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Biomedical subjects

I Nordback

Publications and source records attributed to I Nordback.

At least 37 records · Page 2Linked to original sources
PubMed1999

Cholecystokinin in the early course of acute post-ERCP pancreatitis.

BACKGROUND: A high dose of cholecystokinin (CCK) agonist cerulein can induce acute pancreatitis in animals. The role of CCK in the induction of acute pancreatitis in humans is unclear. We investigated basal plasma CCK levels before and after induction of post-ERCP pancreatitis to determine CCK levels in the early course of the disease. STUDY DESIGN: We determined plasma CCK concentrations in four groups of patients who underwent ERCP: (1) post-ERCP pancreatitis patients (n = 23); (2) patients with post-ERCP hyperamylasemia without pancreatitis (n = 5); (3) patients with post-ERCP abdominal pain without hyperamylasemia (n = 18); and (4) patients with an uneventful post-ERCP period (n = 43). Plasma samples were taken before ERCP, 4 to 8 hours, 10 to 16 hours, and 24 hours after ERCP. Plasma CCK concentrations were determined by a specific and sensitive radioimmunoassay using CCK antiserum (Euro-Diagnostica, Malmö, Sweden). RESULTS: Plasma CCK levels increased five-fold early in the course in post-ERCP pancreatitis patients, but not in post-ERCP hyperamylasemia patients or in uncomplicated ERCP patients, where CCK levels temporarily decreased after ERCP. In patients with abdominal pain, CCK levels did not change. After the early increase, plasma CCK levels declined to almost unmeasurable levels one day after the onset of symptoms in post-ERCP pancreatitis. In other groups CCK levels were close to the pre-ERCP level. CONCLUSIONS: It remains to be shown whether CCK is important in the pathogenesis of post-ERCP pancreatitis or merely a secondary phenomenon. There is a rationale to test CCK antagonists in preventing post-ERCP pancreatitis.

Abdominal Pain↗
PubMed1999

Control of vascular tone in isolated mesenteric arterial segments from hypertensive patients.

1. Experimental hypertension is associated with several functional alterations of vascular endothelium and smooth muscle, but relatively few studies have examined the control of arterial tone in isolated vascular preparations from patients with essential hypertension. Therefore, we compared functional characteristics in vitro of distal ring segments of the mesenteric artery from 17 hypertensive and 22 normotensive humans. 2. Arterial constrictor responses induced by cumulative addition of Ca(2+) in the presence of noradrenaline (NA) were more effectively inhibited by the Ca(2+) entry blocker nifedipine (0.5 nM) in hypertensive than normotensive subjects (by 55.4+/-4.9, n=17 and 35.0+/(-5.2%), n=22, respectively). Also the contractions elicited by high concentrations of KCl were more effectively inhibited by nifedipine in arterial rings from hypertensive than normotensive patients (by 38.9+/(-3.7), n=17 and 20. 2+/(-4.6%), n=22, respectively). However, the concentration-response curves of contractions to NA, serotonin and KCl in the absence of nifedipine were similar between the study groups. 3. The concentration-response curves of endothelium-dependent relaxations to acetylcholine and Ca(2+) ionophore A23187, as well as of endothelium-independent relaxations to the nitric oxide donor nitroprusside, beta-adrenoceptor agonist isoprenaline and K+ channel opener cromakalim did not show any differences between the groups. Moreover, the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (0.1 mM) almost abolished the relaxations to acetylcholine and Ca(2+) ionophore in both groups, indicating that these responses were largely mediated by nitric oxide. The function of arterial sodium pump was evaluated by relaxations elicited by the return of K+ upon contractions induced by K+-free solution. The rate of K+-relaxation was similar in hypertensive and normotensive arteries (for all these responses n=20 - 22 in the normotensive and 15 - 17 in the hypertensive group). 4. These results suggest abnormal function of voltage-dependent Ca(2+) channels in arterial smooth muscle of hypertensive patients, whereas vascular responses to endothelium-dependent and -independent vasodilators and classical contractile agents were similar between hypertensive and normotensive subjects. The present findings support the view that blockade of voltage-dependent Ca(2+) channels is an effective means of reducing arterial tone in essential hypertension.

