Another look at laparoscopic laser cholecystectomy.
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Cholecystectomy↗
Biomedical subjects
D L Kaminski
Publications and source records attributed to D L Kaminski.
Effect of cyclosporine and steroids on canine bile flow.
Cyclosporine and hydrocortisone are the main immunosuppressants used in transplant surgery. The purpose of this study was to determine the effect of intravenous administration of cyclosporine and hydrocortisone on bile flow in dogs. Cyclosporine in doses of 0.5, 1.0 and 1.5 mg.kg-1.hr-1 were administered along with 18 mumol/min intravenous sodium taurocholate to dogs with chronic biliary and gastric fistulas. Bile volume and bile chloride concentration and output were increased by cyclosporine in a dose-related manner, whereas bile salt concentration decreased and bile salt output was unchanged. Hydrocortisone produced small but significant increases in bile flow only at the highest dose of hydrocortisone administered. Subsequently, experiments were performed when sodium taurocholate was administered in progressively increasing doses (9, 18 and 36 mumol/min), with the dose changed every hour. Bile volume, [14C]erythritol clearance in bile and bile salt concentrations were measured with and without cyclosporine and hydrocortisone administration. Cyclosporine increased the bile salt-independent fraction of canalicular bile flow and ductular bile flow. Experiments evaluating the role of the cyclosporine carrier polyoxyethylated castor oil (Cremophor EL) demonstrated that this substance had no independent choleretic activity, whereas cyclosporine dissolved in ethanol and administered without Cremophor EL significantly increased bile flow. The results of this study indicate that cyclosporine stimulates chloride-rich choleresis independent of bile salt secretion.
Animals↗
The effect of capsaicin on gallbladder fluid absorption.
The role of the enteric nervous system of the gallbladder on mucosal water absorption was evaluated by intraluminal administration of capsaicin, a selective stimulant of afferent nerve endings. It has been postulated that the neural responses of the gallbladder are peptidergic and mediated by prostanoids. Anesthetized cats underwent gallbladder perfusion with a physiological buffer solution containing 14C polyethylene glycol as a nonabsorbable tracer to quantitate mucosal water absorption. Capsaicin was added to the perfusate and administered intraluminally at a rate of 5 mg/kg-1/hr-1 for 2 hr. One experiment on five cats was performed when capsaicin was administered and five control experiments were performed when only vehicle was added to the perfusate. Five experiments were performed when indomethacin was administered intravenously (5 mg/kg-1/hr-1) and buffer solution alone was used to perfuse the gallbladder, and five experiments were performed when capsaicin was added to the perfusate and indomethacin was administered intravenously. Additional experiments were performed when lidocaine was added to the perfusate and when lidocaine and capsaicin were administered simultaneously. Gallbladder absorption and perfusate and tissue prostaglandin E and 6 keto prostaglandin F1 alpha concentrations were evaluated. To determine whether capsaicin induced gallbladder inflammation, tissue myeloperoxidase concentrations were measured. Control feline gallbladders absorbed approximately 0.6 ml/hr. Indomethacin alone significantly decreased gallbladder absorption. Capsaicin administration increased gallbladder absorption to approximately 1.6 ml/hr, and this increase was significantly inhibited by indomethacin. (ABSTRACT TRUNCATED AT 250 WORDS)
Absorption↗
The effect of cholecystokinin-receptor antagonists on cholecystokinin-stimulated bile flow in dogs.
