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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CFY male rats anaesthetized with pentobarbital were used in different groups for inducing acute pancreatitis by the retrograde injection either of 1 mg elastase, 5 mg trypsin, 4 mg lysolecithin, 10 mg Na-taurocholate in 0.2 ml volume or of 0.3 m. sunflower oil. In each group laparatomized animals served for control. The animals with pancreatitis were treated either with 15 mug/b.w.kg/hour glucagon or with physiological saline for 72 hours. Twenty-four and 72 hours after inducing pancreatitis glucagon did not influence the significant fall in blood pressure elicited by the intraductal injection of trypsin or elastase or in the plasma calcium level in pancreatitis induced by trypsin or sunflower oil. Neither did glucagon affect the significant increase of plasma lipase activity in pancreatitis induced by trypsin or taurocholate. It also failed to reduce the 24-hour mortality rate and the extension of fat tissue necrosis in the abdominal cavity of pancreatitic animals. In contrast, glucagon treatment significantly reduced the amount of abdominal exudate associated with bile salt induced pancreatitis and, probably due to its pancreatic blood flow increasing effect, seemed to moderate the degree of tissue damage elicited in the pancreas by detergents such as taurocholate or lysolecithin.
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PMID:Glucagon treatment of experimental acute pancreatitis. 123 17

The association of serum amylase activity with the extent of pancreatic injury in acute pancreatitis is unclear. To clarify this relationship, we induced acute pancreatitis ranging from mild to lethal in 118 Sprague-Dawley rats (350-450 g). This was achieved by controlled intraductal infusion of low- or high-dose bile salt, with or without enterokinase, followed by intravenous cerulein or saline for 6 hr. Serum amylase was measured at baseline and 6 hr. Pancreatic histopathology was evaluated by two blinded pathologists employing total surface scoring (N = 118) and morphometric 20-field documentation (N = 22). Serum amylase correlated best with edema (r = 0.61) and fat necrosis (r = 0.58), less well with acinar necrosis (r = 0.53) and inflammation (r = 0.50), and poorly with hemorrhage (r = 0.33) and perivascular infiltrate (r = 0.31). Inasmuch as edema and fat necrosis are not important determinants of severity, these observations could explain the poor prognostic value of serum amylase activity in patients with acute pancreatitis.
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PMID:Histopathologic correlates of serum amylase activity in acute experimental pancreatitis. 138 Apr 25

Severe necrotizing pancreatitis is accompanied by release of hemorrhagic ascites fluid (HAF), which is thought to be related to the occurrence and frequency of cardiocirculatory and pulmonary failure as a consequence of acute pancreatitis. The purpose of this study was to evaluate the role of HAF due to these systemic complications. Experiments were performed in 25 pigs (mean b.wt. 22 +/- 1 kg) under general anesthesia and mechanical ventilation. The animals received 50 ml/kg b.wt. i.p. of either physiologic saline solution (control CO, n = 9) or hemorrhagic ascites fluid (HAF, n = 16). HAF was obtained from 16 pigs with pancreatitis induced by intraductal infusion of bile salt. Eight animals in the HAF group were pretreated with indomethacin (10 mg/kg i.v. INDO/HAF). All animals were followed up for 6 h. Mean arterial pressure, cardiac output, and stroke volume fell significantly in the HAF (-25%, -27%, -27%) and in the INDO/HAF groups (-24%, -20%, -17%) as compared with controls (-6%, -6%, -6%). Also, left ventricular end-diastolic pressure (LVEDP) decreased by 52% and 48% in both HAF recipient groups, whereas LVEDP was unchanged in the control group. Myocardial contractility (Vmax) remained unaltered in all experimental groups. No significant differences in gas exchange and lung dry/wet weight ratio were observed. Lipase and PGI2 of the unpretreated HAF group rised to 203% and 198% in arterial blood at 6 h compared with unaltered levels in the control group. No increase of prostanoid concentrations was detected in the indomethacin-pretreated group, whereas lipase increase by a comparable extent as in the HAF group. We conclude that the early consequences of HAF are mainly characterized by systemic hypotension due to hypovolemia.
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PMID:Hemodynamic effects following intraperitoneal infusion of pancreatic ascites fluid. 141 Aug 1