Adult↗
PubMed1999

Extrapancreatic organ impairment in caerulein induced pancreatitis.

BACKGROUND AND AIMS: Multiorgan function failures are the major fatal complications in acute pancreatitis. In this experiment, we studied 1) the manifestation and time course of extrapancreatic organ damage in an acute pancreatitis model and 2) whether the obstructive liver damage in this model is caused by the obstruction of common biliopancreatic duct compressed by oedematous pancreas. MATERIAL AND METHODS: 80 male Wistar rats were divided into two groups: control and caerulein groups (five subgroups in each group). In the caerulein group, the acute pancreatitis was induced by caerulein intraperitoneal injections. In the controls equal volume of saline was injected. Two subgroups, one in caerulein and one in control groups, had an intrapancreatic bile duct stent inserted transduodenally before the injections. The pancreas, liver, lung and kidney tissues and blood samples were obtained for the measurement or analysis of interstitial oedema, plasma amylase, alanine aminotransferase, bilirubin, urea, creatinine, alkaline phosphatase, lactate dehydrogenase, blood gas and electron microscopy at 1, 6, 12 and 24 hours after the last injection in unstented animals, and at 6 hours in stented animals. RESULTS: Lungs and kidney remained unchanged. Liver damage was found during the first 6-12 hours, manifest as increased plasma alanine aminotransferase and bilirubin and dilatation of bile canaliculi and hepatocyte damage in electron microscopy. The intrapancreatic bile duct stent did not resolve these changes. CONCLUSIONS: The liver may be the first evolved extrapancreatic organ in the early stage in this mild oedematous pancreatitis model and the hepatocyte damage is not caused by the obstruction of common biliopancreatic duct compressed by the oedematous pancreas.

Animals↗
PubMed1999

Extrapancreatic multiorgan injury in a severe sublethal acute pancreatitis model.

In order to develop a new severe but sublethal acute pancreatitis model for the study of clinically relevant extrapancreatic multiorgan injury, we have induced acute pancreatitis in a rat model by intraductal injection with low dose and moderate concentration of bile acid under low pressure. We examined the structural and functional features in the pancreas, lung, liver and kidney. The animals were divided into two groups: the bile acid injection group and the control group. In the bile acid injection group, acute necrotizing pancreatitis was induced by intraductal administration of 0.2 ml of 2.0% bile acid under 30 cm H2O pressure, while the controls underwent the sham operation. The two groups were divided into six subgroups (8 rats for each) and sacrificed at 12, 24, 36, 48, 72 and 144 h, respectively. The pancreatitis induced hyperamylasemia, ascites, pancreatic oedema, haemorrhage, acinar cell necrosis and extensive fat necrosis without early mortality. Accompanied with the pancreatic injury, the function and histologic changes have developed continuously in the kidney and liver for 72 and 144 h in the bile acid injection animals respectively. No pancreatitis associated pulmonary changes were found. Taking into account the results with the two previously developed models of pancreatitis, we conclude that the extrapancreatic injury in acute pancreatitis is found in the liver, kidney and lung, in that order, depending on the severity of pancreatitis. The present sublethal pancreatitis model, in comparison with the two previously studied acute pancreatitis models, is perfect for pathogenetic and therapeutic study of liver and renal changes in acute necrotizing pancreatitis.

Acute Disease↗
PubMed1999

Extrapancreatic organ manifestations in a moderately severe acute pancreatitis model.

