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At least 919 records · Page 51Linked to original sources
PubMed2005

Intraoperative tumor localization using laparoscopic ultrasonography in laparoscopic-assisted gastrectomy.

BACKGROUND: During laparoscopic-assisted gastrectomy, it is impossible to identify early gastric cancer (EGC) lesions; therefore, a precise localization technique is needed. In this study, we used laparoscopic ultrasonography (LUS) after endoscopic clipping as a method of localizing EGC and evaluated the effectiveness of this method. METHODS: A prospective study of 17 patients who had undergone laparoscopic-assisted gastrectomy was performed. Three endoscopic clips were applied just proximal to the tumor during the preoperative endoscopy. The applied clips were detected from the serosal side of the stomach using LUS. The serosal surface of the lesion was marked with dye. RESULTS: In all patients, endoscopic clips were applied proximal to the lesion without complications, and the applied clips were confirmed by plain abdominal radiography. The clips were successfully detected by LUS in all patients. In the resected specimen, the serosal surface, marked with dye, was always just above the clips in the anterior wall or on the anterior wall opposite the clips applied in the posterior wall. The mean detection time was 4.7 min (range, 2-8). With this procedure, two patients underwent total gastrectomy and 15 patients underwent distal subtotal gastrectomy with gastroduodenostomy or gastrojejunostomy. Histological examination confirmed that the resection margins were tumor free in all patients. There was no operative morbidity related to the LUS procedure. CONCLUSIONS: Using LUS to detect endoscopic clips is an easy, safe, and accurate method to localize EGC lesions in laparoscopic-assisted gastrectomy.

Adult↗
PubMed1998

Small carcinoma of the pancreas. Factors of prognostic relevance.

UNLABELLED: Tumor size seems to be one of the primary prognostic factors that influence outcome in pancreatic cancer patients. This finding is reflected in both the Japanese and the International Union against Cancer (UICC) staging systems, in which T categories have a major influence on stage grouping. To investigate whether small tumor size is a prognostic indicator in patients with pancreatic carcinoma, we evaluated (in a prospective study) patients with a small pancreatic cancer, categorized as T1a (<2 cm) or T1b (<4 cm) tumors according to the UICC (1997). PATIENTS AND RESULTS: Of 670 treated patients with pan-creatic malignancies, 26 (3.8%) had a small pancreatic tumor (20 T1b; 6 T1a), Twenty-one patients were treated by pylorus-preserving duodenopancreatectomy, 4 patients re-ceived a left pancreatic resection, and 1 patient underwent a total pancreatectomy. All procedures included extensive soft tissue clearance. Local growth pattern was analyzed according to the Japan Pancreas Society (JPS) criteria for pancreatic cancer, i.e., lymph node involvement - N1 (limited to group 1 nodes) was found in 6/26 patients. Serosal infiltration - S1 (single area) was found in 6/26 and S2 (multiple areas) in 6/26; S3 (infiltration to adjacent organs) was found in 1/26. Retroperitoneal infiltration - Rp1 (adjacent to the pancreas) was found in 7/26 and Rp2 (not limited to adjacent tissues, but no other organs involved) was found in 3/26. Venous involvement (Pv2) was found in 1/26. The 5- and 10-year survival rate for the 26 patients was 46%. Interestingly, the T1a tumor patients had a significantly lower 5 year survival rate than the T1b patients (32% vs 58%; P < 0.05). Of prognostic relevance was lymph node metastasis, and retroperitoneal and serosal involvement and these patients had a significantly lower 5-year survival rate than those without such involvement regardless of tumor size (P < 0. 01). CONCLUSIONS: An overall 5-year survival rate of 46% is exceptionally good. Unfortunately, among pancreatic cancer patients those with a small carcinoma represent a highly selected group, representing less than 5% in our series. Interestingly tumor size is of less prognostic relevance than lymph node, retroperitoneal, and serosal involvement. Radical resection with extensive soft tissue clearance therefore seems essential to achieve such a high survival rate.

Chi-Square Distribution↗
PubMed1999

Histopathologic criteria for local excision of colorectal cancer: multivariate analysis.