Cholecystokinin is a choleretic in dogs. Some of the effects of cholecystokinin in stimulating bile flow in dogs are produced by cholecystokinin stimulating the release of other choleretic hormones such as insulin and glucagon. The purpose of this study was to determine the effects of cholecystokinin receptor antagonists on canine hepatic bile flow and insulin and glucagon release from the pancreas. Cholecystokinin octapeptide (CCK-8) and intraduodenal fat were administered to dogs that had undergone cholecystectomy with chronic biliary fistulas with and without the administration of cholecystokinin receptor antagonists. Bile secretion and systemic venous insulin, glucagon, and cholecystokinin levels were measured. The cholecystokinin receptor antagonists benzotript and CR 1409 had no effect on bile flow or hormone levels when administered without cholecystokinin, whereas proglumide produced a large increase in bile flow without altering hormone levels. The response produced by proglumide may be the result of an osmotic effect produced by the substance being secreted in bile and its stimulating bile salt secretion in bile. CCK-8 and intraduodenal fat increased bile flow, bile chloride secretion, and cholecystokinin, insulin, and glucagon concentrations in venous blood. The cholecystokinin receptor antagonists benzotript and CR 1409 significantly decreased the bile flow and insulin and glucagon changes produced by exogenous CCK-8. The effect of intraduodenal fat on bile flow was not inhibited by the cholecystokinin receptor antagonists, whereas the increased insulin and glucagon levels were decreased significantly. Intraduodenal fat may release other choleretic hormones not affected by cholecystokinin receptor antagonists. The choleresis produced by exogenous CCK-8 is inhibited by cholecystokinin receptor antagonists, perhaps by inhibiting the release of the choleretic hormones insulin and glucagon.
Animals↗
Prostanoids and leukotrienes in experimental feline cholecystitis.
Current information suggests that arachidonic acid metabolites are involved in the development of cholecystitis. The purpose of this study was to evaluate eicosanoid formation during the development of experimental cholecystitis in cats. Lysophosphatidylcholine is found in the gallbladders of patients with cholecystitis and is known to be a cytolytic, membrane-damaging substance. Anesthetized cats underwent gallbladder perfusion with and without 1.5 mmol/L lysophosphatidylcholine. Additional experiments were performed when calcium ionophore were added to the perfusates and experiments were performed when cats were treated with indomethacin and underwent perfusion with lysophosphatidylcholine. Changes in the gallbladder were determined by evaluating mucosal water transport as measured by determining the changes in concentration in a nonabsorbable marker, by protein secretion and by beta-glucuronidase accumulation in gallbladder tissue as an index of inflammation. Eicosanoid formation was evaluated by measuring perfusate concentrations and gallbladder homogenate concentrations by radioimmunoassay of prostaglandin E, 6 keto prostaglandin F1 alpha, leukotriene B4 and leukotriene C4. Lysophosphatidylcholine perfusion reversed the control patterns of absorption and produced water exsorption, produced an efflux of protein into the perfusate and increased beta-glucuronidase activity. These changes were accompanied by increased production of prostaglandin E and 6 keto prostaglandin F1 alpha in gallbladder perfusate and homogenate. The concentration of leukotriene C4 in gallbladder effusate was increased by lysophosphatidylcholine when compared with control values. Indomethacin inhibited the protein efflux, decreased beta-glucuronidase levels and decreased prostaglandin E and 6 keto prostaglandin F1 alpha formation when compared with values produced by lysophosphatidylcholine alone. Cyclooxygenase inhibition did not alter the secretion of water into the gallbladder or perfusate leukotriene C4 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Long-term outcome of reversal of small intestinal bypass operations.
Between 1976 and 1987, 43 patients underwent reversal of jejunoileal bypass operations because of metabolic complications of the operation. Electrolyte imbalance, malnutrition, and diarrhea (16 patients); cirrhosis (9); nephrolithiasis (9); arthritis (7); and pathologic fractures (1) were the primary indications for reconstruction. Many patients had multiple complications of the jejunoileal bypass operation. Twenty-nine patients underwent gastroplasty at the time of reversal and 14 did not. Seventy three +/- 5 months after reversal, patients with a gastroplasty weighed significantly less than patients without a gastroplasty. Patients with electrolyte imbalance, malnutrition, and diarrhea were all improved after reconstruction. Two patients with cirrhosis died of liver failure after reconstruction; the distinguishing preoperative characteristic was ascites. Postoperative interval liver biopsies indicated improvement in histologic appearance in four patients and no change in three. Nephrolithiasis improved or disappeared in all patients after reconstruction, whereas arthritis improved in 5 of 7 patients. Gastroplasty produced no benefit in alleviation of metabolic complications of jejunoileal bypass operations. Although the survival rate in these patients at last follow-up was 95 percent, 28 percent were incapacitated. Simultaneous gastroplasty performed at the time of reversal significantly decreases body weight when compared with patients undergoing reversal without a gastroplasty.
