Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatitis was induced in 11 miniature pigs by infusing a bile salt-trypsin solution into the pancreatic duct. Seven animals served as sham-operated controls. Serum ionized calcium, total calcium, albumin, total protein, inorganic phosphorus, urea nitrogen, magnesium, insulin, glucagon, and hematocrit were determined every six to 12 h over a period of one week in both test and control animals. We observed significant decreases in ionized and total calcium, modest decreases in albumin, and significant increases in the inorganic phosphorus, urea nitrogen, and hematocrit in the pancreatitic pigs. The latter two findings were consistent with early acute hypovolemia. Glucagon and insulin appeared to play no role in the hypocalcemia. Glucagon concentrations increased to the same degree in both test and control animals, probably as a result of the stress of being handled and operated on. The highest concentrations of inorganic phosphorus and the lowest concentrations of both ionized and total calcium were seen 18 h after the induction of pancreatitis in the test animals. These findings suggest that parathyrin (parathormone) was not being secreted in adequate amounts, or that the target organs were unresponsive to parathyrin.
 ...
PMID:Biochemical changes in a porcine model of acute pancreatitis. 65 76

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.
 ...
PMID:Glucagon treatment of experimental acute pancreatitis. 123 17

Acute haemorrhagic pancreatitis was induced in greyhound dogs by a bile salt/trypsin injection into the main pancreatic duct. Prostaglandin-like activity in the pancreatic venous blood, right atrial blood, and arterial blood was measured by bioassay. Activity rose significantly in the pancreatic venous blood of test dogs but not in controls. Chromatographic analysis of the peritoneal exudate from the dogs with pancreatitis showed high levels of prostaglandin E-like material (mean 43 ng/ml prostaglandin E2 equivalents). It seems likely that prostaglandins contribute to the induced pancreatitis.
 ...
PMID:Prostaglandin release in canine acute haemorrhagic pancreatitis. 126 76

To study the degree of protease activation at reperfusion of a pancreatic allograft after cold storage for 24 hr, 18 porcine whole-organ pancreaticoduodenal allograft transplantations were performed. Twelve grafts were flushed with and stored in Perfadex. In six of these, a hyperosmotic salt solution was injected into the graft aorta at reperfusion. Six grafts were flushed and stored in UW solution. Eleven of twelve grafts in the Perfadex groups were functioning on the first postoperative day, compared with one of six in the UW solution group. There was a significantly more pronounced protease activation among grafts stored in UW solution than in the other groups, with a subsequent breakthrough of the local protease protection barrier made up of protease inhibitors. In surviving pigs (n = 14), biochemical signs of protease activation evolved in plasma, including formation of trypsin-protease inhibitor complexes, a decline in C3 and kininogen levels, and a decline in functionally active alpha 2-macroglobulin, functionally active antithrombin III, and plasma kallikrein inhibitory activity. These biochemical signs of pancreatitis correlated with a deteriorated graft function on the second postoperative day, indicating that graft tissue damage occurred due to protease activation.
 ...
PMID:Protease activation following reperfusion of porcine pancreatic allografts. 127 75

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.
 ...
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.
 ...
PMID:Morphometric characteristics and homogeneity of a new model of acute pancreatitis in the rat. 152 49

Acute necrotizing pancreatitis induced by infusion of bile salt into the pancreatic duct in rats is consistently associated with acute lung injury similar to the adult respiratory distress syndrome. The role of platelet-activating factor (PAF) in this pancreatitis-associated remote organ failure (lung injury) was investigated. Pulmonary tissue levels of PAF were increased gradually and reached a level of 1345 +/- 455 pg/g (6 times the control level) at 12 hours after induction of pancreatitis, whereas pancreatic PAF levels were undetectable and blood PAF remained unchanged. This local pulmonary PAF accumulation occurred at approximately the same time as the progression of lung injury. Pulmonary responses detected (i.e., eicosanoid production, leukocytic infiltration, Evan's blue extravasation, beta-glucuronidase release) were attenuated to varying degrees by treatment of rats in which pancreatitis was initiated with the PAF receptor antagonists (WEB2170 and BN52021). Rat lung lavages were examined after a 12-hour course of pancreatitis and no changes in PAF concentration, surfactant content, and phospholipase A2 (PLA2) activity were noted. Intravenous administration of PLA2 promoted pulmonary PAF production in experimental rats with pancreatitis but not in normal rats. This observation indicates that PLA2, which was determined to be elevated in plasma during pancreatitis, may be responsible for the accumulation of PAF in the lung. In conclusion, pancreatitis-associated lung injury appears to result from an endogenous inflammatory response in which PAF may play an important role.
 ...
PMID:Role of platelet-activating factor in pancreatitis-associated acute lung injury in the rat. 156 55

