Changes of gastrointestinal myoelectric activity and bile acid pool size after cholecystectomy in guinea pigs (original) (raw)
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Digestive Diseases and Sciences, 1999
Nine gallstone patients with normal gallbladder function as assessed by hepatobiliary scintigraphy were included. Fasting and postprandial duodenal motility were studied before and one month after an uncomplicated laparoscopic cholecystectomy. An ambulatory continuous pressure recording was obtained from 5 PM to 8 AM with a sampling frequency of 4 Hz. At 6 PM, the patients received a 1400-kJ standard meal. The size of the bile acid pool after cholecystectomy was measured according to the dilution principle using [C14]cholic acid as the marker. Preoperatively the migrating motor complex (MMC) cycle was 0.48/hr (quartiles 0.42-0.68) compared to 0.68/hr (0.43-0.77) postoperatively. This difference was not significant. An increase in the MMC cycle frequency was observed postoperatively in three patients, and a decrease was seen in four patients. The migration velocity was 5.61 cm/min (4.26-8.01) preoperatively and 7.16 cm/min (4.79-9.71) postoperatively, a difference that was not significant. The time period from meal ingestion to appearance of phase III was 297 min (218-431) at the preoperative examination and 443 min (192-494) at the postoperative examination. This difference was not significant. The size of the bile acid pool after cholecystectomy was 3.68 mmol (2.69-8.47) and was not significantly correlated to the frequency of the MMC cycle or the time period from food ingestion to phase III activity. It is concluded that in gallstone patients with a normally functioning gallbladder, cholecystectomy does not alter duodenal motility, which was not correlated to the size of the bile acid pool.
Enterohepatic circulation of bile acids after cholecystectomy
Gut, 1978
Bile acid metabolism was investigated in 10 patients after cholecystectomy, 10 gallstone patients, and 10 control subjects. Diurnal variations of serum levels of cholic and chenodeoxycholic acid conjugates were not abolished by cholecystectomy. Cholic acid pool size was significantly reduced in cholecystectomised patients and the fractional turnover rate and the rate of intestinal degradation of bile acid showed a significant increase. In cholecystectomised patients fasting bile was supersaturated in cholesterol, though less than in gallstone patients, but, in both, feeding resulted in improvement of cholesterol solubility in bile. These data suggest that after cholecystectomy the small intestine alone acts as a pump in regulating the dynamics of the enterohepatic circulation of bile acids and that the improvement of cholesterol solubility in bile is due to a more rapid circulation of the bile acid pool in fasting cholecystectomised patients.
Quarterly Journal of Experimental Physiology, 1981
The role of enterohepatic circulation of bile salts in biliary secretion in conscious rabbits has been investigated before and after cholecystectomy. Bile flow was higher and bile salt concentration lower in cholecystectomized than in intact rabbits: this could have been caused by a negative feedback effect on bile salt synthesis as the circulating bile salt pool increased. The effects of cholecystectomy on flow and bile salt concentration balanced each other. Bile flow and bile salt concentration declined after interruption of the enterohepatic circulation in both cholecystectomized and intact rabbits. Furthermore, the percentage of the flow of bile independent of bile salt secretion increased, while that independent of total analysed solutes decreased after the enterohepatic circulation was broken. These results confirm that the decrease in bile flow after interruption of the enterohepatic circulation is due to loss of bile salts and not of electrolytes. * See Methods.
The gallbladder of the guinea pig: Its concentrating and contractile abilities
Comparative Biochemistry and Physiology Part A: Physiology, 1974
Bile aspirated from guinea pig gallbladders had a higher concentration of bile salts than did hepatic bile. 2. When hepatic bile was left in the gallbladders, absorption of water and ions occurred. The relative rate of reabsorption, about 6 per cent of the simultaneous rate of bile production, was less than reported for dogs (about 70 per cent). 3. Gallbladders contracted spontaneously and in response to i.v. cholecystokinin-pancreozymin, and to large amounts of intraduodenal acid. 4. In guinea pigs, which eat frequently, concentrating and contractile ability of the gallbladder is less than in species such as dogs, in which digestion is episodic.
