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PubMedDate not supplied

Long-term effects of endoscopic papillary balloon dilation on gallbladder motility.

We prospectively studied long-term (5 years) effects of endoscopic papillary balloon dilation (EPBD) on gallbladder motility. Thirteen patients with intact gallbladders (six with and seven without gallbladder stones) who had undergone EPBD for choledocholithiasis were enrolled in this study. Gallbladder volumes, while fasting and after dried egg yolk ingestion, were determined by ultrasonography, before and at 7 days, 1 month, and 1, 2, and 5 years after EPBD. Before EPBD, the gallbladder had a larger fasting volume and lower yolk-stimulated maximum contraction than in normal controls. Seven days after EPBD, fasting volume was decreased and maximum contraction was increased, regardless of whether the patient had gallbladder stones, showing significant differences from the pre-EPBD values. At 1 month to 5 years after EPBD, these changes were far less evident and gallbladder function did not differ significantly from baseline. EPBD does not adversely affect gallbladder motility in the long-term (5 years).

Aged↗

PubMed2005

Magnitude of combination therapy of radical resection and external beam radiotherapy for patients with carcinomas of the extrahepatic bile duct and gallbladder.

The present study sought to identify the therapeutic efficacy of adjuvant external beam radiotherapy (EBRT) for carcinomas of the extrahepatic bile duct (EHBD) and gallbladder. Twenty-one patients with pathologically verified EHBD carcinoma and 18 patients with gallbladder carcinoma were analyzed retrospectively by Cox regression analysis for predictors of survival. The overall 5-year survival rates after resection were 33% for EHBD carcinoma and 56% for gallbladder carcinoma. The overall 5-year survival rate for EHBD carcinoma was 60% in 8 patients without microscopic residual disease (R0), 15% in 9 patients with microscopic residual tumor (R1), and 0% in 4 patients with macroscopic residual tumor (R2). The overall 5-year survival rate of gallbladder carcinoma patients was also decreased with R status equal to 73%, 40%, and 0% for R0, R1 and R2, respectively. Adjuvant radiotherapy significantly improved the 5-year survival rate in 7 patients with R1 disease of EHBD carcinoma (P = .035), compared with survival in 2 patients who underwent resection alone. However, no significant difference was noted in the 5-year survival rate between the resection plus EBRT group and the resection alone group for gallbladder carcinoma. Multivariate analysis revealed that histopathologic grade (G) was an independent predictor of survival for EHBD carcinoma and that direct invasion of liver parenchyma was a predictor of survival for gallbladder carcinoma. This study suggests that curative resection provides the best survival for patients with EHBD and gallbladder carcinoma, and that radiotherapy may play a beneficial role in controlling local-regional residual EHBD carcinoma tumors. However, new strategies for adjuvant therapy are needed to improve survival in patients with gallbladder carcinoma.

Aged↗

PubMed1999

Clinical aspects of gallbladder motor function and dysfunction.

Impaired gallbladder motility plays an important role in the pathogenesis of benign gallbladder disorders. Defective gallbladder muscle contraction is associated with supersaturated bile with cholesterol and with pregnancy due to high circulating levels of progesterone. These abnormalities result in bile stasis that facilitates gallstone growth. A defective gallbladder muscle contraction may also contribute to the pathogenesis of acute and chronic cholecystitis. In addition, an impaired gallbladder contraction may be the source of recurrent biliary colicky pain in patients with acalculus gallbladder disease. The gallbladders of these patients have an abnormal ejection fraction of less than 35% in response to an intravenous infusion of cholecystokinin (CCK). Although histology of the gallbladder wall is grossly normal, the muscle cells are functionally abnormal, with an impaired response to agonists that act on membrane and cytosolic receptors.

Biliary Dyskinesia↗

PubMed1984

The effect of a progestin on gallbladder function in young women.

