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

The etiology of acute pancreatitis, apart from alcohol abuse and cholelithiasis may also include a vascular component responsible for pancreatic ischemia. It is now acknowledged that chronic pancreatitis may be a consequence of the acute variant, but it remains unclear what factors influence this sequence of morphological changes. In order to clarify this issue we proposed a model of experimental acute pancreatitis in rats induced by a 30 min reduction of blood flow in inferior splenic artery followed by reperfusion. Rats were sacrificed at 1 h, 12 h, 24 h, and 2, 3, 5, 7, 14, 21, 28 days after cessation of ischemia. We performed histopathological examination of pancreatic tissue and measured pancreatic blood flow, plasma amylase activity and interleukin-1 beta concentration. The present findings indicate that transient pancreatic ischemia leads to the development of acute necro-haemorrhagic pancreatitis. The morphological features of acute inflammation are correlated positively with functional disorders. In some cases the features of chronic pancreatitis may appear transiently after the acute phase, whereas the repair of postinflammatory injury involves the regeneration of acinar cells.
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PMID:Morphological changes and morphological-functional correlations in acute experimental ischemia/reperfusion pancreatitis in rats. 1124 88

Ischemia of the gastrointestinal mucosa is characterized by acidosis in the submucosal layer during the majority of interventions, which necessitates monitoring of tissue pH (pHi) of the abdominal organs during aortocoronary bypass surgery and the immediate postoperative period. The pHi was measured by gastrotonometry with a nasogastral tube (Trip catheter) and Tonocap-TC200 device (Datex Engstrom, Finland); pHi was measured in 17 patients in department of intensive care on days 1 or 2 after cardiosurgical interventions with at least 120-min artificial circulation and in 23 patients during the operation. Surgical treatment consisted in correction of acquired valvular diseases, myocardial revascularization (shunting operations), and combinations of these operations. The first stage of investigation revealed a relationship between decreased pHi level to the acid values and complicated course of the postoperative period. The second stage showed that postoperative complications occurred in 27.2% cases only in patients subjected to long artificial circulation bypass (more than 120 min). The frequency of complications were 2-fold more in the patients with tissue acidosis (pHi < 7.35) during surgery than in patients with normal and alkaline pHi values. The following complications occurred: acute pancreatitis, acute peptic ulcer, acute renal and polyorgan failure. Comparative analysis of pHi and other metabolic markers of arterial blood showed a correlation between these parameters, but pHi was more specific for the diagnosis of tissue ischemia. Hence, a low invasive highly specific method of gaseous gastrotonometry helps evaluate the blood supply to abdominal organs during and after cardiac surgery with artificial circulation and predict postoperative gastrointestinal and grave systemic complications (sepsis, acute renal failure, and polyorgan failure).
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PMID:[Significance of tissue pH in the prognosis of postoperative complications in heart surgery patients]. 1133 11

The objective of this study was to assess the biochemical and histological signs of pancreatic damage development and pancreatic recovery in the course of ischemia-reperfusion induced pancreatitis. Acute pancreatitis was induced in rats by limitation of pancreatic blood flow (PBF) in inferior splenic artery for 30 min using microvascular clips, followed by reperfusion. Rats were sacrificed at the time: 1 h, 12 h, 24 h, and 2, 3, 5, 7, 10, 14, 21 and 28 days after ischemia. PBF was measured using laser Doppler flowmeter. Plasma amylase, interleukin 1beta (IL-1beta) and interleukin 10 (IL-10) concentration, pancreatic DNA synthesis, as well as, morphological features of pancreatic damage were examined. Ischemia with reperfusion caused acute necrotizing pancreatitis followed by pancreatic regeneration. After removal of microvascular clips, PBF was reduced and the maximal fall of PBF was observed 24 h after ischemia, then PBF grew reaching the control value at 28th day. Plasma amylase activity was increased between 12th h and 3rd day with maximum at 24 h after ischemia. Also plasma IL-1beta and IL-10 were elevated with maximal value at the first and second day after ischemia, respectively. DNA synthesis was maximally reduced at the first day (by 70%) and from second day the reversion of this tendency was observed with full restoration of pancreatic DNA synthesis within four weeks. Morphological features of pancreatic tissue showed necrosis, strongly pronounced edema and leukocyte infiltration. Maximal intensity of morphological signs of pancreatic damage was observed between first and second day of reperfusion. During pancreatic regeneration between second and tenth day after ischemia the temporary appearance of chronic pancreatitis-like features such as fibrosis, acinar cell loss, formation of tubular complexes and dilatation of ducts was observed. The regeneration was completed within four weeks after pancreatitis development. We conclude that partial and temporary pancreatic ischemia followed by reperfusion causes acute necrotizing pancreatitis with subsequent regeneration within four weeks. Pancreatic repair after necrotizing pancreatitis is connected with the increase in plasma IL-10 concentration and transitory formation of tubular complexes.
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PMID:Pancreatic damage and regeneration in the course of ischemia-reperfusion induced pancreatitis in rats. 1145 2