BACKGROUND: Local treatment of colorectal cancer, including endoscopic removal of colonic polyps and transanal resection of rectal tumors, has become widely accepted. However, risk factors predicting the presence of lymph node metastasis have not been fully investigated. To determine the criteria for local excision of colorectal cancer, histopathologic factors independently predicting the lymph node metastasis were investigated. METHODS: We performed a retrospective histopathologic study on 335 patients who underwent resection of colorectal cancer and dissection of regional lymph nodes between 1982 and 1996. Features of node-positive tumors (n = 150) were compared with those of node-negative tumors (n = 185), with special reference to the histopathologic findings of the resected tumor. Multivariate analysis was done using the stepwise logistic regression test. RESULTS: Node-positive tumors, when compared with node-negative tumors, were characterized by tumor larger than 6 cm (42% vs. 22%), serosal invasion (88% vs. 56%), lymphatic invasion (32% vs. 5%), venous invasion (9% vs. 2%), and histology other than well-differentiated (66% vs. 29%). Multivariate analysis showed that factors independently associated with lymph node metastasis were serosal invasion, lymphatic invasion, and histologic type. When these three risk factors were negative, lymph node metastasis was rare (5%). When one, two, or three factors were positive, the frequency of lymph node metastasis was 38%, 66%, and 85%, respectively. CONCLUSIONS: In colorectal cancer, factors independently associated with lymph node metastasis are serosal invasion, lymphatic invasion, and histologic type. When these three parameters are favorable, local treatment of colorectal cancer does not require additional lymph node dissection.

Colorectal Neoplasms↗
PubMed1993

Laparoscopic capacitance: a mystery measured. Experiments in pigs with confirmation in the engineering laboratory.

OBJECTIVES: Our purpose was to determine whether capacitive currents induced in operative laparoscopes during endoscopic electrosurgery can cause unintentional injury and to measure these currents in the laboratory. STUDY DESIGN: In five anesthetized live pigs we tested whether capacitive currents generated in operative laparoscopes by unipolar instruments cause serosal injury. These currents were then measured in the clinical engineering laboratory. RESULTS: In the setting examined by us serosal injury by capacitive currents occurred only with high generator output power. In the laboratory the maximum power of these capacitive currents measured 2.5 W. CONCLUSIONS: Capacitive coupling between unipolar instruments and 10 mm operating laparoscopes requires relatively high generator output to cause serosal injury. Lower generator output settings may cause injury with electrosurgical generators capable of higher voltages than the units used in this study (Valleylab SSE2L and Force 2).

Abdominal Muscles↗
PubMed1978

Non-step intracellular voltage response of epithelial and oxyntic cells in frog gastric mucosa.

Intracellular analyses of the electrical potential response to current pulses were performed in epithelial and oxyntic cells of the frog gastric mucosa. Independently of the use of Cl- or SO(2-)4 solutions and of the transmucosal potential difference measured, the resistance and slow potential changes observed across the mucosal surface of epithelial cells are not different from those registered across the serosal surface. In the oxyntic cells the resistance and slow potential changes are significantly higher across the mucosal than across the serosal surface, when the solution in contact with the serosal surface is positive with respect to the solution in contact with the mucosal surface. These differences were not observed when the transmucosal potential difference was reversed. It is proposed that the ionic concentration changes, by effect of current flow across the mucosa, occur in the oxyntic cells and that these changes are the origin of the slow transmucosal potential change. The epithelial cells act as a passive shunt.

Animals↗
PubMed1978

Amylase transport across ileal epithelium in vitro.

Amylase transport was measured across the rabbit ileum in vitro employing a modified Ussing chamber. Amylase was moved preferentially in the mucosal to serosal direction. Its rate of transfer was 2--3 orders of magnitude greater than that for inulin. Mucosal to serosal transport of exogenous amylase was completely inhibited in the absence of oxygen. There was also a constant release of endogenous amylase from intestinal tissue into both mucosal and serosal compartments in the absence of an exogenous source. An estimate of the rate of amylase absorption indicates that it may be of sufficient magnitude to account for the enteropancreatic circulation of amylase secreted by the pancreas during augmented secretion.