Female sex hormones have been considered to be a risk factor for the development of cholesterol gallstone disease, because of increased cholesterol saturation of bile. Impaired gallbladder function is an additional factor which is suspect but unproved. We investigated gallbladder function in 10 young women on two occasions: first during the follicular phase of the menstrual cycle, when endogenous progesterone is low, and again after the ingestion of medroxyprogesterone acetate, 10 mg/day for 10 days, just prior to the next menstrual period. Another group, 15 young women, was studied during their luteal phase, when endogenous progesterone is high. Gallbladder filling and emptying in response to cholecystokinin (0.02 U/kg-min) was quantitated by 99mTc-HIDA cholescintigraphy. Gallbladder filling and emptying were no different in women in the follicular phase than in women in the luteal phase of the menstrual cycle. In both menstrual phases, the administration of the exogenous progestin significantly (p less than 0.05) reduced the fraction of hepatic bile entering the gallbladder. Gallbladder emptying was also depressed: the total amount ejected was less, the time to empty half the contents was prolonged, and the rate was slower (p less than 0.05). Thus, different phases of the normal menstrual cycle do not appear to have any effect on gallbladder function. Administration of an exogenous progestin, however, significantly impairs both gallbladder filling and emptying, factors which could predispose to the formation of cholesterol gallstones.

Adolescent↗

PubMed1987

Pharmacologic characterization of excitatory and inhibitory cholecystokinin receptors of the cat gallbladder and sphincter of Oddi.

The pharmacologic properties and specificity of cholecystokinin (CCK) receptors of the biliary tract were investigated by testing various sulfated and desulfated CCK fractions and by using specific CCK-gastrin antagonists. Sulfated CCK-7 (5-80 pmol/kg) caused gallbladder contraction and sphincter of Oddi relaxation. Denervation with tetrodotoxin decreased the gallbladder response by 50% and changed the sphincter of Oddi response from relaxation to contraction. Desulfated CCK-7 (80-400 pmol/kg) caused a weak gallbladder contraction that was unaffected by tetrodotoxin. The gallbladder did not respond to CCK-3 (10-80 nmol/kg) or to CCK-2 (10-160 nmol/kg) in doses that completely relaxed the sphincter of Oddi. These doses, however, were 5-2000 times higher than the maximal dose of sulfated CCK-7. After denervation with tetrodotoxin, desulfated CCK-7 (10-400 pmol/kg) induced a weak sphincter of Oddi contraction even with doses five times greater than the maximal dose of sulfated CCK-7. The denervated sphincter of Oddi did not respond to CCK-3 (10-80 nmol/kg) or CCK-2 (10-160 nmol/kg). Furthermore, a continuous proglumide infusion (5-20 mg/kg X min) and bolus doses of dibutyryl cyclic guanosine monophosphate (250-1000 micrograms/kg) blocked the effect of sulfated CCK-8 on the gallbladder and sphincter of Oddi. Higher doses of these antagonists were needed, however, to block the CCK effect on the sphincter of Oddi than on the gallbladder. In contrast, high doses of desulfated CCK-7 (100 pmol/kg) or CCK-3 (200 nmol/kg) did not antagonize the effect of sulfated CCK-8 (10-80 pmol/kg) on the gallbladder. These findings suggest the existence of three sets of specific CCK receptors with molecular configuration requirements determined by the type of cell where these receptors are located: on the postganglionic cholinergic neurons, on the smooth muscle cells of the gallbladder, and sphincter of Oddi, or on the postganglionic noncholinergic, nonadrenergic inhibitory neurons.

Ampulla of Vater↗

PubMed1988

Impairment of gallbladder emptying in diabetes mellitus.

