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Biomedical subjects

I Ihse

Publications and source records attributed to I Ihse.

At least 73 records · Page 4Linked to original sources
PubMed1995

Antioxidant and calcium channel blockers counteract endothelial barrier injury induced by acute pancreatitis in rats.

BACKGROUND: Multiple organ failure is the major mortality-related complication in severe acute pancreatitis. Endothelial barrier injury may be involved in its pathophysiology. METHODS: The present study evaluated alterations in endothelial barrier integrity in different organs/tissues 12 h after induction of acute pancreatitis by intraductal infusions of bile. Potential effects of oxygen free radicals and calcium influx were evaluated by pretreatment with an antioxidant, N-acetyl-L-cysteine, and calcium channel antagonists, verapamil and diltiazem. RESULTS: Tissue edema, reflected by an increase in tissue water content, was noted in the stomach, proximal small intestine, cecum, spleen, pancreas, kidneys, liver, lungs, heart, and brain in rats with pancreatitis. Also, an increased endothelial barrier permeability, as evidenced by the leakage of radiolabeled human serum albumin from blood to tissues, occurred in the stomach, proximal small intestine, colon, peritoneum, spleen, pancreas, kidneys, liver, lungs, and heart, accompanied by altered liver functions, increased levels of pancreatic enzymes, compromised renal function, and delayed intestinal motility. N-acetyl-L-cysteine prevented tissue edema and endothelial permeability changes in most organs/tissues, whereas the effects of verapamil and diltiazem were less marked. The preventive effects occurred in an organ-dependent manner. CONCLUSIONS: Endothelial barrier injury is found in all investigated organs/tissues in acute experimental pancreatitis. Oxygen free radicals and calcium influx may play a role in the development of these changes.

Acetylcysteine↗
PubMed1995

Intravascular ultrasound of the portal vein--normal anatomy.

The purpose of this study was to evaluate the appearance of the normal portal vein with intravascular ultrasound. The portal vein was studied in 10 patients with colorectal carcinoma without known liver or pancreatic disease. For the intravascular portovenous examination, a 2.0-mm, 20-MHz ultrasound catheter was used. The field of view was 30 mm. The wall of the portal vein appeared as a single hyperechoic layer 0.5 to 0.8 mm in thickness. Normal structures adjacent to the portal vein, such as the common bile duct, the hepatic artery or small lymph nodes, were clearly separated from the lumen of the portal vein by the wall of the vein together with some periportal fat. In most cases the parenchyma of the pancreas could be separated from the wall of the vein.

Adult↗
PubMed1994

Surgical management of pure pancreatic fistulas.

This paper reports on 13 patients with pure pancreatic fistulas defined as persistent lesions originating directly from the gland tissue and not from a pancreatico-intestinal or pancreatico-gastric anastomosis. Six fistulas were external and seven internal. All external fistulas were postoperative whereas all the internal ones were due to chronic pancreatitis. Conservative treatment of 2 to 36 months duration was unsuccessful, so that all patients underwent surgery. To establish a proper surgical strategy, preoperative mapping of the fistula by endoscopic retrograde cholangiopancreaticography (ERCP), fistulography and/or computerized tomography proved of value. In eleven patients, pancreatic fistula flow was surgically redirected into the gastrointestinal tract, while the remaining two were submitted to a pancreatic left resection. There were no hospital deaths and the complication rate was low. During the follow-up time of 6 to 96 months no recurrent fistulas were seen.

Adult↗
PubMed1993

Improved glucose metabolism after subtotal pancreatectomy for pancreatic cancer.

Diabetes occurs frequently in patients with pancreatic cancer. To investigate the impact to tumour removal, seven patients were studied before and after 85 per cent subtotal pancreatectomy for adenocarcinoma of the pancreas. The frequency of diabetes was determined by the oral glucose tolerance test. Fasting levels of C peptide and insulin were measured in plasma, and insulin secretion was investigated by hyperglycaemic glucose clamp and glucagon stimulation. Six of the seven patients were diabetic before surgery and four required insulin treatment. Improvements in diabetic status and glucose metabolism were found in all seven patients after operation, as demonstrated by increased glucose metabolic capacity during hyperglycaemia. This occurred despite a postoperative reduction in insulin secretion and is explained by the observed augmentation of whole-body insulin sensitivity after surgery. A diabetogenic factor may be produced by pancreatic adenocarcinoma that may be responsible, directly or indirectly, for the high frequency of diabetes in patients with pancreatic cancer.

Adenocarcinoma↗
PubMed1993

Bacterial peritonitis with hyperamylasemia in the absence of ultrastructural changes of pancreas. A light and electron microscopic study in the rat.