Ischemia/reperfusion injury plays an important role in the development of graft pancreatitis and thrombosis after pancreas transplantation. Up to now there are few therapeutic options for this severe complication because very little is known about pancreatic ischemia/reperfusion injury. The same pathomechanisms may also be involved in the induction and determination of the course of acute pancreatitis. We observed the effect of 2 h of warm in situ ischemia on the postischemic tissue oxygenation, histological organ damage, and pancreatic enzymes. Experiments were performed in 21 male Wistar rats. In sham-operated animals without ischemia, the pancreas was not dissected. In the ischemia/reperfusion group a pancreatic tail-segment was carefully separated from the head, and ischemia was induced by clamping the splenic vessels for 2 h, after flushing the pancreatic tail-segment with heparinized saline. Animals treated similarly, but with opening of the clamps some seconds after induction of ischemia, served as controls. The animals were observed for 2 h after reperfusion. Tissue oxygenation was monitored by a PO2-sensitive probe (LICOX, GMS, Kiel, Germany) which was implanted into the pancreatic tissue. Blood samples were taken before, 5 min, 60 min, and 120 min after reperfusion. At the end of the experiment the pancreatic tail was excised for histological examination; biopsies froin the non-ischemic pancreatic head served as intraindividual control to exclude side effects on the nonischemic pancreatic head. In the ischemia/reperfusion group, PO2ti was significantly lower 1 h (18.0+/-1.7 mmHg) and 2 h (16.4+/-1.6 mmHg) after reperfusion compared with baseline conditions (32.8+/-5.2 mmHg) and the control group (1 h 30.6+/-1.9 mmHg, 2 h 32.4+/-2.4 mmHg). Histological injury score and plasma lipase activity were significantly higher in the ischemia/reperfusion group compared with the control group. Thus we describe a new experimental model of complete normothermic in situ ischemia of a pancreatic tail-segment with the possibility of flushing the pancreatic tail-segment and selective local application of drugs to the pancreas.
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PMID:Ischemia/reperfusion-induced pancreatitis in rats: a new model of complete normothermic in situ ischemia of a pancreatic tail-segment. 1146 2

Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures.
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PMID:Acute pancreatic damage associated with convulsive status epilepticus: a report of three cases. 1173 95

Pancreatic microvascular control is a complex physiological process which is incompletely understood. Blood flow in the pancreas is altered by a large number of endogenous and exogenous factors in the context of acute and chronic pancreatitis. The frequency of progression from acute pancreatitis to a chronic form is a controversial question. In acute pancreatitis reductions in blood flow and alterations of microvascular integrity resulting in impaired tissue oxygenation play an important part in the progression and possibly the initiation of the disease. Endothelin and nitric oxide are believed to be two of the most effective vasoactive mediators. The beneficial effect of therapeutic strategies affecting vasoactive mediators is confirmed in experimental studies. Chronic disease is associated with decreased pancreatic blood flow and histological changes in the vasculature in both patients and animal models. Further studies are needed to clarify whether ischemia in chronic pancreatitis is more important in perpetuating the disease or as primary cause of the inflammatory processes.
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PMID:Importance of microcirculatory disturbances in the pathogenesis of pancreatitis. 1175 96

Reported causes of pancreatitis in pregnancy include: gallstone disease, hyperlipidemia, alcohol ingestion, viral, and idiopathic. Few reports associate pancreatitis with pregnancy-induced hypertension. A 35-year-old women with pregnancy-induced hypertension and spontaneous rupture of membranes was admitted for induction of labor. Her postpartum course was complicated by acute renal failure that responded well to treatment with Lasix and Albumin. Subsequently, the patient developed acute pancreatitis and recovered following conservative treatment. It is possible that the pancreatic ischemia due to generalized vasoconstriction of preeclampsia and loop diuretics in the setting of oliguria with renal failure, had a synergistic effect on the pancreas. Therefore, we suggest that in postpartum women with pregnancy-induced hypertension and acute renal failure, diuretics should be cautiously used because they may increase the risk of pancreatitis.
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PMID:Pregnancy-induced hypertension complicated by postpartum renal failure and pancreatitis: a case report. 1201 78