Individuals with diabetes mellitus are reported to have a twofold to threefold increase in the incidence of cholesterol gallstones. A frequently cited but unproven pathophysiologic mechanism for this phenomenon is reduced gallbladder muscle function, which results in stasis and allows for cholesterol gallstone crystal formation and gallstone growth. To date, gallbladder motor function has not been investigated in a well-characterized diabetic population. Therefore, using radionuclide cholescintigraphy, gallbladder filling and subsequent emptying produced in response to an infusion of the octapeptide of cholecystokinin in 30 diabetic patients and 20 control individuals were studied. No difference in any parameter used to assess gallbladder filling was demonstrated in the diabetics when compared with controls. In contrast, gallbladder emptying induced with cholecystokinin-octapeptide (20 ng/kg body wt . h) was reduced in diabetics compared with controls (55% +/- 5% vs. 74% +/- 4%, p less than 0.01). The peak emptying rate in the diabetics was also decreased (5.0% +/- 0.5% per minute) compared with the controls (7.0% +/- 0.6% per minute, p less than 0.02). The observed decreased gallbladder emptying found in diabetics was not related to obesity, type of diabetes, diabetic control, or presence or absence of peripheral neuropathy. The most severe impairment of gallbladder emptying occurred, however, in diabetics with an associated autonomic neuropathy. This subgroup demonstrated a significant reduction in the percentage of gallbladder emptying (40% +/- 8% vs. 62% +/- 5%, p less than 0.04) and the peak ejection rate (3.5% +/- 0.5% per minute vs. 5.6% +/- 0.6%, p less than 0.02) compared with the diabetics without autonomic neuropathy.

Diabetes Mellitus↗

PubMed1989

Effects of loxiglumide on gallbladder emptying in healthy volunteers.

This study evaluates the effects of the specific cholecystokinin receptor antagonist loxiglumide on gall-bladder emptying after a meal or after intravenous infusion of caerulein in humans. Ten healthy male volunteers were studied five times on separate days. The following five studies were performed in randomized order: (a) caerulein was intravenously infused at doses increasing from 7.5 to 120 ng/kg.h without the antagonist; (b) in addition to increasing doses of caerulein, loxiglumide was given intravenously at doses of 0.2, 1.0, or 5.0 mg/kg.h; (c) a solid-liquid 800-kcal meal was given without loxiglumide; (d) the 800-kcal meal was given with simultaneous infusion of 1 or 5 mg/kg.h loxiglumide; and (e) loxiglumide (5 mg/kg.h) was given. without caerulein or the test meal. Gallbladder volume was measured by ultrasound. Loxiglumide dose-dependently inhibited gallbladder emptying induced by caerulein or the meal. High doses of the antagonist did not only abolish meal-induced gallbladder emptying but increased gallbladder volume after administration of caerulein or the meal when compared with prior fasting values. The antagonist given alone markedly increased gallbladder volumes compared with prior fasting values. In conclusion, given alone markedly increased gallbladder volumes compared with prior fasting values. In conclusion, cholecystokinin is the hormone primarily and mainly responsible for mediation of gallbladder emptying after a regular meal. Cholecystokinin might also play a physiologic role in the regulation of the fasting tone of the gallbladder.

Adult↗

PubMed1990

Effect of loxiglumide on gallbladder contractile response to cerulein and food in humans.

The present study investigated the effect of loxiglumide, a new selective cholecystokinin-receptor antagonist, on the gallbladder contractile responses to caerulein and to food in humans. In 6 healthy men, the gallbladder emptying driven by intravenous infusion of stepwise increasing doses of cerulein (10-80 ng/kg . h) and that induced by a 550-cal standard meal were monitored by ultrasonography. In both sets of experiments, the effect of loxiglumide was tested at various infusional rates against a control infusion of saline. An infusional rate of 2.5 mg/kg . h of loxiglumide abolished the gallbladder response even to maximal doses of cerulein, whereas a rate of 1.0 mg/kg . h counteracted the cholecystokinetic activity of cerulein up to the dose of 20 ng/kg . h. In postprandial experiments, the cholecystokinin antagonist dose-dependently inhibited the physiologic gallbladder contraction. The maximal gallbladder emptying, which always occurred 85 min after the meal, was 71.1% +/- 3.3% of basal volume in control studies, 39.2% +/- 1.8% during infusion of 2.5 mg/kg . h of loxiglumide, and 17.3% +/- 5.9% when 5.0 mg/kg . h were infused. A dose of 7.5 mg/kg . h of loxiglumide was able to prevent any postprandial emptying of the gallbladder. The present study shows that a selective cholecystokinin receptorial blockade competitively antagonizes cerulein-induced gallbladder contraction and dose-dependently inhibits postprandial gallbladder emptying.