Bacterial peritonitis was induced in rats by injecting two concentrations of E. coli (10(6) cfu/mL or 10(8) cfu/mL) and B. fragilis (10(8) cfu/mL or 5 x 10(8) cfu/mL) ip. Twenty-four hours later the serum amylase activity was significantly increased in both groups. At light microscopy scattered polymorphonuclear leukocytes were observed in the pancreatic glands of both controls and rats receiving bacteria. In the peripancreatic fat microabscesses were seen in 5 of 10 animals receiving the higher dose of bacteria. There were no fat necroses. Morphometric analysis of the pancreatic ultrastructure revealed a marginal but statistically nonsignificant increase of the volume density of connective tissue stroma indicating slight edema. There were no apparent changes seen within the acinar cells. Morphometrically the granule volume density, numerical density of granule profiles, numerical granule density, nuclear volume density, and numerical condensing vacuole density were similar between controls and animals receiving bacteria. We conclude that, although bacterial peritonitis caused hyperamylasemia, no obvious morphologic damage was found in the exocrine pancreas.

Amylases↗
PubMed1993

Effects of pancreaticobiliary diversion and gastric fundectomy on azaserine-induced pancreatic carcinogenesis in the rat.

The effects of pancreaticobiliary diversion (PBD) and gastric fundectomy on the pancreas in azaserine-treated rats were studied over 14 months. Sham-operated azaserine-treated animals served as controls. A significant increase in pancreatic weight and total DNA and protein content was found in PBD-operated and fundectomized animals. DNA flow cytometry showed a significantly increased ratio of tetraploid to diploid cells in pancreatic tissue in both experimental groups. Mean values of all these variables were significantly higher after PBD than after fundectomy. Acidophilic atypical acinar cell foci of the pancreas were observed in all of the experimental and 75% of the control animals. The volume density of these foci was significantly higher in each experimental group than in the controls. The volume density, radioactive thymidine labeling index, and mitotic index of the foci were significantly higher after PBD than after fundectomy. Changes consistent with pancreatic adenoma were diagnosed in the PBD group only. It is concluded that not only PBD with endogenous hypercholecystokininemia, but also fundectomy with endogenous hypergastrinemia lasting about half of the life span in rats, induces pancreatic hypertrophy and enhances the development of precancerous pancreatic changes after azaserine treatment. In comparison with PBD, fundectomy caused less pronounced changes and no observable neoplasia.

Animals↗
PubMed1993

Release of platelet-activating factor in acute experimental pancreatitis.

This study demonstrates the formation of platelet-activating factor (PAF) in rats with acute experimental pancreatitis (AEP). The AEP was induced by infusing sodium taurodeoxycholate and trypsin into the bile-pancreatic duct. The PAF content was increased in blood samples and in pulmonary and pancreatic tissue as compared with control animals. Significant amounts of PAF were also found in peritoneal fluid. The PAF content did increase in blood samples and in pulmonary tissue after administration of endotoxin intravenously. The effects of intraperitoneal PAF administration were also studied and showed an increase of polymorphonuclear cells in blood samples. These findings suggest that acute pancreatitis might generate and release PAF. Whether PAF release is associated with the pathophysiology of complications in acute pancreatitis remains to be elucidated.

Acute Disease↗
PubMed1993

Pancreatic pain: is there a medical alternative to surgery?

The non-surgical management of chronic pancreatic pain is reviewed. In accordance with the suggested multifactorial origin of pancreatic pain, different treatment principles are practised. Besides conventional analgesic drugs, oral pancreatic enzymes seem efficient in a subgroup of patients with chronic pancreatitis. Endoscopic treatment aiming at reduction of the pancreatic duct-tissue pressure is promising, but it is still in its infancy. Coeliac nerve blockage is recommended in patients with pancreatic cancer and pain, whereas external radiotherapy plays a role in a diminishing number of these patients. Treatment of chronic pancreatic pain is an example of a complex clinical problem in which a multidisciplinary approach is mandatory.

Abdominal Pain↗
PubMed1993

Enterochromaffin-like cells in rat stomach respond to short-term infusion of high doses of cholecystokinin but not to long-term, sustained, moderate hyperCCKemia caused by continuous cholecystokinin infusion or pancreaticobiliary diversion.

The histamine-producing enterochromaffin-like (ECL) cells in the oxyntic mucosa are controlled by gastrin. An acute gastrin challenge induces release and accelerated resynthesis of ECL cell histamine. Long-term stimulation with gastrin causes ECL cell hyperplasia. We set out to study whether the ECL cells respond not only to gastrin but also to cholecystokinin (CCK). A wide dose range of gastrin-14 sulfated and -17 non-sulfated and CCK-8 sulfated (CCK-8s) and non-sulfated (CCK-8) was infused intravenously to rats for 3 h. The activity of the histamine-forming enzyme was measured at termination of infusion. Gastrins and CCK-8s were equally effective in activating the enzyme, whereas sulfated CCK-8 was notably less potent than the other three peptides. Clearly, the receptor responsible for activation of the ECL cells distinguishes poorly between gastrin-17 and CCK-8s, which is in line with the characteristics of the CCK-B receptor. Moreover, neither the response to gastrin-17 nor that to CCK-8s was affected by concomitant infusion of devazepide (200 micrograms/kg/h), a selective CCK-A-receptor antagonist. One group of rats received CCK-8s continuously via a minipump. Another group of rats was subjected to pancreaticobiliary diversion (PBD), which increases the plasma CCK concentration 10- to 20-fold. The rats were killed 7 or 10 weeks later, respectively, and the stomachs were analyzed with regard to mucosal growth and ECL cell hyperplasia. HyperCCKemic rats had increased pancreatic weights but showed no signs of growth stimulation in the stomach and no ECL cell hyperplasia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Pancreatic cancer is associated with impaired glucose metabolism.