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.
 ...
PMID:A somatostatin analogue is protective against retrograde bile salt-induced pancreatitis in the rat. 171 27

Non-insulin-dependent (type II) diabetes mellitus is an inherited metabolic disorder characterized by hyperglycemia with resistance to ketosis. The onset is usually after age 40 years. Patients are variably symptomatic and frequently obese, hyperlipidemic and hypertensive. Clinical, pathological and biochemical evidence suggests that the disease is caused by a combined defect of insulin secretion and insulin resistance. Goals in the treatment of hyperglycemia, dyslipidemia and hypertension should be appropriate to the patient's age, the status of diabetic complications and the safety of the regimen. Nonpharmacologic management includes meal planning to achieve a suitable weight, such that carbohydrates supply 50% to 60% of the daily energy intake, with limitation of saturated fats, cholesterol and salt when indicated, and physical activity appropriate to the patient's age and cardiovascular status. Follow-up should include regular visits with the physician, access to diabetes education, self-monitoring of the blood or urine glucose level and laboratory-based measurement of the plasma levels of glucose and glycated hemoglobin. If unacceptably high plasma glucose levels (e.g., 8 mmol/L or more before meals) persist the use of orally given hypoglycemic agents (a sulfonylurea agent or metformin or both) is indicated. Temporary insulin therapy may be needed during intercurrent illness, surgery or pregnancy. Long-term insulin therapy is recommended in patients with continuing symptoms or hyperglycemia despite treatment with diet modification and orally given hypoglycemic agents. The risk of pancreatitis may be reduced by treating severe hypertriglyceridemia (fasting serum level greater than 10 mmol/L) and atherosclerotic disease through dietary and, if necessary, pharmacologic management of dyslipidemia. Antihypertensive agents are available that have fewer adverse metabolic effects than thiazides and beta-adrenergic receptor blockers. New drugs are being developed that will enhance effective insulin secretion and action and inhibit the progress of complications.
 ...
PMID:Non-insulin-dependent (type II) diabetes mellitus. 174 94

The property of the pancreatic ductal system that restricts free ionic diffusion has been termed the "pancreatic duct mucosal barrier," damage to which may be important in the pathogenesis of acute gallstone pancreatitis. The bile-pancreatic duct of the rat (BPD) was perfused in situ with a standard ionic solution. The normal duct was permeable to both chloride and bicarbonate ions, and flux (JCl-, JHCO3-) appeared to occur by passive ionic diffusion. Measurement of absolute ionic flux and transductal potential difference (PD) gave control values of JCl-, +0.92 +/- 0.15 mumol/cm/hr; JHCO3-, -1.71 +/- 0.12 mumol/cm/hr; PD -2.3 +/- 0.20 mV. The preparation was stable over the experimental period, and the results obtained were reproducible between animals. Glycodeoxycholate compromised the integrity of the BPD with an increase in ionic flux and a reduction in PD with corresponding alterations in mucosal ultrastructure. Increasing concentrations of bile salt produced more severe damage to the BPD. The BPD of the rat is therefore analogous to the pancreatic duct of the cat in possessing a mucosal barrier, and the barrier is damaged by bile salts. This preparation may be useful for studying pancreatic duct integrity, a concept of importance in the pathogenesis of acute gallstone pancreatitis.
 ...
PMID:Ionic flux and mucosal ultrastructure in the rat bile-pancreatic duct. Effect of bile salt perfusion on duct integrity. 244 Jun 46


1 2 3 4 5 6 Next >>