Adult↗

PubMed1993

Regulation of canine gallbladder motility by brain peptides.

BACKGROUND: Brain peptides alter most gastrointestinal functions, but their effects on gallbladder motility have not been examined in detail. METHODS: Studies were conducted in awake, male beagle dogs. RESULTS: Of 30 brain peptides evaluated, thyrotropin-releasing hormone (TRH) and calcitonin gene-related peptide (CGRP) inhibited CCK- and meal-induced gallbladder contraction. These responses were abolished by ganglionic blockade. Truncal vagotomy prevented the central inhibitory action of TRH but not that of CGRP, whereas noradrenergic blockade prevented the central inhibitory action of CGRP but not that of TRH. Muscarinic blockade did not prevent the relaxing effect of cerebral TRH but pretreatment with the vasoactive intestinal peptide (VIP) antagonist, (4Cl-D-Phe6-Leu17)VIP, significantly attenuated gallbladder relaxation induced by cerebral TRH: the combination of both VIP and muscarinic antagonists abolished TRH-induced gallbladder relaxation. alpha-Adrenergic receptor blockade but neither beta-adrenergic blockade nor adrenalectomy abolished gallbladder relaxation induced by cerebral CGRP. Intravenous infusion of VIP and norepinephrine inhibited CCK-induced gallbladder contraction and these responses were abolished dose dependently by intravenous infusion of (4Cl-D-Phe6-Leu17)VIP and phentolamine, respectively. CONCLUSIONS: Cerebral TRH inhibits canine gallbladder contraction by stimulation of vagal outflow and subsequent release of VIP acting via its specific receptor whereas cerebral CGRP inhibits gallbladder contraction by stimulation of sympathetic, noradrenergic outflow via alpha-adrenergic receptors.

Amino Acid Sequence↗

PubMed1985

Effect of pancreatic polypeptide on gallbladder filling.

Recent studies suggest that pancreatic polypeptide (PP) alters gallbladder pressure and reduces delivery of bile to the duodenum. Whether this peptide influences gallbladder emptying and/or filling is not clear. Using the prairie dog model, we tested the hypothesis that exogenous PP induces gallbladder filling. Animals maintained on control diets underwent laparotomy with placement of catheters into the gallbladder and common bile duct. The gallbladder was perfused with [14C]polyethtyleneglycol ([14C]PEG)-labeled lactated Ringer's solution (LR) at 0.1 ml/min. Effluent from the common bile duct was collected at 5-min intervals during 30-min intravenous infusions of LR, LR + 2% serum albumin, and LR + 2% serum albumin + bovine PP (10 and 50 ng/kg/min). Gallbladder pressure was continuously recorded. Total and incremental fillings were calculated based on volume and [14C]PEG concentration changes. Infusion of PP, 50 ng/kg/min, induced significant gallbladder filling. The filling response was progressive and peaked during the final 10 min of peptide infusion. These findings coupled with the observation that serum PP levels are increased for up to 6 hr postprandially suggest that PP may play an important role in the regulation of interdigestive gallbladder filling.

Animals↗

PubMed1988

Postprandial sphincter of Oddi myoelectric activity and gallbladder emptying.