OBJECTIVE: To investigate glucose metabolism and insulin secretion on patients with pancreatic cancer compared with healthy control subjects. DESIGN: Open study. SETTING: Linköping University Hospital, Sweden. SUBJECTS: 44 consecutive patients referred for radical operations for pancreatic carcinoma, and eight healthy age and sex matched volunteers. INTERVENTIONS: Hyperglycaemic glucose clamp in 36 of patients and all volunteers. MAIN OUTCOME MEASURES: Glucose tolerance according to WHO criteria, plasma insulin and C-peptide concentrations, and insulin secretion measurements both during hyperglycaemia and after stimulation by glucagon. RESULTS: Thirty-three patients (75%) had either impaired glucose tolerance or diabetes. Fasting insulin concentrations were raised in the non-insulin-requiring diabetic patients, but similar in the insulin-requiring group compared with healthy control subjects and patients with normal glucose tolerance. In neither diabetic group was insulin secretion affected during hyperglycaemia. After stimulation with glucagon, insulin secretion increased in non-insulin-requiring diabetic patients but remained unchanged in those who required insulin. Glucose metabolic capacity and whole body insulin sensitivity were reduced in patients with diabetes and with impaired glucose tolerance, and the reduction was more pronounced in diabetic patients. CONCLUSIONS: There is a high incidence of impaired glucose tolerance and diabetes in patients with pancreatic cancer, which cannot be explained by impaired secretion of insulin. Other factors that reduce insulin sensitivity seem to have a role in the development of diabetes in this group of patients.

Adenocarcinoma↗
PubMed1993

Bacterial translocation during acute pancreatitis in rats.

OBJECTIVE: To see if bile-induced pancreatitis could cause bacterial translocation to mesenteric lymph nodes, and therefore pancreatic necrosis, in rats. DESIGN: Controlled experiment. MATERIAL: 18 Male Wistar rats. INTERVENTIONS: Pancreatitis was induced in the experimental group (n = 12) by infusion of 0.2 ml of a solution containing 4 mumol (20 mumol/ml) sodium taurodeoxycholate into the pancreatic duct over one minute. The controls had sham operations (no infusion). Two days later repeat laparotomy was done on all surviving animals and samples taken for microbiological analysis. All animals were weighed at the beginning and end of the experiment. RESULTS: Bacteria were isolated from the mesenteric lymph nodes in all survivors in the experimental group (9/12), and from the pancreas in all but one. Blood and peritoneal fluid were colonised in 5 and 7 rats, respectively. Escherichia coli was the most common organism isolated. Positive anaerobic cultures were obtained from mesenteric lymph nodes in 5, and from the pancreas in one. Rats with pancreatitis developed overgrowth of both aerobic and anaerobic bacteria in the caecum and the ileum, but on light microscopic examination the proximal and distal intestinal mucosa did not differ between control and experimental rats. Bacterial translocation increased as the condition of the animals worsened. CONCLUSION: Acute pancreatitis in rats causes systemic bacterial colonisation, probably as a result of bacterial translocation, which may therefore be a mechanism of pancreatic infection.

Acute Disease↗
PubMed1993

Recurrence of exocrine pancreatic cancer--local or hepatic?

The results of radical surgery for pancreatic cancer depend, like all other cancer surgery, on the technique used, and the biology of the disease. We have analysed the site and time of recurrence after pancreatectomy for exocrine pancreatic cancer in 74 patients who died more than six months postoperatively. All patients had recurrent disease, 64 patients had local recurrence in the pancreatic bed and 68 had liver metastases. Local recurrence without liver metastases was found in six patients, and ten had liver metastases, but no local recurrence. Both the time from operation to clinically evident recurrence and the postoperative survival time were significantly longer for patients with local recurrence only. Although not statistically significant, there was a tendency (5 out of 8) for smaller, well-differentiated tumors without spread outside the pancreas to be associated with local recurrences without liver metastases. We conclude that, in retrospect, the surgical procedures used were inappropriate and inadequate. To cure these patients, a more radical operation and/or effective adjuvant treatment is needed.

Adenocarcinoma↗