Digestive Diseases and Sciences, 2004
The present investigation was undertaken to delineate the in vitro responsiveness of cholelithiatic gallbladders to cholecystokinin (CCK) and compared with those evoked by carbachol, histamine, or electrical stimulation. Gallbladder muscular strips (2-3 mm wide and 15-20 mm long) from patients undergoing cholecystectomy were used for recording the in vitro contractions evoked by electrical and chemical (carbachol, histamine, or cholecystokinin) stimulation. Stimulation of strips with trains of pulses (5-msec duration, 70 V at 100 Hz) of varying train durations (0.01 to 9 sec) elicited duration-dependent increase in the amplitude of contractions and the maximal contractions were seen with 5 sec. Atropine (0.4 µM) significantly attenuated these contractions, leaving about 34% of contractions, which in turn was abolished by xylocaine. Carbachol produced a concentrationdependent (0.004-0.4 µM) increase in force of contraction and the maximal response was seen at 0.4 µM and abolished by atropine (0.4 µM). Histamine also produced contractions and the maximal contractions were about 35% of the maximal carbachol response. Histamine-induced contractions were not abolished by atropine but were abolished by xylocaine. CCK up to 10 µM failed to evoke any contraction, even though the strips were responsive to carbachol. The results indicate that cholelithiatic gallbladders exhibited responses to electrical stimulation through cholinergic and histaminergic plexuses and they were insensitive to CCK.
American Journal of Surgery, 1990
In order to evaluate the effect of cholecystectomy on the gastric mucosa, the duodenogastric reflux of total and single bile acids, the number of parietal and gastrin cells, and the volume of gastric acid secretion were examined in 15 patients with gallstones and functioning gallbladders before and 6 months after cholecystectomy. The duodenogastric reflux of the total bile acids increased from a mean preoperative value of 1.9 #mol/hour to a mean postoperative value of 21 #mol/hour (p = 0.008). The duodenogastric reflux of all single bile acids increased after cholecystectomy, with a higher increase in glycoconjugated compared with tauroconjugated bile acids. The parietal cells decreased from a mean preoperative value of 82.8 to a mean postoperative value of 68.7 (p = 0.05), whereas there was only a mild increase in the number of gastrin cells; the output of gastric acid remained unchanged. The variation of the gastrin cells before and after cholecystectomy was negatively correlated only with the variation of taurocholic acid (r = -0.50, p = 0.05), while the variation of the parietal cells was mildly correlated with all single bile acids (r = 0.35-0.50, 0.05 < p <0.02). These findings show an increased duodenogastric reflux of bile acids 6 months after cholecystectomy with a mild morphologic alteration of the gastric mucosa. C holecystectomy is a common surgical operation, and it is important to be aware of its eventual side effects. Surgical removal of the gallbladder alters the composition of hepatic bile [1-5] and probably increases the risk of colorectal cancer [6-10], but little is known about its effect on the stomach.
Disrupted bile flow affects interdigestive small bowel motility in rats
Surgery, 1997
The role of bile flow in the regulation of small bowel motility and the migrating myoelectric complex (MMC) is unclear. We aimed to study the effects of biliary diversion or obstruction on the MMC in a newly developed rat model. In rats, myoelectrodes were implanted in the jejunum, and the proximal common bile duct (CBD) was cannulated and exteriorized at the head, enabling us to manipulate biliary flow without influencing pancreatic flow and without the need of anesthesia or additional surgery. Group A were controls without CBD cannulas. Biliary circulation was exteriorized but kept intact in group B; bile was diverted externally in group C; and the CBD was obstructed in group D. MMCs were recorded in unrestrained conditions by jejunal electromyography before and after biliary diversion or obstruction. Spontaneous recanalization of the CBD was monitored by measurement of serum bilirubin and by cholangiography. Exteriorization of the CBD without interruption of bile flow did not aff...
Hepatology, 1990
To determine the role of cholecystokinin and the cholinergic system in intestinal stimulation of gallbladder contraction, we studied the effects of atropine on plasma cholecystokinin and gallbladder contraction in six healthy volunteers (four men and two women aged 20 to 27 yr). Effects were noted after intraduodenal fat instillation and after dosage with exogenous cholecystokinin inducing plasma cholecystokinin coneentrations similar to those after intraduodenal fat instillation. At regular intervals before and after administration of each stimulus, plasma cholecystokinin concentrations and gallbladder volumes were measured by radioimmunoassay and real-time ultrasonography, respectively. Intraduodenal infusion of 250 ml2W0 Intralipid induced a peak plasma cholecystokinin increment of 10.2 f 1.6 pmol/L compared with 10.7 f 0.7 pmol/L during infusion of 1 Ivy dog unit per kilogram per hour of cholecystokinin. The increases in plasma cholecystokinin after fat and exogenous cholecystokinin administration were accompanied by similar decreases in gallbladder volume. Integrated gallbladder contraction after fat instillation was 3,%% * 288%. min compared with 3,301% 2 359% . min during cholecystokinin infusion (NS). Atropine (0.015 mg/kg as bolus followed by 0.005 mglkglhr) did not change plasma cholecystokinin concentrations but induced similar inhibition of gallbladder contraction to 2396% 2 511% . rnin (p < 0.05) after intraduodenal fat instillation and to 1,756% 2 456% 1 rnin (p < 0.05) during cholecystokinin infusion.