Feeding initiates gallbladder emptying and bile delivery into the duodenum. It is not yet defined how the sphincter of Oddi regulates flow of bile into the duodenum during gallbladder emptying. The aim of this study was to assess postprandial spike burst activity in the sphincter of Oddi, while quantitating gallbladder emptying with noninvasive radioisotope imaging. Six adult opossums were prepared with bipolar electrodes in the sphincter of Oddi. After 2 weeks of recovery the animals were fasted overnight and positioned under a gamma camera, and myoelectric recordings were begun. After two cycles of the migrating motor complex (MMC), 2 mCi 99Tc-HIDA was infused intravenously and permitted to concentrate in the gallbladder for a period of 30 min. Subsequently, a 30-ml liquid meal, containing 0.9 g protein, 3.5 g carbohydrate, and 3.3 g fat, was instilled into the stomach. Sphincter of Oddi myoelectric activity (spike bursts/min) and gallbladder emptying (expressed as percentage of original 99Tc counts in the gallbladder) were measured at intervals for 120 min following feeding. Feeding resulted in prompt gallbladder emptying. Sphincter of Oddi spike burst activity was not altered significantly in the first 30 min after feeding, suggesting that motor activity in the sphincter of Oddi does not initially influence bile flow. Subsequently, spike burst activity increased progressively, suggesting that sphincter of Oddi motor activity may accelerate bile delivery into the duodenum during later phases of gallbladder emptying.

Ampulla of Vater↗

PubMed1990

The effect of calcium on gallbladder absorption.

The absorption of water and electrolytes is an important physiologic function of the gallbladder which is altered during gallstone formation. Extracellular calcium and calcium channel antagonists are known to affect intestinal absorption, yet their effect on gallbladder absorption is less well defined. We, therefore, tested the hypothesis that changes in extracellular calcium or in calcium channels would alter gallbladder absorption. New Zealand white rabbit gallbladders were removed, filled with a modified Krebs buffer (Ca2+ = 0.7 mM), and suspended in an oxygenated bath of the same buffer. Water absorption was determined gravimetrically by obtaining serial gallbladder weights at 10-min intervals. After a 40-min control period, the serosal bathing solution was changed to one of four experimental solutions (n = 6 for each group): Ca2+ = 0.25, 0.7, or 1.2 mM or Ca2+ = 0.7 mM plus 0.1 mM verapamil. Absorption was determined during an 80-min experimental period with results expressed as the percentage change in gallbladder absorption compared to that of the control period. The 0.25, 0.7, and 1.2 mM Ca2+ groups did not show a significant change in absorption rate from their respective control rates. However, the verapamil group did demonstrate a significant (P less than 0.05) decrease in absorption rate of -69 +/- 8% by the end of the experimental period. These data demonstrate that verapamil inhibits gallbladder absorption while changes in serosal calcium concentration have no effect. We conclude that calcium channels and intracellular calcium may play an important role in modulating gallbladder absorption.

Absorption↗

PubMed1991

Estrogen and progesterone receptors in the gallbladders from patients with gallstones.

Cytosolic receptors for estrogen and progesterone were assayed in 50 gallbladders from 29 women and 21 men who had cholecystectomies because of cholelithiasis. High-affinity (equilibrium dissociation constant, KD = 0.46 +/- 0.23 nmol/L of 24 cases) estrogen receptors were detected in 20 of 29 gallbladders from women (range = 1.6 to 32 fmol/mg protein; mean +/- S.D. = 10.9 +/- 8.1), whereas in men only 4 of 21 specimens contained detectable estrogen receptors. High-affinity (KD = 0.45 +/- 0.17 nmol/L; mean +/- S.D. of 41 cases) progesterone receptors were found in 25 of 29 gallbladders of women (range = 2 to 62 fmol/mg protein; mean +/- S.D. = 19.2 +/- 14.4) and in 16 of 21 gallbladders of men (range = 4 to 36 fmol/mg protein; mean +/- S.D. = 12.5 +/- 8.5). There is a statistically significant difference between men and women in the proportion of estrogen receptor-positive gallbladders, 19% and 69% for men and women, respectively. Progesterone receptors are present in similar proportion in the gallbladders of men (72.2%) and women (86.2%). In women a positive correlation between estrogen and progesterone receptors was found. Even in the absence of estrogen receptors, the gallbladders of men express progesterone receptors at levels similar to those observed in women. At least in cholelithiasic gallbladders, this suggests that a sex difference exists in the coexpression of estrogen and progesterone receptors. Such a difference could be related with the higher gallstone incidence in women than in men.