Arthritis↗
The role of prostanoids in the production of acute acalculous cholecystitis by platelet-activating factor.
Gallbladder tissue from patients with acute acalculous cholecystitis contains increased amounts of prostanoids when compared to normal gallbladder tissue. Platelet-activating factor (PAF) is a potent stimulus of eicosanoid formation. It has been implicated as a mediator of acute inflammatory processes and systemic responses to shock. In this study the role of PAF in acute acalculous cholecystitis was evaluated. Anesthetized cats underwent gallbladder perfusion with a physiologic buffer solution containing [14C]polyethylene glycol as a nonabsorbable tracer to quantitate mucosal water absorption. Platelet-activating factor was infused into the hepatic artery for 2 hours. Control experiments were performed when vehicle alone was infused. Experiments also were performed when indomethacin was administered intravenously and when indomethacin and PAF were administered. Gallbladder mucosal absorption/secretion and perfusate and tissue prostaglandin E (PGE) and 6 keto prostaglandin F1 alpha (6-keto PGF1 alpha) levels were evaluated. Gallbladder inflammation was evaluated by beta-glucuronidase and myeloperoxidase tissue concentrations and by a histologic scoring system. Platelet-activating factor eliminated gallbladder absorption and produced net fluid secretion associated with dose-related increases in perfusate PGE concentrations and gallbladder tissue PGE and 6 keto PGF1 alpha levels when compared to control values. Platelet-activating factor produced significant inflammation in the gallbladder with increases in the histologic score of inflammation and tissue lysosomal enzyme activities. Indomethacin significantly decreased the fluid secretion, prostanoid levels, and inflammation produced by PAF. The results suggest that PAF may induce acute gallbladder inflammation associated with systemic stress through a prostanoid-mediated mechanism.
6-Ketoprostaglandin F1 alpha↗
Evaluation of prostacyclin production by human gallbladder.
The prostanoids have been demonstrated to be involved in gallbladder physiology and disease. In previous reports, prostaglandin E (PGE) compounds were found to be increased in inflamed human gallbladders. Prostaglandin synthetase inhibition decreased PGE formation by human gallbladders; however, the relief of symptoms of cholecystitis did not correlate well with the decrease in PGE formation. This suggested that other prostanoids may be involved in cholecystitis. The purpose of this study was to evaluate the production of the proinflammatory arachidonic acid metabolite prostacyclin by gallbladders from patients with calculous cholecystitis. The formation of PGE and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of prostacyclin, in normal human gallbladder mucosal cells and muscle tissue was compared with that produced by diseased mucosal cells and muscle tissue. Normal human gallbladders produced small amounts of 6-keto-PGF1 alpha, and no differences in formation rates were evident when muscle tissue was compared with mucosal cells. Diseased gallbladders produced significantly greater amounts of 6-keto-PGF1 alpha than did normal gallbladders, and diseased gallbladder muscle produced approximately four times greater amounts of 6-keto-PGF1 alpha than did diseased gallbladder mucosa. Prostacyclin formation is increased in diseased human gallbladders and may be an important mediator of the inflammatory changes of cholecystitis.
Acute Disease↗
Effect of bradykinin on feline gallbladder water transport and prostanoid formation.
