[Diagnostic peritoneal lavage in blunt abdominal injuries].
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Biomedical subjects
Publications and source records attributed to J Stadaas.
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Acute pancreatitis was induced in pigs by manual retrograde injection of Na-Taurocholate into the pancreatic duct. Using chromogenic peptide substrate assays, increased plasma kallikrein activity (KK), paralleled by a reduction in functional plasma kallikrein inhibition values (KKI) were found in the peritoneal exudate in untreated animals. Several of the untreated animals experienced an increased trypsin activity (TRY) in the same exudate. Five out of eight animals died during a 6 hour observation period. Pretreatment with either Cl-INH or aprotinin given intravenously, resulted in a significantly increase in KKI capacity paralleled by unchanged KK and TRY activities in the peritoneal exudate. Furthermore, inhibitor pretreatment significantly improved hemodynamic performances (AP and CO) and the survival rate. The study underlines the pathophysiological importance of trypsin and the plasma kallikrein-kinin system during acute, severe pancreatitis.
Acute pancreatitis was induced in pigs by retrograde injection of Na-taurocholate into the pancreatic duct. By means of chromogenic peptide substrate assays, increased plasma kallikrein activity, parallel with a reduction of plasma prekallikrein and functional kallikrein inhibition values, was found in peritoneal exudate. In plasma, however, no changes in the kallikrein-kinin system were found during the 6-h observation time. The study demonstrates the presence of components of the plasma kallikrein-kinin system in peritoneal fluid and suggests that the peritoneal cavity to a great extent is a functionally separate compartment from plasma. Activation of the plasma kallikrein-kinin system in peritoneal exudate during acute experimental pancreatitis appears to be of importance for the initial symptoms and the development of shock seen during this condition.
The median number of mast cells (with 95% confidence interval) in jejunal specimens from 79 individuals was 108 (93-121)/mm2 section area. The distribution was unimodal and slightly skewed to the right. No relation was found between mast cell number and sex, age, height, or weight. A history of possible allergic manifestations did not influence the mast cell number.
The effects of high-dose corticosteroids (HDC) on activities within the proteolytic cascade systems were studied in vitro and in vivo using chromogenic peptide substrate assays. In in vitro experiments 20 mg methylprednisolone sodium succinate (Solu-Medrol) per ml plasma significantly inhibited activation of plasma prekallikrein, prothrombin and plasminogen and reduced functional plasma kallikrein inhibition, antithrombin and antiplasmin activities. The effects of HDC on activities within these proteolytic cascade systems were further evaluated in experimental acute pancreatitis in pigs. Acute pancreatitis was induced by injection of Na-taurocholate into the pancreatic duct. Seven test animals received methylprednisolone sodium succinate 30 mg per kg intravenously for 30 minutes before the induction of pancreatitis as pretreatment. Eight animals remained untreated. Trypsin (TRY), plasma prekallikrein (PKK), plasma kallikrein (KK) and functional plasma kallikrein inhibition capacity (KKI) were studied in the peritoneal exudate. Cardiac output (CO) and mean arterial pressure (MAP) were monitored regularly before and during a 6 hour observation period. During untreated pancreatitis a reduction of PKK levels of about 40% were found, paralleled by an increased KK activity and a reduction of KKI capacity. Several of the animals experienced high TRY activities. The mortality rate was 63% (5 out of 8 animals). In the pretreated groups, all animals survived the observation period. CO and MAP were significantly less reduced than the untreated group at 6 hours. HDC was also found to reduce significantly plasma kallikrein activities in the peritoneal exudate compared with untreated animals. No changes in TRY activities were found in pretreated animals. Furthermore, plasma prekallikrein and functional plasma kallikrein inhibition values in the exudate were elevated significantly in HDC treated animals compared with untreated animals.
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Using chromogenic peptide substrate assay technique, components of the plasma kallikrein-kinin system and trypsin activity were studied in plasma and peritoneal exudate during acute pancreatitis in pigs. In the plasma no significant changes occurred, but increased kallikrein activity was found in the peritoneal exudate. This finding was paralleled by a reduction in prekallikrein levels and functional kallikrein inhibition values. The trypsin activity in peritoneal exudate, however, increased inconstantly. These results emphasize the significance of peritoneal protease-antiprotease imbalance during acute pancreatitis.
