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排序方式: 共有142条查询结果,搜索用时 15 毫秒
1.
OSWALDO M. TISCORNIA M.D. F.A.C.G. DENIS LEVESQUE M.D. HENRI SARLES M.D. ALEXANDRE BRETHOLZ M.D. MIGHEL VOIROL M.D. JOAO P. MENDES DE OLIVEIRA M.D. MANFRED SINGER M.D. PIERRE DEMOL M.D. 《The American journal of gastroenterology》1977,67(2):121-130
In five dogs with chronic gastric fistulas (Thomas cannula) and a new type of chronic pancreatic fistula which permits collection of pure nonactivated pancreatic juice after ingestion of a test meal, the following series of experiments were performed: In the first series, a test meal (400 gm. canned dog meat) was given with 200 ml. saline simultaneously infused through the gastric cannula. In response to this stimulus, the 20-minute peak pancreatic flow rate and bicarbonate output were respectively 33% and 34%, of the maximal secretion of the pancreatic gland obtained with secretin in six control dogs provided with gastric and the classical Thomas duodenal fistula. The 20-minute peak protein output represented 84% of the maximal secretory capacity attained with dose-response curves to CCK in the same group of control animals.
In the second series either 1.5 or 2.0 gm./kg. ethanol were given instead of saline. Intragastric ethanol induced a dissociation of pancreatic secretion: a significant inhibition of flow rate, of bicarbonate concentration and output and a significant rise of protein concentration; protein output remaining unchanged.
It is postulated that ethanol, acting on the stomach and duodenojejunum, evokes, independently of its gastrin-releasing capacity', an unknown humoral or nervous mechanism that counteracts the ethanol-elicited cholinergic-mediated inhibition of pancreatic protein secretion which has been previously described. 相似文献
In the second series either 1.5 or 2.0 gm./kg. ethanol were given instead of saline. Intragastric ethanol induced a dissociation of pancreatic secretion: a significant inhibition of flow rate, of bicarbonate concentration and output and a significant rise of protein concentration; protein output remaining unchanged.
It is postulated that ethanol, acting on the stomach and duodenojejunum, evokes, independently of its gastrin-releasing capacity', an unknown humoral or nervous mechanism that counteracts the ethanol-elicited cholinergic-mediated inhibition of pancreatic protein secretion which has been previously described. 相似文献
2.
A New Variant of Hereditary Hemolytic Anemia With Stomatocytosis and Erythrocyte Cation Abnormality 总被引:4,自引:1,他引:4
MILLER DENIS R.; RICKLES FREDERICK R.; LICHTMAN MARSHALL A.; LA CELLE PAUL L.; BATES JONATHAN; WEED ROBERT I. 《Blood》1971,38(2):184-204
A new variant of congenital hemolyticanemia associated with stomatocytosis,reticulocytosis, decreased osmotic fragility, type I autohemolysis and shortened erythrocyte survival without specific splenic sequestration was discoveredin three siblings of Swiss-German ancestry. Increased intracellular sodium(two to three times normal) and slightlydecreased intracellular potassium weredetected. Total sodium efflux was eight-fold greater than normal but total potassium influx was normal and ouabain-sensitive potassium influx was decreased.The ouabain-sensitive sodium efflux:potassium influx ratio was 26:1 ratherthan the 3:2 ratio noted in normal cells.The consanguineous parents, four othersiblings, and 44 other family membershad mild stomatocytosis, reticulocytosis,and, when studied, decreased osmoticfragility, increased autohemolysis, intermediate abnormalities of cation content,cation flux, and moderate shortening oferythrocyte survival. Autosomal dominant inheritance was suggested. Noabnormalities of RBC enzymes, hemoglobin or lipids were observed. No abnormalities of membrane protein weredetected on acrylamide gel. Substratedepletion of these hypermetabolic cellsresulted in intracellular dehydrationwith potassium loss in excess of sodiumgain and decreased deformability. Although the exact nature of the defectresponsible for hemolysis is unknown,this syndrome differs from other hereditary hemolytic anemias associated withstomatocytosis. Submitted on December 21, 1970 Revised on March 16, 1971 Accepted on March 29, 1971 相似文献
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GUSTAVO GLOTZ de LIMA DENIS ROY MARIO TALAJIC MARC DUBUC 《Pacing and clinical electrophysiology : PACE》1998,21(5):1152-1154
The anatomical substrate for AV nodal reentrant tachycardia (AVNRT) is well known and is due to anterograde conduction through a siow conducting pathway and retrograde conduction using a fast conducting path way. In this report, we describe a patient with AVNRT who also presented with frequent episodes of paroxysmal nonreentrant tachycardia due to the occurrence of two conducted ventricular beats for each sinus depolarization. Palpitations and arrhythmias were abolished after radiofrequency ablation of the slow pathway. 相似文献
8.
Treatment Failure With Rhythm and Rate Control Strategies in Patients With Atrial Fibrillation and Congestive Heart Failure: An AF‐CHF Substudy
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KATIA DYRDA M.D. M.Sc. DENIS ROY M.D. HUGUES LEDUC M.Sc. MARIO TALAJIC M.D. LYNNE WARNER STEVENSON M.D. PETER G. GUERRA M.D. JASON ANDRADE M.D. MARC DUBUC M.D. LAURENT MACLE M.D. BERNARD THIBAULT M.D. LENA RIVARD M.D. PAUL KHAIRY M.D. Ph.D. 《Journal of cardiovascular electrophysiology》2015,26(12):1327-1332
9.
BENJAMIN BERTE M.D. JATIN RELAN Ph.D. FREDERIC SACHER M.D. Ph.D. XAVIER PILLOIS M.D. Ph.D. ANTHONY APPETITI SEIGO YAMASHITA M.D. Ph.D. SAAGAR MAHIDA M.D. Ph.D. FREDERIC CASASSUS M.D. DARREN HOOKS M.D. Ph.D. JEAN‐MARC SELLAL M.D. SANA AMRAOUI M.D. ARNAUD DENIS M.D. NICOLAS DERVAL M.D. HUBERT COCHET M.D. Ph.D. MÉLÈZE HOCINI M.D. MICHEL HAÏSSAGUERRE M.D. Ph.D. RUKSHEN WEERASOORIYA M.D. Ph.D. PIERRE JAÏS M.D. Ph.D. 《Journal of cardiovascular electrophysiology》2015,26(11):1213-1223
10.
Age,Atrial Fibrillation,and Structural Heart Disease Are the Main Determinants of Left Atrial Fibrosis Detected by Delayed‐Enhanced Magnetic Resonance Imaging in a General Cardiology Population
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HUBERT COCHET M.D. Ph.D. AMAURY MOURIES M.D. HUBERT NIVET M.D. FREDERIC SACHER M.D. Ph.D. NICOLAS DERVAL M.D. ARNAUD DENIS M.D. MATHILDE MERLE Ph.D. JATIN RELAN Ph.D. MÉLÈZE HOCINI M.D. MICHEL HAÏSSAGUERRE M.D. FRANÇOIS LAURENT M.D. MICHEL MONTAUDON M.D. Ph.D. PIERRE JAÏS M.D. 《Journal of cardiovascular electrophysiology》2015,26(5):484-492