Amylases↗
PubMed1983

Non-electrolyte diffusion across the frog gastric mucosa under osmotic gradients.

Serosal-to-mucosal and mucosal-to-serosal diffusion of 14C-labelled inulin, sucrose, erythritol and propionamide was compared with 3HHO diffusion in mucosae incubated with isosmotic solutions at both surfaces, as well as isosmotic solution at serosal surface and hyperosmotic solution at the mucosal surface. The use of a hyperosmotic solution at the mucosal surface significantly increases unidirectional diffusion fluxes of inulin and of sucrose. To a nonsignificant extent, it affects the fluxes of erythritol and propionamide and significantly reduces the 3HHO diffusion. A size increment of the diffusion path utilized by the larger molecules is proposed.

Amides↗
PubMed1984

Maximal flux responses after multiple challenges with vasopressin.

Antidiuretic hormone (ADH) increases transepithelial flux of water and particular solutes across the amphibian urinary bladder and mammalian collecting duct by increasing the permeability of the apical surface. We find that if each challenge with ADH is ended by replacing the medium bathing both the mucosal and serosal surfaces of the toad bladder, then rechallenge with the same supramaximal dose of ADH 36-100 min later produces flux equivalent to or greater than the original response, but rechallenge after 15 min produces only 68% of the original response. If the medium bathing the mucosal surface is neither replaced nor returned to its original volume, complete recovery of the osmotic flux response to ADH does not occur. Maximal restimulation by ADH occurs with transepithelial osmotic gradients between 119 and 180 mosmol/kg during both challenges (the serosal bath is always isotonic amphibian Ringers). In addition, ADH-containing serosal baths that have maximally activated transport across bladders for 30-60 min can be reused and again produce maximal activation of ADH responses in fresh bladders or in the original bladders after washing. These results are in contradistinction to reports of desensitization of transepithelial flux upon rechallenge with ADH after an initial stimulation under many conditions. Our findings suggest that desensitization in vitro may result from experimental design rather than intrinsic biological characteristics of the system.

Animals↗
PubMed1984

Chloride-induced increment in short-circuiting current of the turtle bladder. Effects of in-vivo acid-base state.

Evidence for the participation of conductive and non-conductive (exchange) transmembrane anion pathways in the luminal acidification, alkalinization, and chloride-reabsorptive functions of the turtle bladder is provided from the pattern of Cl- -induced changes in transepithelial electrical parameters of isolated urinary bladders from three groups of donor turtles: control or post-absorptive turtles (those killed 5 days after feeding); acidotic turtles (NH4Cl-loaded); and alkalotic turtles (NaHCO3-loaded). The predominance of each of the three aforementioned transport functions as well as the response to Cl- -addition is altered by the in-vivo electrolyte balance of the turtle. In post-absorptive bladders, which are poised for acidification and Cl- reabsorption, the mucosal and serosal addition of Cl- to Na+-free, (HCO3- + CO2)-containing media increases the negative short-circuiting current (Isc). In acidotic bladders, which are poised for acidification but not Cl- reabsorption, mucosal Cl- addition has no effect on this Isc whereas serosal Cl- addition increases the negative Isc in a manner identical to that observed in the post-absorptive bladders. Alkalotic bladders do not possess an acidification function but instead are poised for Cl- reabsorption and cAMP-dependent electrogenic alkali secretion (positive Isc). In these bladders, serosal Cl- addition is without effect while mucosal Cl- addition produces transient changes in this positive Isc. It is found that these results can be replicated by a model of the turtle bladder in which transmembrane Cl- and HCO3- conductive and exchange paths mediate transepithelial acidification, alkalinization and Cl- reabsorption.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Intracellular Ca2+ concentration and the antidiuretic hormone-induced increase in water permeability: effects of ionophore A23187 and quinidine.