Continuing evaluation of the pathophysiology of gallbladder disease has demonstrated significant relationships between gallbladder mucosal fluid transport, gallbladder inflammation, and prostanoid formation. Inflamed gallbladder mucosa secretes, rather than absorbs, fluid, a process associated with prostaglandin formation. Bradykinin has been previously implicated in the pathogenesis of cholecystitis and, in the intestine, bradykinin stimulates mucosal fluid secretion by a prostaglandin-mediated mechanism. Bradykinin was infused into the gallbladder lumen and administered intraarterially into the hepatic artery of perfused cat gallbladders. Both methods of bradykinin administration reversed the mucosal absorption present during control experiments as measured by concentration changes in a nonabsorbable marker. Perfusate and gallbladder tissue prostaglandin E concentrations were significantly increased by bradykinin when compared to control values. Concentrations of 6-keto PGF1 alpha in perfusate solutions and in gallbladder tissue were significantly increased, suggesting bradykinin increased prostacyclin formation. Bradykinin administration significantly increased inflammation, as evaluated by a histologic scoring system. Indomethacin was administered intravenously along with luminal perfusion of the gallbladder with bradykinin. Indomethacin significantly decreased gallbladder fluid secretion and prostanoid formation, but not histologic inflammation, when compared to values produced by bradykinin alone. An increase in systemic vascular and bile kinin concentrations produces gallbladder mucosal water secretion, a process which may be mediated by prostanoids. Histologic inflammation produced by bradykinin was not prevented by indomethacin.
6-Ketoprostaglandin F1 alpha↗
Role of glucagon and insulin in canine bile flow stimulated by endogenous cholecystokinin release.
The role of endogenous cholecystokinin (CCK) in stimulating hepatic bile flow was evaluated. Attention was directed at discerning the relative importance of the ability of CCK to stimulate the release from the pancreas of the choleretic hormones glucagon and insulin. Utilizing dogs with chronic biliary and gastric fistulas, duodenal infusion of a lipid emulsion resulted in an increase in cholecystokinin concentration and hepatic bile flow. Endogenous CCK stimulation was associated with a significant increase in the concentrations of both glucagon and insulin. In an effort to separate the potential choleretic response of CCK from that of glucagon and insulin, subsequent experiments were performed on anesthetized dogs that had the source of glucagon and insulin eliminated by pancreatectomy and gastrectomy. The duodenum and its arterial blood supply and venous drainage were carefully preserved, and intraduodenal infusion of emulsified lipid resulted in an exaggerated increase in systemic CCK concentrations. Although CCK release occurred in the absence of the pancreatic and gastric changes in bile flow, glucagon and insulin were eliminated. The results of this study indicate that intraduodenal lipid increases hepatic bile flow by glucagon- and insulin-mediated CCK stimulation. There is no evidence to support any direct choleretic activity of CCK.
Animals↗
Arachidonic acid metabolites in hepatobiliary physiology and disease.
Arachidonic acid metabolites are involved in a wide spectrum of hepatobiliary physiologic functions and disease. Prostanoids alter hepatic bile flow. Prostaglandins with a C9 ketooxygen stimulate a bicarbonate-rich choleresis and those with a C9 hydroxyloxygen produce a chloride-rich choleresis. Prostaglandin F2 alpha stimulates the release of the potent choleretic glucagon and the stimulatory effect of prostaglandin F2 alpha on bile flow is inhibited by cyclooxygenase inhibitors, suggesting that prostaglandins play a role in the release of choleretic hormones as well as in their action. Prostanoids are involved in gallbladder contraction and water absorption. Prostaglandins produce gallbladder contraction in various species and cause gallbladder relaxation in other species. Prostaglandins also may be mediators of cholecystokinetic hormone action; however, cyclooxygenase inhibitors do not inhibit the effect of cholecystokinetic hormones in all species. Prostanoids alter the normal process of water absorption by gallbladder mucosa and induce net water secretion. The inflamed gallbladder secretes rather than absorbs fluid. The demonstration that prostaglandin E2 inhibits gallbladder fluid absorption has led to subsequent studies that demonstrated that the secretion of fluid into the inflamed gallbladder lumen may be mediated by prostanoids. In cholecystitis, the prostanoids may mediate the distention produced by mucosal fluid secretion and the contraction of the diseased gallbladder. The inflammatory changes produced in various experimental models of cholecystitis can be prevented by cyclooxygenase inhibitors. Cyclooxygenase inhibitors decrease gallbladder prostaglandin formation and are effective in producing relief of the symptoms of gallbladder disease. In experimental cholesterol gallstone formation, prostaglandins are involved in the production of mucin, which acts as a nidus for stone formation, and cyclooxygenase inhibitors prevent the formation of experimental cholesterol gallstones. Prostaglandins have been shown to be cytoprotective in various types of experimental hepatic injury and leukotrienes have been shown to be injurious to hepatocytes and biliary tract tissues. Specific prostanoids and lipoxygenase inhibitors may be valuable in treating patients with various acute hepatic inflammatory disease processes. Continued evaluation of the role of arachidonic acid metabolites in hepatobiliary physiology and disease may lead to important new therapeutic modalities.
