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G Thiefin

Publications and source records attributed to G Thiefin.

32 records · Page 2Linked to original sources
PubMed1994

[Subcutaneous seeding on the tract of percutaneous cytologic puncture with a fine needle of a hepatic metastasis from colonic adenocarcinoma].

Subcutaneous seeding after percutaneous ultrasonically guided fine needle aspiration of liver tumours is a rare complication and only a few cases have been reported. We report a new case of cutaneous implantation following a fine needle (21.5 gauge of external diameter) aspiration biopsy of a superficial colonic liver metastasis, as shown by a subcutaneous nodule and increased serum carcinoembryonnary-antigen. We discuss the risk factors of this rare complication, especially the thickness of the liver parenchyma along the needle tract and precautions which can be taken for prevention.

Adenocarcinoma↗
PubMed1992

Superior mesenteric artery is more important than inferior mesenteric artery in maintaining colonic mucosal perfusion and integrity in rats.

Mucosal hemodynamics (by reflectance spectrophotometry) and mucosal damage (by histologic examination) following acute colonic ischemia were evaluated in different anatomic locations in the colon of anesthetized rats. The reflectance spectrophotometer provides an index of mucosal hemoglobin concentration (IHB) and an index of oxygen saturation of hemoglobin (ISO2). The patterns of ischemia without congestion (decreases IHB, decreases ISO2) during superior mesenteric artery occlusion, and ischemia with congestion (increases IHB, decreases ISO2) during portal vein occlusion, previously demonstrated in the stomach and duodenum, are also applicable to the colon. The significant linear correlations between changes (as percent of baseline) in IHB, ISO2, and hydrogen gas clearance suggest that changes in these indices are adequate indicators of changes in colonic mucosal perfusion. Superior mesenteric artery ligation produced significant reductions in both indices, and an increase in damage in the mucosa of the cecum, transverse colon, splenic flexure, and left colon, but not the rectum. Inferior mesenteric artery ligation produced only slight reduction in these indices and minimal damage only in the mucosa of the splenic flexure. These results support the hypothesis that the superior mesenteric artery is more important than the inferior mesenteric artery in maintaining colonic perfusion and colonic mucosal integrity in the rat.

Animals↗
PubMed1991

Vagal afferent innervation and regulation of gastric function.

In this article, we have presented evidence that vagal capsaicin-sensitive afferent fibers are involved in the regulation of gastric mucosal and motor function. Gastric acid secretion stimulated by gastric distension, histamine and central injection of TRH analog are all partly dependent on vagal capsaicin-sensitive afferent mechanisms. It is possible that as vagal efferent activity releases histamine, the common final pathway is the reduction in the response to histamine. At present, it is unclear as to the mechanism by which capsaicin-sensitive afferents are involved in the secretory response to histamine. With regard to the gastric acid and mucosal blood flow responses to TRH, it is not clear whether the sensory neurons represent a component of the efferent pathway that is activated by TRH or whether their role is to set the sensitivity of, or exert feedback control on this efferent pathway. As perineural capsaicin application decreases peptide content in the peripheral terminal fields of sensory neurons and these peptides may produce local effector functions within the tissue, it is possible that alterations in the gastric responses to TRH result from a decrease in the local effector functions of vagal neurons. From the experiments on electrical stimulation of the vagus nerve, it is evident that antidromic stimulation of vagal afferents can stimulate gastric mucosal blood flow, although under these experimental conditions there was no evidence for a capsaicin-sensitive stimulation of gastric acid secretion. The physiological relevance of this stimulation of gastric mucosal blood flow is at present unclear, but it is possible that physiological stimuli, such as distension or nutrients, may stimulate afferents and signal for an increase in gastric mucosal blood flow. In addition, pathophysiological or noxious stimulation of vagal afferents may also signal for an increase in gastric mucosal blood flow and may play a role in the response of the mucosa to injury.

Animals↗
PubMed1991

[Cardiopexy using the hepatic ligament in the treatment of gastroesophageal reflux. Apropos of 200 cases].