The hydroosmotic responses induced by oxytocin and 8-bromo-cyclic AMP, in frog and toad urinary bladders, were recorded minute by minute. 3HHO and 45Ca unidirectional fluxes as well as prostaglandin B2 liberation were also measured. It was observed that: (1) Addition of the calcium ionophore A23187 or quinidine to the serosal bath inhibited the response to oxytocin, but not to 8-bromo-cyclic AMP, while increasing prostaglandin E1 liberation into the serosal but not into the mucosal bath. (2) Addition of A23187 to the mucosal bath induced a transient and temperature-dependent inhibition of the response elicited by 8-bromo-cyclic AMP. The time-course of this reduction in water permeability and its sensitivity to medium temperature were similar to those observed after the withdrawal of agonist, but clearly different of those observed after intracellular acidification. (3) The hydroosmotic response was also transitorily inhibited when the Ca2+ concentration was step-changed in the mucosal bath. (4) When added to the mucosal or to the serosal baths, the ionophore increased either the apical or the laterobasal Ca2+ permeabilities. It is concluded that manipulation of intracellular Ca2+ interferes with the hydroosmotic response at two different levels. (1) A first target point located 'pre-cyclic-AMP production'. This effect would be mediated by prostaglandin liberation. (2) A second target point located after cyclic AMP production and before the 'temperature-dependent rate-limiting step'. This effect is probably related to the mechanism controlling the insertion and removal of water channels.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1988

Benzodiazepines stimulate sodium ion transport in frog skin epithelium.

Benzodiazepine binding sites are present in a variety of non-neuronal tissues including the kidney where they are localized to distal nephron segments. It is postulated that renal binding sites are involved in modulating ion transport. This study examined the effects of two benzodiazepines on sodium transport in frog skin epithelium, a model system for sodium transport in renal collecting duct. Treatment of short-circuited frog skin with diazepam (a non-selective benzodiazepine agonist) stimulated amiloride-sensitive short-circuit current, reflecting stimulation of active sodium transport. The diazepam response was equally effective with either serosal or mucosal application of the drug. Maximal stimulation of the current (42 +/- 8%) was achieved with 10 microM diazepam (serosal). Short-circuit current was similarly augmented by serosal or mucosal addition of Ro5-4864, a benzodiazepine agonist with selective activity at peripheral (non-neuronal) receptors. The natriferic response to diazepam was additive to that of vasopressin or cyclic AMP suggesting that the mode of action of benzodiazepines is probably distinct from the cyclic AMP pathway. Thus, frog skin appears to be a useful model to examine the epithelial effects of benzodiazepines. Whether stimulation of sodium transport, however, involves peripheral-type benzodiazepine receptors in this tissue requires further studies.

Animals↗
PubMed1988

Catecholamine stimulation of ion transport in the toad urinary bladder.

We have observed that serosal catecholamines increase the amplitude of the short-circuit current (Isc) in the toad urinary bladder by as much as 450%. Chemical sympathectomy with 10(-6) M 6-hydroxydopamine and the sympathomimetic effects of 10(-5) M tyramine indicate a reservoir of amines in the serosal stroma of the tissue. The urinary epithelium from the toad responds to six adrenoceptor agonists: (-)-epinephrine, (-)-norepinephrine, (-)-phenylephrine, clonidine, methoxamine and oxymetazoline. The alpha 2-adrenoceptor agonist clonidine is most potent for stimulating Isc. Some agonists were found to diminish Isc. Apparently this is related to a simultaneous increase in the transepithelial flux of both chloride and sodium. The Isc response to the catecholamines is also inhibited by several adrenoceptor antagonists. The alpha 2-adrenoceptor antagonist yohimbine is more effective than the alpha 1-antagonist prazosin for blocking the stimulation of epithelial transport. As a result of these studies, we have tentatively classified the serosal adrenoceptor of the toad urinary bladder as alpha 2.

Adrenergic alpha-Agonists↗
PubMed1989

The effect of vanadate on glucose transport and metabolism in rat small intestine.