Arachidonic Acids↗
Orthotopic liver transplantation resulting in amitriptyline toxicity in the recipient.
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Adult↗
Initial results of a program in liver transplantation.
St. Louis University established a liver transplant program in early 1988. The authors report on the program's first 10 months in operation, emphasizing the careful planning and cooperation the medical center must undertake to ensure the program's success.
Female↗
A simplified technique for the extirpation of the gastric bubble using an endo-overtube.
Since 1982, the medical literature as well as the lay press discussed an artificial bezoar, the gastric bubble, as an adjuvant in the treatment of morbid obesity. Approved by the FDA, the Garren-Edwards Gastric Bubble has been reported by the company to have been placed over 17,000 times. Due to a reported increased rate of deflation after three months, removal and reimplantation of a new bubble is recommended. After deflation, some difficulty in retrieval of the bubble has been reported. The authors report a new technique for bubble extraction. The bubble is visualized through a gastroscope and deflated using bicap cautery. The gastroscope is removed. The endo-overtube is placed on the gastroscope and this assembly is reintroduced through the esophagus to the level of the GE junction. The deflated bubble is visualized, grasped with a forceps, and withdrawn into the endo-overtube until becoming wedged. The entire assembly (gastroscope, overtube, forceps, and gastric bubble) are removed. With this technique, bubble removal has been simplified and has decreased the procedure length to approximately fifteen minutes.
Equipment and Supplies↗
Role of glucagon in cholecystokinin-stimulated bile flow in dogs.
Although many choleretic agents are known, their physiological roles and interrelationships in increasing bile flow remain largely undetermined. Exogenous cholecystokinin (CCK), glucagon, and insulin are stimulants of hepatic bile flow in animals and humans. Of possible importance in the choleresis produced by CCK is the stimulation by exogenous CCK of glucagon and insulin release from the pancreas. This research evaluates the role of glucagon and insulin in the choleresis produced by CCK. Dogs with chronic biliary and gastric fistulas were used. The synthetic octapeptide of CCK (CCK-8) administered in increasing doses produced progressive increases in bile volume, bile bicarbonate secretion, and bile chloride concentration and output. The choleresis produced by CCK-8 was qualitatively similar to that produced by intravenous glucagon. CCK-8 administration in increasing doses produced progressive increases in plasma glucagon. When bile flow changes during CCK-8 administration were correlated with changes in plasma glucagon, significant correlation existed. CCK-8 significantly increased serum insulin concentration only at the highest dose of CCK-8 administered. Somatostatin is an inhibitor of hormone release. Administration of somatostatin, along with CCK-8, inhibited the choleresis and the increased plasma glucagon produced by CCK-8 administration alone. During acute experiments in anesthetized dogs, the pancreas and stomach were removed to eliminate endogenous glucagon and insulin release. (ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Pancreatitis after biliary tract surgery.