In order to study the extent of clinically relevant extrapancreatic organ injury in a moderately severe pancreatitis model, we examined the structural and functional features of the pancreas, lung, liver and kidney in a rat model simulating gallstone pancreatitis. The animals were divided into three groups: the low-ligation group, the high-ligation group and the control group, and sacrificed at 6, 24, 42, 60 and 96 h. In the low-ligation group, moderately severe acute pancreatitis was induced by the ligation of the common biliopancreatic duct plus intralipid intragastric injection, while controls underwent the ligation of the bile duct above the pancreas (the high-ligation group) or only sham operation (the control group) with fat injection. The pancreatitis induced hyperamylasemia, pancreatic oedema, haemorrhage, acinar cell necrosis and extensive fat necrosis. Accompanied with a peak value of serum amylase activity 24 h after the induction, the kidney changes developed, characterized by decrease in urine output, increase in serum urea and creatinine, and proximal convoluted tubular damage under electron microscope. There were no pancreatitis associated lung or liver changes. These results suggest that this model can be used to study the pathogenesis and therapy of renal injury during acute moderately severe pancreatitis.

Acute Disease↗
PubMed1998

Difference in microbes contaminating pancreatic necrosis in biliary and alcoholic pancreatitis.

CONCLUSION: There are differences in the microbiology of infected pancreatic necrosis in alcoholic and biliary pancreatitis. One possible explanation may be different routes of contamination. BACKGROUND: Infection is a severe complication in acute pancreatitis. Bacteria are found in 40-70% of all patients suffering from necrotizing pancreatitis. We investigated whether there were any differences in microbes isolated from pancreatic necrosis in biliary and alcoholic pancreatitis. METHODS: Microbiological tests were conducted on necrosis taken at the operation for pancreatitis with the etiology of (group A) alcoholic pancreatitis (n = 47) and (group B) biliary pancreatitis (n = 23). Patients with simultaneous cholecystitis were excluded. The time from the first symptoms to the operation or the extent of necrosis did not differ between the groups. RESULTS: Microbes were isolated more often in the cultures from group B than group A (17/23 = 74% vs 15/47 = 32%, p = 0.001). The most common were Gram-positive bacteria in group A and Gram-negative bacteria in group B. From the first week, from the onset of symptoms to the operation. Gram-negative bacteria were isolated significantly more often in the cultures from group B patients than from group A patients (8/10 = 80% vs 1/5 = 20%, p = 0.04). In multivariate analysis, we found that biliary pancreatitis was an independent risk factor (adds ratio 5.5, 95% confidence interval [CI] 0.59-52.10) of contamination of necrosis with Gram-negative bacteria.

Adult↗
PubMed1998

Hyperamylasemia after cardiopulmonary bypass: pancreatic cellular injury or impaired renal excretion of amylase?

BACKGROUND: Postoperative hyperamylasemia and even acute pancreatitis are associated with coronary artery bypass grafting (CABG). The mechanism of hyperamylasemia and pancreatic acinar cell damage was studied in 20 patients undergoing CABG. METHODS: Serial blood and urine samples at eight time points before, during, and 24 hours after the CABG were collected. Salivary and pancreatic isoamylases, the fractional clearance of isoamylases (i.e., relative to creatinine clearance), pancreatic phospholipase A2 (a specific serum marker of pancreatic acinar cell injury), and cystatin C (a sensitive marker of glomerular filtration rate) were measured. RESULTS: Mild serum hyperamylasemia (300 to 1000 units/L) was found in 11 of 20 (55%) and severe (> 1000 units/L) in 6 of 20 (30%) patients with no signs of clinical acute pancreatitis. Hyperamylasemia occurred from 6 to 24 hours after the CABG and was mainly caused by pancreatic isoamylase. Serum pancreatic phospholipase A2 concentration remained unchanged, which excludes acinar cell damage. Although renal glomerular filtration was normal during CABG as measured by serum cystatin C and creatinine clearance, the fractional clearance of isoamylases decreased. CONCLUSIONS: The decreased rate of excretion into urine, rather than pancreatic cellular damage, is the major source of hyperamylasemia after CABG.

Amylases↗
PubMed1998

Effects of botulinum toxin A on the sphincter of Oddi: an in vivo and in vitro study.