The effect of sodium orthovanadate on the absorption, transmural transport and metabolism of glucose was studied by perfusion of isolated loops of rat jejunum in vitro. The presence of 1 mM vanadate in the serosal medium diminished absorption from 539 +/- 19 (n = 12) to 246 +/- 19 (P less than 0.001) mumol/h per g dry weight and transmural transport from 333 +/- 17 to 14 +/- 19 (P less than 0.001) mumol/h per g dry weight, whereas glucose utilisation was unaffected. The rate of release of lactate into the serosal medium was also diminished from 168 +/- 14 to 75 +/- 5 mumol/h per g dry weight (P less than 0.001). The observed rates were linear with respect to time and vanadate was effective within 5 min. In contrast, the rate of release of lactate into the luminal perfusate was strongly enhanced. Moreover, the progress curve showed a positive transient with an apparent lag time of 18.0 +/- 0.3 min, during which the rate increased to a value 9.2-times that of the control. Under the final steady-state conditions, the ratio of mucosal to serosal lactate production was 5.2 +/- 0.2 compared with 0.25 +/- 0.06 for the control, so that the effect of vanadate was to reverse the vectorial disposition of lactate. The concentration dependence of the effect of vanadate on absorption and metabolism was similar to that observed for the inhibition by vanadate of Na+/K+-ATPase activity in mucosal homogenates. The results are discussed in terms of the dissipation of transmembrane Na+ gradients as a result of the inhibition of the Na+/K+-ATPase.

Animals↗
PubMed1980

Prostaglandin release from rat stomach following vagal stimulation or administration of acetylcholine.

The rat isolated stomach was perfused via the coeliac artery and prostaglandin-like material released from the mucosa into the lumen (luminal fraction) and from blood vessels and surrounding serosal wall (serosal fraction) was bioassayed using rat fundus strips. Prostaglandin F2 alpha was identified by chromatographic and mass spectrometric techniques. The amount of prostaglandin F2 alpha released upon either vagal nerve stimulation or acetylcholine infusion increased significantly over basal levels, in association with increased gastric peristaltic activity. The quantity of prostaglandin released into the luminal fraction greatly exceeded the amount liberated into the serosal samples and this increase was dependent upon the rate of stimulation. Infusion of either atropine or hexamethonium markedly reduced both the prostaglandin output and the gastric contraction elicited by stimulation. Pretreating the stomach with indomethacin considerably decreased prostaglandin outflow. The role of endogenous prostaglanding F2 alpha in relation to parasympathetic neurotransmission in the stomach is discussed.

Acetylcholine↗
PubMed1985

The action of two mast cell stabilising agents and verapamil on rat gastric acid secretion in vitro.

The actions of two mast cell stabilising agents, FPL 52694 and disodium cromoglycate and the Ca2+ channel antagonist verapamil on acid secretion by the rat isolated stomach have been studied. FPL 52694 (1-5 mM) in the serosal medium stimulated acid secretion. This was antagonised by prostaglandin E2 but not by atropine, metiamide, propranolol or tetrodotoxin. FPL 52694 (1-5 mM) in the mucosal medium had an inhibitory effect on basal acid secretion and that stimulated by pentagastrin and histamine. The inhibition reversed only slowly after removal of FPL 52694. Disodium cromoglycate and serosal application of verapamil had no significant effects on acid output. Removal of calcium from the bathing solutions and mucosal verapamil inhibited basal secretion. Topically applied, FPL 52694 is a potent inhibitor of acid secretion in vitro. This effect may involve an action upon the availability of calcium to the tissue. The stimulatory effects of serosal FPL 52694 are discussed in relation to previous in vivo findings.

Animals↗
PubMed1989

Platelet activating factor is a potent colonic secretagogue with actions independent of specific PAF receptors.