Pancreatitis associated with biliary tract operations continues to be an important clinical problem. The results of biliary tract operations performed on 1256 patients were carefully scrutinized for the presence of postoperative hyperamylasemia and pancreatitis persisting after 48 hours. Patients were evaluated in the context of the presence or absence of preoperative pancreatic dysfunction. Similarly, various operative risk factors were evaluated, including cholangiography, choledocholithiasis, common duct exploration, choledochoscopy, choledochoduodenostomy, and sphincteroplasty. Operative cholangiography did not induce postoperative pancreatitis. The incidence of postoperative pancreatitis following cholecystectomy was 0.6%, which was significantly greater than the incidence following common duct exploration (8.4%). Pancreatitis following biliary tract surgery seemed to be not directly related to the performance of choledochoscopy, sphincteroplasty, or choledochoduodenostomy, as it developed with similar frequency in patients undergoing common duct exploration alone. The timing of operative therapy in patients with biliary tract pancreatitis did not significantly alter the frequency with which pancreatitis persisted in the postoperative period. In 970 patients undergoing cholecystectomy, one patient who had preoperative pancreatitis died of postoperative pancreatitis. Of 286 patients undergoing common duct exploration, seven patients died with pancreatitis. In three of these patients there was no active preoperative pancreatitis, and in one of these patients pancreatitis was the cause of death. Four patients with preoperative pancreatitis eventually died of pancreatitis in the postoperative period. Pancreatitis is an important complication of biliary tract disease and operations, and all efforts should be extended to suppress its occurrence and development.
Amylases↗
Effect of stimulation of endogenous glucagon secretion by amino acid administration on canine hepatic bile flow.
Exogenous glucagon administration is associated with stimulation of hepatic bile flow. The physiologic role that glucagon plays in the control of hepatic bile flow remains indeterminant. The purpose of this study was to evaluate amino acid administration, a stimulus of endogenous glucagon release, on canine hepatic bile flow. The experiments were performed utilizing cholecystectomized dogs with chronic biliary fistulas. The enterohepatic circulation of bile salts was artificially maintained by intravenous bile salt administration. Intravenous L-arginine stimulated endogenous glucagon release and hepatic bile secretion. Intravenous amino acid administration produced significant increases in hepatic bile flow and plasma glucagon and was significantly more potent than intravenous arginine. Intravenous amino acid administration produced small but significant increases in serum insulin but did not significantly change plasma concentrations of cholecystokinin. The results of this study suggest that endogenous glucagon secretion produces a choleresis and supports a role for glucagon in the physiologic control of canine hepatic bile flow.
Amino Acids↗
Effects of somatostatin on acute canine experimental pancreatitis.
Somatostatin is an inhibitory hormone that decreases the secretion and end organ response of cholecystokinin (CCK). Inhibition of hormonal stimulation of pancreatic exocrine secretion by somatostatin may improve the course of acute pancreatitis. Anesthetized dogs underwent cholecystectomy and cannulation of the pancreatic duct, thoracic duct, and portal vein. Twenty experiments were performed in random order with 5 dogs in each group. Hourly measurements of lymph flow and portal and thoracic duct amylase were made. Portal blood insulin, glucagon, and CCK concentrations were determined by radioimmunoassay on samples obtained at the beginning and end of the experiments. Pancreatitis was induced by injecting, under constant pressure, 10 ml bile into the pancreatic duct during 1 min. Somatostatin was administered intravenously (20 micrograms/kg/hr). After 5 h, the dogs were killed, pancreas glands removed and weighed and tissue samples obtained for histologic evaluation. There was a significant increase in lymph amylase output and portal venous amylase and CCK concentrations in the dogs with pancreatitis compared to the control dogs. In dogs with pancreatitis, lymphatic amylase secretion and portal CCK concentrations were significantly decreased by somatostatin. Somatostatin did not significantly alter portal amylase concentrations, pancreas gland weights or histologic inflammation when compared to values from dogs with pancreatitis not treated with somatostatin.
Acute Disease↗