BACKGROUND: Botulinum toxin A is a potent inhibitor of the release of acetylcholine from nerve endings. Local injection of botulinum toxin has recently been suggested to be helpful in sphincter of Oddi dyskinesia by decreasing sphincter of Oddi pressure. AIMS: To explore the mechanism of action of botulinum toxin A on sphincter of Oddi (SO) muscle. METHODS: Four piglets underwent duodenoscopy and SO manometry was performed. After obtaining a baseline pressure, the SO was injected with normal saline and the experiment repeated after one week. The SO was then injected endoscopically with botulinum toxin (40 U) with follow up manometry one week later. The sphincter of Oddi was removed from 10 pigs, cut into three rings, and placed in an organ bath. The force of contraction was measured and registered on a polygraph. Rings were stimulated by 70 V (10 Hz, 0.5 ms) electrical field stimulation for 20 seconds, exogenous acetylcholine (100 microM), and KCl (125 mM). Botulinum toxin (0.1 U/ml) or atropine (1 microM) was added to the incubation medium and the stimulation was repeated. RESULTS: Mean basal SO pressure in the pigs remained unchanged after saline injection but decreased to about 50% of baseline value following botulinum toxin injection (p = 0.04). The contractions induced by direct stimulation of SO smooth muscle with KCl were not significantly affected by either atropine or botulinum toxin. In all rings exogenous acetylcholine induced contractions, which were totally blocked by atropine, but not by botulinum toxin. Electrical field stimulation induced contractions that were inhibited by both atropine and botulinum toxin. CONCLUSION: Botulinum toxin inhibits pig sphincter of Oddi smooth muscle contractions by a presynaptic cholinergic mechanism, similar to that described in skeletal muscle.

Acetylcholine↗
PubMed1997

The presence of the gallbladder is associated with the severity of acute biliary pancreatitis.

CONCLUSION: The presence of the gallbladder at the onset of acute biliary pancreatitis is associated with increased severity of the disease. One possible explanation is that gallbladder contraction might induce bile reflux into the pancreatic duct during the transfer of a gallstone through the ampulla. BACKGROUND: In clinical practice there is an impression that the presence of the gallbladder in patients with biliary pancreatitis may be associated with increased severity of the disease, compared to patients who have undergone cholecystectomy. METHODS: To test this hypothesis, we studied 266 cases with biliary pancreatitis. Patients were divided into two groups: (A) those who had a gallbladder in situ at the onset of biliary pancreatitis (n = 234, 88%) and (B) those who had undergone previous cholecystectomy (n = 32, 12%). RESULTS: Pancreatitis was more severe in group A than in group B, according to Glasgow criteria (> or = 3 positive, 66/210 = 31% vs 4/29 = 14%, p = 0.04); development of complications (77/234 = 33% vs 4/32 = 13%, p = 0.01); and mortality (40/234 = 17% vs 1/32 = 3%, p = 0.03). Furthermore, serum C-reactive protein levels on admission were over 150 mg/L twice as often in group A as in group B.

Acute Disease↗
PubMed1997

The inhibitory role of nitric oxide in the control of porcine and human sphincter of Oddi activity.

BACKGROUND: The possible role of nitric oxide in the regulation of the sphincter of Oddi is not known in species with a resistor-like sphincter of Oddi such as humans and pigs. METHODS: Sphincter of Oddi perfusion manometry and simultaneous electromyography (EMG) were recorded transduodenally in eight anaesthetised pigs. Acetylcholine (4 micrograms/kg) was given intra-arterially, with or without sodium nitroprusside (10-100 micrograms/kg), an exogenous nitric oxide donor. For in vitro studies the sphincter was removed from the eight pigs and from six patients undergoing pancreaticoduodenectomy, cut into rings, and the amplitude of contraction was measured in an ex vivo bath. Each ring was stimulated with acetylcholine (100 microM) and KCl (125 mM). The stimulation was repeated after incubation with L-NAME (a stereospecific competitive inhibitor of nitric oxide synthase), with L-NAME plus L-arginine (a substrate for nitric oxide synthase), and with sodium nitroprusside. The sphincter rings were then submersed in liquid nitrogen and stored. Immunohistochemical analysis was used to localise nitric oxide synthase in the pig and human sphincter specimens. RESULTS: In vivo EMG revealed 2-3 phasic bursts per minute with the basal pressure variation 6-40 mm Hg. Acetylcholine induced a large electrical burst and the pressure increased by (mean (SE)) 20 (10) mm Hg (p < 0.01) for 17 (4) seconds. After sodium nitroprusside (10 micrograms/kg) acetylcholine did not induce pressure changes and electrical activity was almost abolished. In vitro, L-NAME increased the KCl induced sphincter contraction in both pig and human specimens (p < 0.01). In human, but not in pig, specimens L-NAME increased the amplitude of acetylcholine induced contraction (p < 0.01). L-Arginine partly reversed the effect of L-NAME in both pig and human specimens. Sodium nitroprusside decreased the acetylcholine and KCl induced contractions in both pig and human specimens. Immunohistochemical studies localised nitric oxide synthase to rich plexi of nerve fibres in the mucosa and the muscle in both pig and human sphincter of Oddi. CONCLUSIONS: The sphincter of Oddi in both pigs and humans has endogenous nitric oxide synthase activity and immunoreactivity. Inhibition of endogenous nitric oxide production enhances contractility while exogenous nitric oxide decreases sphincter contractility and electrical activity.