The authors report 200 cases of cardiopexy with the ligamentum teres (Rampal-Marchal's procedure) associated with a 180 degree posterior fundoplication, in the surgical treatment of gastroesophageal reflux. 200 patients with severe reflux (76% oesophagitis) were operated on with this procedure over a 10 year period. Symptoms of reflux disappeared immediately in 99% cases, with healing of oesophagitis in 124 out of the 127 patients controlled with endoscopy, and a significant increase of inferior sphincteric pressure (from 11 cm H2O to 25 cm H2O). Objective controls by post-prandial pHmetry evidenced persistant reflux with 10 patients, but 9 of them are totally free of symptoms. Operative mortality was 1.5%. Transient dysphagia was observed in 32% cases. All the patients were reviewed with a mean follow up of 23 months. 4 clinical recurrences of reflux were observed (2%) but no oesophagitis was found on endoscopic controls with these 4 patients, and only one had to be reoperated on. Actuarial chance to remain free of recurrence was estimated at 97.8% up to 48 months according to the Kaplan-Maier's method. Cardiopexy with the ligamentum teres ensures the lengthening of the abdominal portion of the oesophagus and anchors the antireflux assembly within the pressure environment of the abdomen in a strong and flexible way. It seems to be the best procedure for the treatment of GE reflux.

Cardia↗
PubMed1990

Capsaicin-sensitive afferent fibers contribute to gastric mucosal blood flow response to electrical vagal stimulation.

Electrical stimulation of the peripheral vagus produces a noncholinergic increase in gastric mucosal blood flow (GMBF) via unknown mechanisms. The purpose of this study was 1) to investigate whether a portion of the increase in GMBF during prolonged electrical vagal stimulation involves a mechanism separate from augmented acid secretion and 2) to determine whether antidromic activation of afferent fibers contributes to the vascular or secretory responses to electrical vagal stimulation. Electrical vagal stimulation (40 V, 6 Hz, 2 ms) applied for 30 min to the distal cut end of the subdiaphragmatic ventral vagus significantly increased gastric acid secretion and GMBF measured by hydrogen gas clearance. Atropine (0.15 mg/kg iv) or omeprazole (10 mumol/kg iv) completely abolished the secretory response to electrical vagal stimulation, while a significant increase in GMBF remained. Pretreatment with perineural application of the sensory neurotoxin capsaicin to both cervical vagi significantly reduced by 48% the increase in GMBF but not gastric acid secretion; atropine completely abolished the remaining vascular response in capsaicin-treated rats. These results suggest that prolonged electrical vagal stimulation induces a sustained increase in GMBF partially independent of augmented acid secretion and that the noncholinergic portion of the vascular response is mediated by capsaicin-sensitive vagal afferent fibers.

Afferent Pathways↗
PubMed1990

Prevention by aluminium phosphate of gastric lesions induced by ethanol in the rat: role of endogenous prostaglandins and sulfhydryls.

This study was designed to demonstrate the cytoprotective effect of an antacid containing aluminium phosphate (Phosphalugel) against ethanol-induced gastric injury in the rat and to determine whether this cytoprotective effect is mediated by endogenous prostaglandins and sulfhydryls. We have quantitatively evaluated gastric mucosal lesions using macroscopic and histological techniques one hour after ethanol administration. Two ml of aluminium phosphate given orally one hour before administration of 2 ml of 100% ethanol significantly (p less than 0.01) reduced the area of macroscopic lesions induced by ethanol (3.3 +/- 0.9%) when compared to distilled water (20 +/- 4.8%). The histological study showed that aluminium phosphate prevented deep tissue necrosis. However, it did not protect surface epithelial cells against ethanol injury. Pretreatment with indomethacin, 5 mg/kg sc one hour before aluminium phosphate, slightly but significantly (p less than 0.05) reduced the cytoprotective effect of aluminium phosphate. Macroscopic lesions occupied 4.3 +/- 0.94% and 1.88 +/- 0.41% of total mucosal area in indomethacin group and in vehicle group, respectively. On the other hand, the sulfhydryl blocker, N-ethyl-maleimide, 10 mg/kg sc, given one hour before aluminium phosphate, completely abolished the cytoprotective effect of aluminium phosphate (32.92 +/- 4.85% in N-ethyl-maleimide group versus 3.78 +/- 1.41% in vehicle group; p less than 0.01). These results show that aluminium phosphate has a cytoprotective effect against ethanol injury in the rat. This property appears to be mediated by both endogenous prostaglandins and sulfhydryls.