Cholelithiasis↗

PubMed1989

Effect of cholecystokinin octapeptide and somatostatin on the motility of guinea pig and canine gallbladder.

Species differences have been observed in the effect of cholecystokinin octapeptide (CCK OP) on the canine and guinea pig gallbladder smooth muscle motility. 1. CCK OP was more potent stimulant in canine than in guinea pig gallbladder smooth muscles. Its pD2 values were 10 and 9.2, respectively. 2. The acetylcholine (10(-4) M)-induced maximum contractions in canine gallbladder muscle strips were by 50% lower as compared to the CCK OP (10(-8) M) maximum responses while in guinea pig gallbladder muscle strips the acetylcholine (ACh) maximum responses were by 20% lower than the CCK OP maximum responses. 3. CCK OP increased [3H]ACh release by 27% in canine gallbladder and by 40% in guinea pig gallbladder. 4. Somatostatin (SOM) had not any direct myogenic effect in guinea pig and canine gallbladder but it decreased [3H]ACh release from gallbladder intrinsic cholinergic neurons.

Acetylcholine↗

PubMed1992

Bradykinin and not cholecystokinin stimulates exaggerated prostanoid release from the inflamed rabbit gallbladder.

The relationship of bradykinin and cholecystokinin (CCK) to inflamed gallbladder prostanoid synthesis and release was examined in rabbits treated with common bile duct ligation (BDL) for 24 or 72 h. Gallbladders removed from control and BDL groups were incubated in oxygenated Krebs buffer at 37 degrees C (pH 7.4) for 60 min. The slices were then placed every 20 min in vials containing increasing doses of bradykinin (30-3000 ng) or CCK (30-1000 ng). Incubation fluid was analyzed by RIA for 6-keto-prostaglandin (PG)F1 alpha (PGI2 metabolite), PGE2 and thromboxane (TX) B2. Bradykinin stimulated control gallbladder 6-keto-PGF1 alpha and PGE2 release was modest. Gallbladders from 24- and 72-h BDL groups released 3- to 10-fold higher levels of 6-keto-PGF1 alpha and PGE2 (not TXB2) following bradykinin stimulation when compared to controls, which was abolished with indomethacin pretreatment. CCK did not stimulate gallbladder prostanoid release in the control or BDL groups. These data show that bradykinin and not CCK stimulated PGI2 and PGE2 release from inflamed rabbit gallbladder. Increased BDL gallbladder PGI2 release may be prolonged or augmented by bradykinin as gallbladder distention and progressive acute inflammation stimulate local bradykinin formation.

Acute Disease↗

PubMed2004

[Iatrogenic perforation of the gallbladder during laparoscopic cholecystectomy does not influence the prognosis. Prospective study].

BACKGROUND: Perforation of the gallbladder and spillage of gallstones frequently occur in laparoscopic cholecystectomy. As stones may be lost and as spilled bile is known to be contaminated, influence on morbidity may be expected. AIMS: To evaluate the immediate and late consequences on morbidity of peroperative gallbladder perforation during laparoscopic cholecystectomy (LC) in an universitary hospital center. PATIENTS AND METHODS: One hundred and twenty one LC were prospectively evaluated with a mean follow-up of 30 months. Elective operations on 30 men and 91 women with a mean age of 56.4 years (18-85) were carried out for symptomatic cholecystolithiasis in 97 cases (80%), and in 24 cases for complicated cholecystolithiasis. The "french technique" was used for all LC, with systematic intra-operative cholangiography and ultra Sonography. Thirty-seven (30.5%) LC were performed by surgical trainees, 84 LC by confirmed surgeons. The consequences of ultra-operative gallbladder perforation were evaluated in the immediate postoperative period, especially for septic complications, and thereafter, patients were followed up 1, 6, 12 and 24 months postoperatively. RESULTS: Ultra-operative gallbladder perforation occurred in 24 cases (20%), in 83.3% during gallbladder dissection. Gallstone spillage occurred six times, and all spilled stones were removed. Gallbladder perforation was more frequent (but non significant) in acute cholecystitis (25 vs 19%, ns). A clear correlation to the skill and experience of the surgeon is shown (32.4 vs 14.2%, P =0.01). Gallbladder perforation is accompanied by an elevated (nonsignificant) postoperative morbidity (16.6 vs 7.2%, P =0.62) which is, in fact related to older patient and more acute cholecystitis in this group. No reoperations were necessary. One and two years follow-up revealed no long-term complications specially due to lost gallstones. CONCLUSION: Peroperative gallbladder perforation during LC carries no morbidity, provided a total and complete recuperation of gallstones spilled and local treatment of bile contamination with local irrigation and antibiotics. This complication is correlated to the surgeon's skill and experience.