Several candidate mediators of acute inflammation such as E-type prostaglandins, histamine and bradykinin are potent pro-diarrhoeal colonic secretagogues. They act to increase serosal to mucosal transport of chloride and passive water efflux. We investigated the effects of platelet activating factor (PAF) on muscle-stripped rat colon, measuring transepithelial potential difference (p.d.) and, under voltage clamp conditions, short circuit current (Isc). PAF induced dose-dependent increases in p.d. and Isc, with an approximate EC50 of 1.5 X 10(-10) M; similar concentrations of lyso-PAF had a much smaller but discernible effect. PAF and lyso-PAF both displayed 'sidedness' with serosal application effective and mucosal application ineffective. Inhibitor studies suggest that chloride is the principal ion carrier, but the specific PAF receptor antagonists kadsurenone, L652731, CV 3988 and WEB 2086 did not block the response. Unlike bradykinin, PAF did not cause the release of PGE2 into the serosal bathing fluid, and its action was not attenuated by the cyclo-oxygenase inhibitors piroxicam, mefenamic acid or flurbiprofen. We conclude that PAF has a powerful pro-diarrhoeal secretory action on colonic epithelium which is not mediated by the previously defined PAF receptor(s) and is independent of prostanoid generation.

Animals↗
PubMed1991

Modulation of Na+, Cl- and HCO3- transport by carbachol in pig distal jejunum.

Acetylcholine and cholinomimetics such as carbachol are potent stimulants of epithelial Cl- secretion in the small and large intestines of several mammalian species. In this study, the effects of carbachol were characterized in vitro on active ion transport in sheets of submucosa-mucosa from the distal jejunum of swine. Carbachol (10 microM) produced an increase in serosa-positive short-circuit current (Isc) in this tissue after its serosal, but not luminal administration. The Na(+)-K(+)-Cl- transport blocker bumetanide (10 microM) produced a 50% decrease in the carbachol-induced Isc elevation after its serosal administration. Peak increases in Isc evoked by carbachol were significantly reduced by 60-85% in tissues bathed in media lacking Cl-, HCO3-, or both anions. The initial drug-induced increase in net charge transfer from serosa to lumen was dependent upon both HCO3- and Cl-, whereas sustained elevations in charge transfer were dependent upon extracellular Cl- only. Radiotracer flux analyses revealed that the drug decreased net Na+ absorption and increased Cl- secretion. In the absence of HCO3-, carbachol decreased Cl- absorption. The effects of carbachol on HCO3- transport were examined by pH-stat titration. The drug rapidly alkalinized the luminal medium immediately after its serosal administration. These results suggest that carbachol stimulates electrogenic anion secretion in the mucosa of the porcine distal jejunum. Furthermore, the ability of carbachol to inhibit spontaneous Na+ absorption is dependent upon extracellular HCO3-.

Animals↗
PubMed1991

Regulation of ion transport in porcine distal colon: effects of putative neurotransmitters.

Porcine distal colon epithelium was mounted in Ussing chambers and bathed with porcine Ringer's solution. The effects of vasoactive intestinal polypeptide, norepinephrine, and carbamylcholine on Na and Cl fluxes and transepithelial electrical parameters were determined after their serosal administration. Vasoactive intestinal peptide increased the Cl-dependent component of the short-circuit current with a half-maximal effect at 115 nmol/L. Transepithelial Na and Cl flux studies demonstrated that the increase in current was caused by stimulation of Cl secretion. Norepinephrine also stimulated Cl secretion and increased the serosal-to-mucosal Na flux, producing a half-maximal effect at 1.6 mumol/L. Selective blockade of alpha 1 adrenoceptors by 0.5 mumol/L prazosin produced an eightfold decrease in norepinephrine potency. Carbamylcholine produced a significant increase in Cl secretion and decreased absorption of both Na and Cl with a concentration of 10 mumol/L producing a half-maximal effect. The muscarinic cholinoceptor blocker atropine (0.1 mumol/L) produced a 22-fold decrease in carbamylcholine potency. The effects of all three transmitter substances were unaffected after pretreatment of tissues with the neuronal conduction-blocker tetrodotoxin or an inhibitor of arachidonic acid metabolism. These results indicate that (a) vasoactive intestinal polypeptide stimulates Cl secretion without affecting Na absorption; (b) norepinephrine acting through alpha 1 adrenoceptors stimulates net Cl secretion and activates a serosal-to-mucosal Na transport mechanism; and (c) carbamylcholine acting through muscarinic receptors stimulates Cl secretion and inhibits Na and Cl absorption.

Animals↗