Pancreatic microcirculatory disturbance plays an important role in th e pathogenesis of acute pancreatitis, and it involves a series of changes including vasoconstriction, ischaemia, increased vascular permeability, impairment of nutritive tissue perfusion, ischaemia/reperfusion, leukocyte adherence, hemorrheological changes and impaired lymphatic drainage. Ischaemia possibly acts as an initiating factor of pancreatic microcirculatory injury in acute pancreatitis, or as an aggravating/continuing mechanism. The end-artery feature of the intralobular arterioles suggests that the pancreatic microcirculation is highly susceptible to ischaemia. Various vasoactive mediators, as bradykinin, platelet activating factor, endothelin and nitric oxide participate in the development of microcirculatory failure.
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PMID:Influencing factors of pancreatic microcirculatory impairment in acute panceatitis. 1204 59

Adenosine protects against cellular damage and dysfunction under several adverse conditions including inflammation and ischemia. In this study, we examined the effects of 3-[1-(6,7-diethoxy-2-morpholinoquinazolin-4-yl)piperidin-4-yl]-1,6-dimethyl-2,4(1H,3H)-quinazolinedione hydrochloride (KF24345), an adenosine uptake inhibitor, on experimental acute pancreatitis induced by choline-deficient and ethionine-supplemented diet in mice. KF24345, administered with the diet onset and every 24 h thereafter, prevented hyperamylasemia, acinar cell injury and serum tumor necrosis factor-alpha elevation and ultimately decreased mortality. Therapeutic treatment with KF24345, which started 32 h after the diet onset, also decreased mortality. The beneficial effect of KF24345 on mortality was abolished by the pretreatment with 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM 241385), a selective adenosine A(2A) receptor antagonist. An intravenous injection of KF24345 at 48 h after the diet onset increased plasma adenosine concentrations in mice with acute pancreatitis. These results suggest that KF24345 shows anti-pancreatitis effects via endogenous adenosine and adenosine A(2A) receptors. The adenosine uptake inhibition could be a new therapeutic approach for acute pancreatitis.
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PMID:KF24345, an adenosine uptake inhibitor, ameliorates the severity and mortality of lethal acute pancreatitis via endogenous adenosine in mice. 1240 9

Melatonin, a pineal secretory product, synthesized from l-tryptophan, has received increased attention because of its antioxidative and immunomodulatory properties. It has been detected in the gut and shown to protect the gastric mucosa, and liver from acute damage, but the role of melatonin in the protection of the pancreas against acute inflammation is not clear. The aim of this study was to investigate the effects of melatonin and its precursor, l-tryptophan, on caerulein-induced pancreatitis (CIP) and on ischemia/reperfusion (I/R)-provoked pancreatitis in rats. CIP was induced by subcutaneous infusion of caerulein to the rats (25 microg/kg). I/R was induced by clamping of the inferior splenic artery for 30 min followed by 2 hr of reperfusion. Melatonin (10, 25 or 50 mg/hr) or l-tryptophan (50, 100 or 250 mg/kg) was given as a bolus intraperitoneal (i.p.) injection 30 min prior to the onset of pancreatitis. CIP and I/R were confirmed by histologic examination and manifested by typical pancreatic edema, by an increase of plasma levels of amylase (by 500% in CIP and by 40% in I/R) and the pro-inflammatory tumor necrosis factor alpha (TNFalpha) (by 500%). Lipid peroxidation products such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), were increased several fold in the pancreas CIP and I/R, whereas pancreatic blood flow (PBF) was significantly reduced in these animals. Pretreatment of rats subjected to CIP or to I/R with melatonin (25 or 50 mg/kg i.p.) or l-tryptophan (100 or 250 mg/kg i.p.) significantly reduced pancreatic edema, plasma levels of amylase and TNFalpha and diminished pancreatic MDA + 4-HNE contents, while enhancing PBF, pancreatic integrity and plasma levels of the anti-inflammatory interleukin 10 (IL-10). This was accompanied by a marked and dose-dependent rise of plasma melatonin immunoreactivity. Gene expression of N-acetyl transferase, an enzyme involved in melatonin biosynthesis, was detected in the pancreas of normal rats and was significantly enhanced in the rats with CIP. We conclude that exogenous melatonin, and that produced from l-tryptophan, attenuates pancreatic damage induced by CIP or by I/R and this effect may be attributable to the reduction in lipid peroxidation and TNFalpha release combined with an increase of plasma anti-inflammatory IL-10 in rats with acute pancreatitis.
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PMID:Protective effect of melatonin and its precursor L-tryptophan on acute pancreatitis induced by caerulein overstimulation or ischemia/reperfusion. 1248 71


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