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The operations of Nissen, Hill, and Belsey are adequate in controlling esophaegeal reflux in the majority of patients. In a small percentage however, objective and subjective evidence of esophagitis persists in spite of repeated operations to restore lower esophageal sphincter competency. These failures are then usually treated by operative procedures of great magnitude involving organ interposition. Repeated antireflux operations directed to the gastroesophageal area may in some instances result in impairment of blood supply with an increased risk of both esophageal and gastric fistulae. In the past many observers have felt that reflux esophagitis resulted solely from the effects of acid-pepsin secretions bathing the distal esophagus. Recently experimental and clinical data have indicated the importance of duodenal contents in the etiology and perpetuation of reflux esophagitis. During a recent two year period, 6 patients with persistent reflux esophagitis uncontrolled by repeated antireflux procedures have been seen on our service. These 6 patients, underwent 12 unsuccessful antireflux operations elsewhere. Three of the 6 patients had also been subjected to vagotomy-antrectomy for a coexisting duodenal ulcer. A marked lowering of gastric acidity took place but esophageal reflux and esophagitis persisted. These three patients were treated on our service by takedown of the Billroth I anastomosis, closure of the duodenal stump and diversion of the duodenal contents into a Roux-en-Y limb. Three other patients who had undergone unsuccessful antireflux procedures alone were subjected to antral resection, Roux-en-Y diversion and transthoracid vagotomy. This simplified appraoch to the treatment of persistent esophageal reflux uncontrolled by repeated antireflux procedures has given satisfactory results. The operation should be considered when technical considerations preclude further surgical attempts to perform another effective antireflux operation. Total duodenal diversion should, however, not be considered as the primary operation for the patient suffering from reflux esophagitis. However, in circumstances discussed above this direct approach appears preferable to major resectional procedures.  相似文献   
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The aim of the present experiments was to determine the role of insulin and glucagon in the regulation of basal glucose production in dogs fasted overnight. A deficiency of either or both pancreatic hormones was achieved by infusin somatostatin (1 mug/kg per min), a potent inhibitor of both insulin and glucagon secretion, alone or in combination with intraportal replacement infusions of either pancreatic hormone. Infusion of somatostatin alone caused the arterial levels of insulin and glucagon to drop rapidly by 72+/-6 and 81+/-8%, respectively. Intraportal infusion of insulin and glucagon at rates of 400 muU/kg per min and 1 ng/kg per min, respectively, resulted in the maintenance of the basal levels of each hormone. Glucose production was measured using tracer (primed constant infusion of [3-3H]glucose) and arteriovenous difference techniques. Isolated glucagon deficiency resulted in a 35+/-5% (P less than 0.05) rapid and sustained decrease in glucose production which was abolished upon restoration of the plasma glucagon level. Isolated insulin deficiency resulted in a 52+/-16% (P less than 0.01) increase in the rate of glucose production which was abolished when the insulin level was restored. Somatostatin had no effect on glucose production when the changes in the pancreatic hormone levels which it normally induces were prevented by simultaneous intraportal infusion of both insulin and glucagon. In conclusion, in the anesthetized dog fasted overnight; (a) basal glucagon is responsible for at least one-third of basal glucose production, (b) basal insulin prevents the increased glucose production which would result from the unrestrained action of glucagon, and (c) somatostatin has no acute effects on glucose turnover other than those it induces through perturbation of pancreatic hormone secretion. This study indicates that the opposing actions of the two pancreatic hormones are important in the regulation of basal glucose production in the postabsorptive state.  相似文献   