Aluminum↗
PubMed1989

Central nervous system action of thyrotropin-releasing hormone to increase gastric mucosal blood flow in the rat.

The central nervous system effects of thyrotropin-releasing hormone (TRH) on gastric acid secretion and mucosal blood flow were studied in rats. Corpus mucosal blood flow was measured by the hydrogen gas clearance technique and acid output by a continuous gastric perfusion method in fasted, urethane-anesthetized rats. Thyrotropin-releasing hormone (1 or 5 micrograms) injected into the cerebral lateral ventricle induced concomitant increases in gastric acid secretion and mucosal blood flow. Intravenous infusion of step doses of TRH (60 and 180 micrograms/kg.h) had no effect on these parameters. Bilateral vagotomy and atropine (0.15 mg/kg) completely blocked the effects of intracerebroventricular injection of TRH (5 micrograms) on gastric acid secretion and mucosal blood flow. In contrast, intravenous omeprazole (20 mumol/kg) completely inhibited the increase in gastric acid secretion but not the increase in mucosal blood flow elicited by intracerebroventricular administration of TRH (5 micrograms). These results demonstrate that TRH acts in the brain to stimulate gastric acid secretion and mucosal blood flow through vagal dependent pathways and peripheral muscarinic receptors. Part of the effect of central TRH on gastric mucosal blood flow is not secondary to the stimulation of acid secretion and appears to represent a direct cholinergic vasodilatory response.

Animals↗
PubMed1989

Dissociated effects of corticotropin-releasing factor on acid secretion and blood flow.

Peripherally administered corticotropin-releasing factor (CRF) inhibits gastric acid secretion in the rat via unknown mechanisms. Because intravenous CRF can produce marked systemic hypotension, the hypothesis that its antisecretory effect is due to a reduction in gastric mucosal blood flow (MBF) was tested. Corpus MBF was measured by hydrogen gas clearance in fasted, urethan-anesthetized rats. CRF (15 nmol.kg-1.h-1 iv) had no significant effect on MBF but significantly decreased systemic blood pressure (BP) by 21.8 +/- 3.4%. This dose of CRF significantly decreased acid secretion stimulated by 40 micrograms.kg-1.h-1 pentagastrin iv but did not decrease MBF despite a 30.3 +/- 2.3% decrease in BP. To avoid the confounding effect of systemic hypotension on MBF, close gastric intra-arterial infusions were performed. CRF (1.7 nmol/h ia) had no effect on BP and did not increase MBF. CRF (3.4 nmol/h ia) slightly decreased BP without modifying MBF. In contrast, histamine (200 micrograms/h ia) significantly increased MBF by 58 +/- 11%. We conclude that 1) the peripheral antisecretory effect of CRF is not related to a decrease in MBF, 2) the maintenance of MBF during CRF-induced hypotension is not due to a direct vasodilator effect of CRF on the gastric microvasculature.

Animals↗
PubMed1989

Protective effect of low dose of enprostil against gastric blood loss induced by aspirin in man.

This study tested the efficacy of enprostil given both at potent antisecretory (35 micrograms twice daily) and weak antisecretory (7 micrograms twice daily) doses in preventing aspirin-induced gastric blood loss measured chemically in gastric washings in 10 volunteers. Aspirin (500 mg four times a day) increased gastric blood loss compared with placebo (p less than 0.001). When enprostil was given in addition to aspirin, gastric blood loss was not significantly different from basal value. The pH of gastric washings was significantly increased by the large but not by the low dose of enprostil compared with placebo. The two doses of enprostil were equally efficacious, suggesting a mucosal protective effect of enprostil independent of acid inhibition.

Adult↗
PubMed1987

[Hepatocellular carcinoma invading the right atrium: clinical, echographic and angiographic study].

The authors report the case of a 54 year old woman suffering from hepatocellular carcinoma with tumor growth into right hepatic vein, inferior vena cava and right atrium. On cardiac examination, a pansystolic bruit and a diastolic rumble were audible at the tricuspid focus. Diagnosis was confirmed by inferior vena cavography and two-dimensional echocardiography, which demonstrated a large mobile mass in the right atrium moving to and fro through the tricuspid valve. This case report emphasizes the value of routine cardiac examination during the course of hepatocellular carcinoma.

Carcinoma, Hepatocellular↗