Acetylcholine↗
PubMed1997

Postoperative hyperamylasaemia in cardiac surgery.

The mechanism of postoperative hyperamylasaemia was studied in 48 patients undergoing coronary artery bypass grafting (CABG). Mild hyperamylasaemia developed in 87% of the patients, and in 10% the serum amylase activity was > 1000 U/l. Serial measurements of serum salivary (S-) and pancreatic (P-) isoamylases indicated that hyperamylasaemia was highest 24 hours after CABG and consisted mainly of P-amylase component. Serum creatinine, creatinine clearance and urinary albumin concentration remained normal after CABG, excluding severe renal damage. The fractional clearance (i.e. relative to creatinine clearance) of P-amylase decreased more than of S-amylase (from 3.6 to 0.9% vs 1.3 to 0.8%). Decreased rate of excretion into urine, rather than pancreatic cellular damage, is the main source of hyperamylasaemia after CABG.

Aged↗
PubMed1997

Haemorrhage into a duodenal cyst with ectopic gastric epithelium, a rare cause of gastric outlet obstruction in an adult.

BACKGROUND: Duodenal duplications, including also cysts with gastric epithelium, are congenital anomalies observed in less than 1 per 100,000 births. They are usually detected in infants or children. AIM: To evaluate and discuss the diagnostic work-up and treatment. MATERIAL AND METHODS: A rare case of haemorrhage in the duodenal cyst in a 32-year-old woman with gastric outlet obstruction is presented. RESULTS: Computed tomography (CT) revealed cystic lesion in the duodenum. Endoscopic retrograde cholangiopancreatography (ERCP) showed normal biliary and pancreatic ducts. Final histology demonstrated cystic lesion in the duodenum which was lined with gastric mucosa. CONCLUSION: Preoperative CT and ERCP are important in the differential diagnosis and planning of treatment in duodenal cystic lesions.

Adult↗
PubMed1997

Prospective evaluation of a treatment protocol in patients with severe acute necrotising pancreatitis.

OBJECTIVE: Audit of the protocol for surgical treatment of patients with acute severe and necrotising pancreatitis (ANP). DESIGN: Prospective open study. SETTINGS: University hospital, Finland. PATIENTS: 33 patients treated for severe (Ranson score 3 or more) and necrotising (as judged on computed tomograms (CT)) pancreatitis between 1992-1993. PROTOCOL: Indications for antibiotic treatment (n = 25 patients) were: fulminant multiorgan disease; recurrent continual parallel increase in temperature, white cell count (WCC) and C-reactive protein concentration; or the presence of bacteria on Gram stain of a percutaneous fine needle aspiration smear of necrosis. Three of the 25 responded to antibiotics. They and eight others with ANP but without these indications were treated conservatively. Twenty-two patients underwent repeated necrosectomy by laparostomy. MAIN OUTCOME MEASURES: Diagnosis of pancreatic infection, morbidity and mortality RESULTS: Of the 22 patients operated on 17 had contaminated necrosis at operation, and this had been predicted by the increasing inflammatory variable and the presence of bacteria in the Gram stain. Five patients operated on died (23%), four of the five having been operated on for fulminant multiorgan disease (80%). Recurrent sepsis developed in five patients, pancreatic fistulas in two, and there were no pseudocysts. Gastrointestinal fistulas developed in 12 patients, but not after we had changed the technique of wound packing. All 11 patients treated conservatively survived. CONCLUSION: A third of patients with ANP can be selected for safe non-operative treatment. Infected ANP can be treated by repeated necrosectomy by laparostomy with low mortality (6%). Early fulminant multiorgan disease should not be treated with laparostomy.

