Laparoscopic surgery. A difference.
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Biomedical subjects
Publications and source records attributed to N Basso.
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The purpose of this study was to investigate the effect of long-term misoprostol administration, at non-antisecretory doses, on N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)-induced gastric carcinogenesis. The incidence of gastric carcinomas and precancerous lesions was evaluated in 50 male 250-g Sprague-Dawley rats after 52 weeks of continuous oral administration of MNNG (120 mg/l; n = 20), MNNG plus misoprostol (2 mg kg-1 day-1; n = 20) or tap water (n = 10) (experiment 1), and in 30 rats treated with MNNG for 30 weeks followed by tap water (n = 15) or by misoprostol (n = 15) for 22 weeks; a third group (n = 10) received tap water only for 52 weeks (experiment 2). After sacrifice, gastric mucosal lesions were macroscopically evaluated and their histology obtained. MNNG consumption was comparable in all groups (6.5 +/- 1.1 mg rat-1 day-1). Misoprostol consumption was 180 +/- 0.25 mg kg-1 day-1 rat-1. In experiment 1 the incidence of gastric carcinomas was 60% in the MNNG group and 25% in the group treated with MNNG plus misoprostol (P less than 0.05). Cytotoxic and hyperplastic gastric mucosal lesions were also significantly reduced by misoprostol. In experiment 2 the incidence of carcinomas was 31% and 38.6% respectively. Misoprostol significantly decreased the incidence of gastric cancer formation when given from the beginning of the experiment. By contrast, when administered after 30 weeks of MNNG treatment it did not interfere with experimental gastric cancer formation. Exogenous prostaglandins are able to prevent the early MNNG-induced gastric mucosal lesions, thus interfering with gastric carcinogenesis.
An increased number of interphasic nucleolar organizer regions containing ribosomal cistrons associated with argyrophilic proteins (AgNORs) has been described in human malignant tumor cells. In this study variations in AgNOR numbers have been compared with changes of cell kinetics, evaluated by the mitotic count (MC) and bromodeoxyuridine labeling index (BrdU LI), during gastric carcinogenesis induced with N-methyl-N'-nitro-N-nitrosoguanidine (NG) in rats. Significant differences (2 P < 0.005) in AgNOR mean numbers, evaluated in the antral isthmic cells, in MC mean values and BrdU LI, evaluated in the whole antral cellular population, were found when comparing areas of acute gastritis, atrophy and hyperplasia in NG-treated rats with the normal mucosa in controls. No differences were observed in MC and BrdU LI between normal antrum and carcinoma cells which showed an AgNORs mean number lower than in the isthmic cells of controls (2 P < 0.005). Moreover, significant correlations were found comparing changes in AgNOR numbers with MC (r = 0.89, P < 0.001) and BrdU LI (r = 0.66, P < 0.001) in different lesions. These data show that evaluation of AgNOR numbers does not allow the identification of malignant cells in NG-induced gastric carcinoma. However AgNOR quantification seems to be a reliable index of cell kinetics and related well with the cellular dividing fraction.
Laparoscopic cholecystectomy is a valid alternative to open cholecystectomy. The Authors present their experience in the management of 208 consecutive patients. The low incidence of complications, the short hospital stay as well as earlier return to work, and lower medical expenses are the advantages of laparoscopic surgery. The latter is, therefore, more suitable for the treatment of benign gallbladder diseases.
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In 17 patients with postoperative recurrent peptic ulcer, incomplete antrectomy (I.A.) was found by endoscopic biopsies in 5. No evidcence of I.A. was found in the remaining 12 patients. Gastric acid output and gastrin levels were measured in basal conditions and following a calcium I.V. infusion (4 mg/kg hr of Ca++ over 4 hr) and a bombesin (BBS) I.V. infusion (15 ng/kg min over 90 min). Basal gastrin levels were significantly differnt in the two groups of patients: BBS infusion augmented significantly serum gastrin levels in all patients with I.S., while BBS infusion had no significant effect on serum gastrin levels in the group of patients without I.A. Acid output following BBS infusion showed a pattern similar to the pattern seen for gastrin. Calcium infusion augmented gastric acid secretion and gastrin levels in the patients with I.A.; however, the response to calcium could not clearly separate in all instances patients with I.A. from patients without I.A. It is concluded that the "BBS infusion test" may be heplful in the diagnosis of I.A. in patients with postoperative peptic ulcer.