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Eighteen male patients between the ages of 25 and 50 were given on a double blind randomized basis (A) 40 gms. galactose (B) 50 gms. arabinogalactan and 0.11 gm. sodium saccharin (C) 2 gm. methyl cellulose and 0.083 gm. sodium saccharin and (D) 4 gm. galactose, all in 200 ml water. Blood glucose, galactose and insulin levels were determined during a six hour period before and after ingestion. The three first mentioned solutions tasted equally sweet, the fourth was essentially tasteless. None of these feedings altered plasma insulin or glucose levels. It appears that in contrast to other conclusions reached by earlier investigators sweet taste is unable to induce insulin secretion through neurogenic pathways.  相似文献   
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The hemodynamic determinants of the time-course of fall in isovolumic left ventricular pressure were assessed in isolated canine left ventricular preparations. Pressure fall was studied in isovolumic beats or during prolonged isovolumic diastole after ejection. Pressure fall was studied in isovolumic relaxation for isovolumic and ejecting beats (r less than or equal to 0.98) and was therefore characterized by a time constant, T. Higher heart rates shortened T slightly from 52.6 +/- 4.5 ms at 110/min to 48.2 +/- 6.0 ms at 160/min (P less than 0.01, n = 8). Higher ventricular volumes under isovolumic conditions resulted in higher peak left ventricular pressure but no significant change in T. T did shorten from 67.1 +/- 5.0 ms in isovolumic beats to 45.8 +/- 2.9 ms in the ejecting beats (P less than 0.001, n = 14). In the ejecting beats, peak systolic pressure was lower, and end-systolic volume smaller. To differentiate the effects of systolic shortening during ejection from those of lower systolic pressure and smaller end-systolic volume, beats with large end-diastolic volumes were compared to beats with smaller end-diastolic volumes. The beats with smaller end-diastolic volumes exhibited less shortening but similar end-systolic volumes and peak systolic pressure. T again shortened to a greater extent in the beats with greater systolic shortening. Calcium chloride and acetylstrophanthidin resulted in no significant change in T, but norepinephrine, which accelerates active relaxation, resulted in a significant shortening of T (65.6 +/- 13.4 vs. 46.3 +/- 7.0 ms, P less than 0.02). During recovery from ischemia, T increased significantly from 59.3 +/- 9.6 to 76.8 +/- 13.1 ms when compared with the preischemic control beat (P less than 0.05). Thus, the present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate. T may be an index of the activity of the active cardiac relaxing system and appears dependent on systolic fiber shortening.  相似文献   
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In this review, the clinical reality, the statistical risk, and the frequency of thromboembolism in pill users are evaluated, 6 cases described, and premonitory signs, treatment, and etiology are discussed. Clinically these thromboembolisms appear in unlikely subjects and unusual bodily locations such as the mesenteric veins, without warning. The risks are 8-11 times higher for pulmonary thrombosis, 3-6 times higher for myocardial infarction, based on previously used higher dosed pills. The frequency is about .5-1/1000, or 500-1000/year in France. Some of the cases described used pills with less than .05 mg estrogen, some were heavy smokers, 1 woman died, 1 had a lower extremity amputation, and 1 woman had demonstrated IgG lamda antibodies against ethinyl estradiol. Premonitory signs are rare, and unsually ignored. The immediate action is to stop the pill and start anticoagulants. The cause of these disorders is not known in detail, but is presumed to be estrogens, therefore, low-dose pills, i.e., those with .05 or .03 mg ethinyl estradiol, should be used if possible. Other risk factors are surgery, age, immobilization, history of vein disorders, smoking, hyperlipidemia, hypertension, especially since the pill potentiates hypertension, hyperlipidemia, and hypercoagulation. Some mechanisms proposed are hyperlipidemia, disturbed blood coagulation factors, decreased fibrinolysis, alterations in the blood vessel endothelium and immunity against the estrogen in the pill.  相似文献   
30.
Cummulative dose-response curves to l-noradrenaline and in presence of different concentrations of TRH (10(-3), 10(-4), 10(-5), 10(-6), 10(-7), and 10(-8) M) were investigated. 25 segments of vas deferens (escrotal tract) were obtained from different surgical patients of urological disorders. At the lower concentration (greater than 10(-7) M), we can not appreciate any influence of TRH on the l-noradrenaline response. Nevertheless there was a reduction of response to l-noradrenaline, with displacement of the curves to the right side, for the high concentrations, and a proportional ratio to the concentration to TRH.  相似文献   
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