Adult↗
PubMed1997

Posterior approach for adrenal surgery: experiences with 59 patients.

BACKGROUND: The laparoscopic approach has become popular for adrenal surgery. AIM: When starting with laparoscopic adrenalectomies we studied our experiences of posterior open approach for different adrenal disorders to obtain reference data. MATERIAL AND METHODS: Between 1983 and 1993 95 adrenalectomies were performed, of which 59 were via the posterior route. There were 51 unilateral (7 phaeochromocytomas, 6 Cushing's syndromes, 33 Conn's syndromes, 1 sex steroid secreting tumour and 4 incidentalomas) and 8 (Cushing's disease) bilateral adrenalectomies. RESULTS: Of the 4 incidentalomas one was a benign adenoma, one was cyst, one was cortical carcinoma, and one was a metastasis from breast cancer. Operative blood loss was median 300 ml, being higher in the bilateral than in the unilateral adrenalectomies (median 500 (range 300-1,250) ml vs. 300 (30-4,500 ml) (P = 0.01). Complications occurred in overall 11 patients (19%) (8 wound infections, 3 postoperative bleeding, 2 pneumonias, 1 urinary infection). Complications were more frequent in Cushing's patients than in the others (6/14 (43%) vs. 5/45 (11%); P = 0.015). Postoperative hospital stay was median 8 (range 5-21) days. The patients started liquids orally and were mobilised on the first post operative day, except for the 3 re-operated patients. Thromboembolic complications did not occur. Narcotics were used postoperatively for median 2 (range 0-7) days. CONCLUSIONS: With the posterior approach mortality and complications related to the pancreas, spleen, colon and duodenum were avoided. Other complications were rare except for the patients with Cushing's disease or syndrome.

Adolescent↗
PubMed1996

Pancreatitis associated protein as an early marker of acute pancreatitis.

BACKGROUND: Measuring serum pancreatitis associated protein (PAP) in acute pancreatitis has proved valuable to monitoring the course of the disease and the recovery of the patient. AIMS: The aim was to analyze the utility of PAP on admission as a diagnostic and prognostic marker of acute pancreatitis. PATIENTS: Values of PAP were prospectively analyzed in 80 healthy volunteers, 164 patients with abdominal pain but without pancreatitis, 109 patients with mild acute pancreatitis, and 38 patients with severe acute pancreatitis. METHODS: The diagnosis of acute pancreatitis was verified with clinical, laboratory, radiological, and in some cases findings at operation or necropsy. RESULTS: Mean (95% confidence intervals) serum PAP values were 27 (24 to 29) micrograms/l in healthy volunteers, 78 (59 to 96) micrograms/l in patients with abdominal pain, 191 (134 to 247) micrograms/l, in patients with mild acute pancreatitis, and 599 (284 to 914) micrograms/l in patients with severe acute pancreatitis. Differences between the groups were significant (p = 0.04 - 0.01). Despite the differences in means, the ranges overlapped between the groups. The sensitivity of PAP on admission to detect acute pancreatitis was 38%-53% and the respective specificity 89%-77% depending on the cut off level. The sensitivity of PAP to detect severe acute pancreatitis was 45%-68% and the specificity 74%-59% depending on the cut off level. CONCLUSIONS: Admission PAP did not distinguish severe from mild acute pancreatitis better than C reactive protein. Measurement of PAP does not give appreciable diagnostic advantages in the early phase of acute pancreatitis.

Acute Disease↗