complications/prevention & control , Postoperative Complications/surgery , Suture TechniquesABSTRACT
The role of intraduodenal bile acids in the regulation of cholecystokinin (CCK), pancreatic polypeptide (PP), and secretin as well as exocrine pancreatic and biliary secretion was investigated by means of a duodenal marker perfusion technique in volunteers. The following solutions were perfused: (1) liquid test meal, (2) test meal with 6 g cholestyramine, (3) test meal with 2 g chenodeoxycholic acid (CDC), (4) test meal with 6 g cholestyramine and 2 g CDC, (5) 6 g cholestyramine alone, and (6) 2 g CDC alone. The test meal caused an immediate increase in CCK and PP plasma levels, whereas secretin was not significantly altered. CCK release was further enhanced by addition of cholestyramine, whereas CDC inhibited release. The stimulatory effect of cholestyramine was abolished by CDC. CDC alone and in combination with the test meal stimulated secretin release. The response of PP to the test meal was not altered by addition of either compound. Cholestyramine and CDC alone caused only a very small increase in CCK levels, whereas PP was stimulated to nearly postprandial values. Meal-stimulated pancreatic and biliary secretion was significantly enhanced by cholestyramine, CDC, and the combination of both. CDC and cholestyramine alone each stimulated enzyme and bile secretion to a greater extent than the test meal. We conclude that intraduodenal bile salts are a modulator of postprandial CCK release. Changes in exocrine pancreatic and biliary and PP secretion do not necessarily parallel CCK concentrations, suggesting that different mediators are involved in the observed bile acid-induced changes in humans.