This article presents an analysis of acute gastroduodenal mucosal lesions (AGML) based on a review of current literature and the personal experience of the authors. The pathology of AGML involes two distinct types of lesions, namely, superficial erosions confined to the acid-secreting gastric mucosa and presenting as erosive hemorrhagic gastritis, and acute ulcers that occur in the alkaline gastric mucosa and duodenum. The etiology of these two lesions is very likely different. Acut gastroduodenal ulcers, best known as stress ulcers, are probably "peptic" lesions, whereas erosive hemorrhagic gastritis appears to be due to pathologic back diffusion of hydrogen ions caused by a breakdown of the gastric mucosal barrier as a result of endogenous factors, such as gastric mucosal ischemia, and sometimes exogenous factors, such as alcohol, urea, and acetylsalicylic acid. Catecholamine hypersecretion resulting from severe stress, such as occurs in hypovolemia, sepsis, and hypercapnea, contributes to ischemia of the gastric mucosa by producing splanchnic vasoconstriction. The key to the diagnosis of AGML is early endoscopy in all cases of upper gastrointestinal bleeding. Therapy for AGML should begin with a trial of medical measures directed at restoring effective perfusion of tissues and removing hydrogen ions from the stomach by gastric washing. Medical therapy is effective in 80% of patients with erosive hemorrhagic gastritis, but surgical treatment is usually required in acute gastroduodenal ulcer. When surgery is necessary for either type of lesion, vagotomy with hemigastrectomy appears to be the most effective operation. The personal experience of the authors has involved 36 patients with AGML who were treated in three periods between 1968 and 1976. The mortality rate of patients with AGML has been reduced from 50% in the first 2 years to zero in the last 2 years by the use of emergency endoscopy for diagnosis, appropriate medical therapy, properly timed and executed surgery, and, most recently, selective angiography.
Thirteen patients with pancreaticoduodenectomy were studied. In three patients presenting with stomal ulcer or bleeding stomitis, endoscopic biopsies showed the presence of retained antral mucosa (RAM). No disease and no RAM was present in the remaining ten patients. Bombesin (BBS) infusion augmented both gastric acid and gastrin secretion in the group with RAM, whereas no change was apparent in the remaining ten patients. The BBS infusion test is useful in detecting stomal ulcer high risk pancreaticoduodenectomy patients.
Plasma renin activity, reninlike activity present at the artery wall, pressor response to exogenous hog renin, renin half-life time, and renin-like activity present at the artery wall 1 hour after injection of renin were measured in conscious rats 1 month after inducing hypertension by renal artery constriction and contralateral nephrectomy (one-kidney hypertension). Plasma renin activity was higher but without statistical significance in one-kidney hypertensive rats when compared with normotensive or sham-operated animals. Renin-like activity present at the artery wall was significantly increased in hypertensive animals only when compared with one-kidney normotensive rats. Pressor responses to renin in one-kidney hypertensive and normotensive rats were of significantly longer duration than in sham-operated animals. The inactivation rate of exogenous renin followed a first-order reaction with a half-life of 6 minutes in sham-operated rats and of 12 minutes in one-kidney hypertensive and normotensive animals. Decreased inactivation of circulating renin could explain the protraction of the pressor response; however, the slope of the regression equation describing the inactivation of renin in all of the rats was steeper than the slope of the pressor response, indicating a dissociation between blood pressure and plasma renin activity. The renin-like activity present at the artery wall 1 hour after injection of renin was determined in the three groups; the arterial tissue of one-kidney hypertensive rats bound more circulating renin than that of normotensive rats and the latter more than that of sham-operated animals, suggesting the participation of this binding capacity in the protraction of the pressor response and in the maintenance of hypertension.
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The action of duodenal acidification, of continuous I.V. infusion of secretin and glucagon and of a one bolus I.V. administration of secretin and glucagon at maximal doses on BBS-induced gastrin secretion has been studied in a group of 18 healthy subjects. Continuous infusion of secretin and glucagon and the acidification of the duodenum did not alter significantly the levels of gastrin stimulated by BBS. Secretin and glucagon administered by a single I.V. bolus paritially inhibit the effect of BBS on gastrin levels. On the basis of these results it is not possible to affirm or to exclude the possibility that BBS is a hormone physiologically present in man.
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