Extreme maldistribution and immediate establishment of severe cellular injury are typical features of traditional bile salt models of acute pancreatitis; both factors complicate assessment and interpretation of therapeutic benefits in trials of experimental therapy. Even more important, both are indications not of the desired induction of pancreatitis but rather of local injury by barotrauma and noxious chemicals. This study contrasts the severity and regional variability of cellular injury in traditional high-dose bile salt models with that seen in a new preparation employing the combination of intravenous (iv) caerulein (CAE) and intraductal (id) low-dose glycodeoxycholic acid (GDOC). Thirty-six male Sprague-Dawley rats (350-450 g) were induced with (group A) high-dose GDOC id (34 mmol/L), low-dose GDOC id (10 mmol/L) (group B), or low-dose GDOC id combined with caerulein iv for 6 h (group C). The regional distribution of histopathologic injury within the pancreas was assessed in 20 fields/organ by two pathologists unaware of the induction technique used. High-dose GDOC id (group A) resulted in extremely heterogenous distribution of injury for all variables (edema, p = 0.001; acinar necrosis, p = 0.0001; inflammation, p = 0.0001; and hemorrhage p = 0.001). The lesions were confined to the head of the pancreas, which showed large areas of necrosis involving entire lobules, whereas adjacent areas were unaffected. Low-dose GDOC id (group B) was more homogenously distributed, but the injury was mild and regional variability (edema, p = 0.0001; acinar necrosis, p less than 0.04; inflammation, p = 0.0001; and hemorrhage p less than 0.05) was still demonstrable. In contrast, low-dose GDOC id combined with CAE iv (group C) produced moderately severe pancreatitis, which equally affected all areas of the gland. There were no geographical differences in acinar necrosis or inflammation. This feature of the new model provides a desirable prerequisite for accurate and reproducible assessment of histopathology in studies aimed at detecting effects of therapy. We suggest that it replace traditional id bile salt infusion models.
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PMID:Morphometric characteristics and homogeneity of a new model of acute pancreatitis in the rat. 152 49

Between Jan. 19, 1989 and Nov. 23, 1990, 170 patients with symptomatic cholelithiasis were evaluated for possible treatment by extracorporeal shockwave lithotripsy (ESWL). Thirty-one patients were not eligible for treatment, 28 (16%) because of nonvisualization of gallstones by ultrasonography and 3 (2%) because polyps were erroneously diagnosed on ultrasonography. Thirteen (8%) patients failed to comply with the protocol, leaving 126 patients for assessment. At the time of writing, the treatment success rate is 57% at 6 months and 69% at 9 months. Treatment failed in 21 (17%) patients because of unsatisfactory fragmentation in 16 (13%) patients, frequent biliary colic in 3 (2%) patients, acute pancreatitis in 1 (0.8%) patient and severe bile-salt-induced diarrhea in 1 (0.8%) patient. Complications included biliary colic (40 patients), mild diarrhea on bile salts (24 patients), severe diarrhea (1 patient), macroscopic hematuria (4 patients), acute pancreatitis (2 patients) and vagal shock (1 patient). This study demonstrates the effectiveness (87%) of the lithotripter in reducing gallstones to fragments 5 mm in diameter or smaller. However, complete disappearance of these fragments with adjuvant bile-salt therapy may take many months.
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PMID:Extracorporeal shockwave lithotripsy of gallstones: clinical experience with 170 patients. 156 22

Despite the proposal that somatostatin or its stable analogue, octreotide (SMS-201,995), may exert an ameliorating effect on acute pancreatitis, data concerning its beneficial effect in this situation are conflicting. This study examines the effects of octreotide on acute pancreatitis, resulting from the retrograde injection of a bile salt (taurocholate) plus saturating trypsin into the common bile-pancreatic duct of the rat. Octreotide given before the induction of pancreatitis significantly reduced the levels of serum amylase and lipase, ascites amylase concentration, degree of leukocyte infiltration, and focal areas of pancreatic tissue necrosis. In contrast, administration of octreotide as soon as 5 min following induction had no demonstrable ameliorating effects on the pancreatitis. These results indicate that octreotide may have application to prophylaxis of acute pancreatitis in cases where bile salts may play a role in pathogenesis, but may not be beneficial in established acute pancreatitis.
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PMID:A somatostatin analogue is protective against retrograde bile salt-induced pancreatitis in the rat. 171 27

Recently we indicated that pancreatic secretory stimulation with pancreozymin superimposed on chronic alcohol intake increases the tissue necrosis in rat pancreas caused by intraductal bile salt administration, and proposed a new theory of the pathogenesis of acute alcoholic pancreatitis. The purpose of the present work was to study whether secretin and alcohol have a similar damage-expanding coeffect in this experimental model of acute pancreatitis. Though secretin treatment seemed to increase the pancreatic necrosis slightly in both alcoholic animals (four groups, n = 5 in each group) and control animals (four groups, n = 5 in each group), no difference was found in the amount of tissue necrosis between alcohol-treated and control animals after secretin treatment and intraductal taurocholate. The mean percentages of necrosis in pancreatic parenchyma were 21.7, 16.1 and 16.3% in alcoholic groups and 15.9, 19.9 and 17.6% in control groups, when secretin was given 15, 45 and 90 min before sodium taurocholate. When preceding secretin stimulation was not given, the mean percentage of necrosis caused by taurocholate was 13.3% in alcoholic animals and 12.0% in control animals. Taken together with our earlier studies the results suggest that the synergism between chronic alcohol intake and pancreozymin formerly reported is neither due to a different response of alcoholic animals from that of control animals to increased flow of pancreatic juice during taurocholate-induced experimental acute pancreatitis nor caused by malnutrition often associated with chronic alcoholism. These results give indirectly further support to the theory that alcohol-induced alterations in the pancreozymin pathway, particularly, may play a crucial role in the pathogenesis of acute alcoholic pancreatitis.
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PMID:Failure of secretin to increase sodium taurocholate-induced pancreatic necrosis in alcoholic rats. 178 67