Adolescent↗

PubMed2005

Oxytocin microinjected into dorsal motor nucleus of the vagus excites gallbladder motility via NMDA receptor-NO-cGMP pathway.

Our recent study indicated that, in the dorsal motor nucleus of the vagus (DMV), the N-methyl-D-aspartic acid (NMDA) receptor-nitric oxide (NO)-cGMP pathway participated in the regulation of gallbladder motility in rabbits. Oxytocin (OT) is involved as a neurotransmitter in autonomic regulation. The aim of the present experiments is to investigate the effect of OT microinjected into DMV on the gallbladder motility and the involvement of NMDA receptor-NO-cGMP pathway. A frog bladder connected with transducer was inserted into the gallbladder to record the gallbladder pressure. Microinjection of OT (10-50 nmol/L, 100 nl) dose dependently increased the strength of gallbladder phasic contraction. The excitatory effect of OT (10 nmol/L, 100 nl) was completely abolished by atosiban (10 mmol/L, 100 nl), the specific OT receptor antagonist, but was not influenced by [deamino-Pen(1), O-Me-Tyr(2),Arg(8)]-vasopressin (10 mmol/L, 100 nl), the V(1) receptor antagonist. Pretreatment of ketamine (10 mmol/L, 100 nl), the NMDA receptor antagonist, suppressed the gallbladder motor response to OT; but pretreatment of 6-Cyaon-7-Nitroquinoxaline-2,3-(1H,4H)-Dione (CNQX; 10 mmol/L, 100 nl), the non-NMDA receptor antagonist, did not affect it. Pretreatment of L-NAME (10 mmol/L, 100 nl), the nitric oxide synthase (NOS) inhibitor, or methyl blue (10 mmol/L, 100 nl), the guanylyl cyclase inhibitor, inhibited the excitatory effect of OT on gallbladder motility. Hence, we deduced that the microinjection of OT into the DMV enhanced the gallbladder motility through binding specific OT receptors and activating the NMDA receptor-NO-cGMP pathway.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMedDate not supplied

Hepatic vein injury during laparoscopic cholecystectomy: the unappreciated proximity of the middle hepatic vein to the gallbladder bed.

Uncontrollable hemorrhage during laparoscopic cholecystectomy occurs in 0.1% to 1.9% of all cases, with 88% originating from the gallbladder bed. The anatomical proximity between major branches of the middle hepatic vein and the gallbladder bed, and hence the risk of intraoperative bleeding, is unclear. CT scans of 20 random patients were retrospectively reviewed to identify the closest distance between branches of the middle hepatic vein and the gallbladder bed. The vein diameter was also recorded. Risk factors for intraoperative bleeding during laparoscopic cholecystectomy were also retrospectively reviewed. Large branches (mean diameter = 2.1 mm) of the middle hepatic vein are directly adjacent to the gallbladder bed in 10% of patients. An additional 10% of cases also possess branches within 1 mm of the gallbladder bed. Chronically scarred and contracted gallbladder disease may increase the risk of significant bleeding, requiring conversion. Twenty percent of all cases will display a large branch of the middle hepatic vein adherent or immediately adjacent to the gallbladder fossa. These patients are at increased risk for intraoperative bleeding. Furthermore, contracted gallbladders with evidence of chronic disease may be at increased risk for significant hemorrhage.

Aged↗