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Antimicrobial prophylaxis with agents active against aerobic and anaerobic micro-organisms leads to a significant reduction of infectious complications following colorectal surgery. A single dose (1600 mg) of tinidazole (a nitroimidazole derivate) and doxycycline (400 mg) will provide serum and tissue values well above minimum inhibitory concentration (MIC) values for more than 24 hours. To reduce the unwanted side effects and cost of prolonged antimicrobial prophylaxis, a prospective controlled clinical multicenter study comparing the effect of a single dose before operation of tinidazole and doxycycline to five days of prophylaxis before operation in 234 patients undergoing elective colorectal surgery was undertaken. Six patients given a single dose of prophylaxis before operation (n = 118) developed infectious complication (5.1%). Prolongation of prophylaxis before operation for four days after operation (n = 116) did not lead to any further reduction of infectious complications. A single dose of tinidazole and doxycycline before operation is a simple and effective prophylaxis against infectious complications following elective colorectal surgery.
The effects of thyrotropin-releasing hormone (TRH) and atropine on the gastric motility after stimulation by insulin-induced hypoglycemia were studied by the intragastric balloon technique. Four healthy young men were examined in two different ways on different days. In one experiment the effect of 50 micrograms TRH, 500 micrograms atropine, and 10 micrograms TRH, all intravenously injected, and in the other 500 micrograms atropine and 50 micrograms TRH were analyzed in this specific sequence. In two subjects the effect of intravenously injected TRH, 200 micrograms, and atropine, 500 micrograms, on the carbacholine-stimulated gastric motility was tested. The hypoglycemic stimulation of the gastric motility was immediately and completely blocked for a period of 9.3 +/- 0.7 min after 50 micrograms TRH and for 3.4 +/- 0.1 min after 10 micrograms TRH. The intragastric basal pressure was immediately reduced in all after TRH injection (-2.5 +/- 0.48 cm H2O pressure). Atropine had no significant effect on the gastric motility after hypoglycemic stimulation. The inhibiting effect of TRH on the carbacholine-stimulated gastric motility was similar to the effect of TRH on the hypoglycemia-stimulated gastric motility. These results demonstrate that TRH effectively inhibits the atropine-resistant stimulation of the gastric motility after insulin-induced hypoglycemia and also has potent relaxing effects on the muscular tonus of the gastric wall.
Acute pancreatitis was induced in pigs by retrograde injection of Na-Taurocholate into the pancreatic duct. Using a chromogenic peptide substrate assay, increased plasma kallikrein activity was found in the peritoneal exudate. This finding was paralleled by reduced prekallikrein and functional kallikrein inhibition values. In plasma, however, no changes in the kallikrein-kinin system were found during the 6 hours observation time. These findings emphasize the significance of peritoneal protease-antiprotease imbalance during acute pancreatitis.
In 1976 endoscopy with at least 20 biopsies and cytology were performed in 108 patients 20-25 years after partial gastrectomy (Billroth II). In one patient advanced carcinoma and in three cases severe dysplasia or carcinoma in situ, were found. At the follow-study in 1979, 7 patients had died of causes other than gastric carcinoma. A re-examination with endoscopy, biopsies and cytology were performed in fifty-eight patients. The present study did not show a progress of dysplasia in the gastric remnant during the three years of follow-up. The observations may suggest that re-examinations with gastroscopy and multiple biopsies every 3-5 years may be satisfactory in detecting carcinoma of the gastric remnant.
Out of 421 patients who had partial gastrectomy 20-25 years ago for gastric or duodenal ulcer, 108 were examined by endoscopy with multiple biopsy. In no case were the endoscopic appearances of the mucosae interpreted as malignant, though in 2 patients the clinical history suggest malignant disease. Histological examination revealed infiltrating carcinoma in 4 patients, 3 of whom had intramucosal carcinoma only. 3 further patients had severe dysplasia (carcinoma-in-situ). Only 1 patient had a near-normal mucosa close to the anastomosis; in the remainder the gastric remnant showed various degress of dysplasia, metaplasia, or chronic atrophic gastritis. In the patients with carcinoma only 28 (12%) of the 226 biopsy specimens revealed the malignant lesion. Patients who have had partial gastrectomy for benign lesions are at high risk of gastric-stump carcinoma. If, 20 years after operation, they have an endoscopy with multiple biopsy, stump carcinoma may be detected early when the prognosis after operation is probably good.
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