Extracorporeal shock wave lithotripsy (ESWL) is successful in fragmenting gallstones, but less than 28 per cent of patients with gallstone disease fulfil the conventional criteria for treatment. However, no data exist to substantiate these selection criteria. In this study, the selection criteria were broadened to include patients with radiolucent stones of any size and number, and radio-opaque stones less than 3 cm in diameter. To date; 108 symptomatic patients with gallstones have received treatment. All patients received up to six outpatient sessions of ESWL (6000 shock waves per session) without sedation or analgesia. The dissolution therapy consisted of combined bile salt and terpene administration. The clearance rates were 9 per cent within 2 months, 21 per cent at 2-4 months, 38 per cent at 4-8 months, 60 per cent at 8-12 months, and 78 per cent at 12-18 months. Of patients with a successful outcome only 19 (18 per cent) would have satisfied traditional selection criteria. There have been no significant complications except in one patient who developed mild acute pancreatitis, which settled on conservative treatment, and two patients who developed acute cholecystitis. This study would suggest that the previously accepted selection criteria underestimate the number of patients suitable for gallstone ESWL and dissolution therapy.
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PMID:Piezoelectric lithotripsy for gallstones: analysis of results in patients with extended selection. 201 62

The effect of pancreatitis on magnetic resonance T1 and T2 relaxation times was evaluated in two different models of acute pancreatitis in the rat. Acute edematous pancreatitis was induced by repetitive intraperitoneal injections of the cholecystokinin-analogue caerulein; acute hemorrhage pancreatitis was induced by retrograde infusion of the bile salt sodium taurocholate into the pancreatic duct. T1 and T2 relaxation times were obtained in vitro from fresh pancreatic specimens at 37 degrees C with a 0.25 resistive spectrometer. In both edematous and hemorrhagic pancreatitis, significant prolongation of T1 and T2 was noted as early as 1.5 hours after the initiation of pancreatitis when compared with normal rat pancreas. Maximal prolongation occurred at 7 hours in the caerulein model with T1 of 966 +/- 46 msec (mean +/- SEM) (normal + 278 +/- 12 msec) and T2 of 75.9 +/- 2.9 msec (normal = 32.8 +/- 3.3 msec), and after 6 hours in the bile salt model with T1 of 798 +/- 40 msec and T2 of 92.5 +/- 3.3 msec. After the time point of maximal prolongation, T1 and T2 gradually decreased toward the normal values. The prolongation of T1 and T2 paralleled each other throughout the time course of pancreatitis in both models. The prolongation of both relaxation times correlated closely with pancreatic weight, water content, and amylase concentration in serum and ascites. The present determination of T1 and T2 relaxation times by in vitro spectrometry suggests that magnetic resonance imaging has the potential for detecting early pathologic changes in acute pancreatitis and thus may be helpful for an early clinical diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental acute pancreatitis. In vitro magnetic resonance characteristics. 244 17

The management of acute pancreatitis has not changed appreciably throughout several decades. Recent evidence has suggested that cholecystokinin (CCK) may play an important role in pancreatic disease. Investigations into the precise role of CCK in acute pancreatitis have been hampered by the lack of a specific CCK receptor antagonist. Using a newly described, highly potent and specific CCK receptor antagonist, L-364,718, the effect of CCK in two models of acute "surgical" pancreatitis was examined: (1) the bile salt ductal perfusion model in the rat and (2) a traumatic model in the guinea pig. At a suboptimal dose for pancreatic enzyme secretion (25 pmol/kg/h), CCK was found to potentiate the severity of the ensuing pancreatitis in both models. Continuous CCK receptor blockade with L-364,718 (25 nmol/kg/h) improved biochemical, morphologic, and survival indexes. This study suggests that physiologic levels of CCK play an important permissive role in the evolution of acute pancreatitis. The use of L-364,718 as an investigative probe or therapeutic tool for acute pancreatitis is worthy of further consideration.
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PMID:Cholecystokinin augmentation of 'surgical' pancreatitis. Benefits of receptor blockade. 246 10


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