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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that oxygen-derived free radicals play a decisive role in the pathogenesis of acute experimental pancreatitis in a model of edematous pancreatitis. Accordingly, allopurinol, a xanthine oxidase inhibitor, was shown to mitigate the development of nonfatal acute pancreatitis in ex vivo perfusion models using dogs. For further evaluation of allopurinol, its effect was studied in two forms of fatal necrotizing acute experimental pancreatitis: sodium taurocholate-induced pancreatitis in rats and choline-deficient ethionine-supplemented diet-induced pancreatitis in mice. Allopurinol did not affect the mortality rate, pancreatic enzyme elevation in serum and ascites, the enzyme content of the pancreas, or any parameter indicating histopathological damage in the pancreas. Although these experiments did not determine the role oxygen-derived free radicals play in the development of pancreatitis, they show, none the less, the absence of any beneficial therapeutic effect of a xanthine oxidase like allopurinol on the development of the disease once it has begun.
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PMID:Xanthine oxidase inhibitor in acute experimental pancreatitis in rats and mice. 276 73

The role of reactive oxygen metabolites in extrapancreatic organ dysfunction associated with acute hemorrhagic pancreatitis was studied in dogs. Experimental pancreatitis was induced by the intraductal infusion of activated trypsin and taurocholate. Cardiac output, pulmonary and systemic blood pressure, pulmonary wedge pressure, central venous pressure, heart rate, blood gases and serum amylase were measured. Cardiac index, pulmonary and systemic vascular resistance, and the right and left stroke work were calculated. Systemic arterial and venous blood pressure and cardiac index gradually declined over 6 hr, while pulmonary mean blood pressure and pulmonary vascular resistance increased. Pretreatment of pancreatitis with catalase and superoxide dismutase prevented the rise in mean pulmonary blood pressure, moderated the rise in pulmonary vascular resistance, and decreased the rate and extent of the fall in cardiac index. These data suggest that reactive oxygen metabolites may play some role in the extraabdominal organ manifestations of acute pancreatitis.
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PMID:Role of reactive oxygen metabolites in early cardiopulmonary changes of acute hemorrhagic pancreatitis. 279 9

After intravenous blood exposure to low-intensity radiation of Helium-Neon laser patients with haemorrhagic pancreatitis exhibited inhibition of the blood proteolytic activity; enhancement of free-radical oxidation, kallikrein-kinin system activity, blood oxygen transport, correction of endotoxic pancreatogenic syndrome. In addition, the positive shifts were also observed in the immunological status, morphofunctional characteristics of the red blood cells and hemoglobin, hepatic and renal functions. In severe pancreatogenic endotoxicosis the highest response was achieved with combined use of hemosorption and intravenous laser irradiation.
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PMID:[Effect of intravenous laser irradiation of blood on the homeostasis in patients with hemorrhagic pancreatitis]. 281 Dec 43

Whenever the surgeon finds himself face to face with a wound (probably this is the only opportunity for a meeting between physician and pathology which seems to be able to leave the "illness" on one side, almost forgotten, as it were), even when immersed in routine, he can hardly help making a number of considerations of a general nature, to which the sentence above in brackets is not entirely extraneous. In practice, we cannot help asking ourselves an apparently simple, almost banal, question: what exactly is trauma? This triggers off a whole series of secondary queries, such as, for instance, what the relationship is between trauma and classical pathology? In the first place, it should be pointed out that "traumatic" pathology is undoubtedly the only instance of pathology in which, as a rule, at least at the outset, one can justifiably talk about the "isolated" role of what can certainly be regarded as an out-of-body factor. If, then, we consider the specifically morphological and pathophysiological aspects of the period subsequent to the traumatic insult, we find ourselves in an even more embarrassing position: we are faced with irreparably devastated organ and body structures, or with a situation which is already on the way to convalescence. One last alternative is that the traumatic insult is merely a memory, a key finding in the case history, a past reality which to all intent and purposes has ceased to exist, and we are faced with extremely complex clinical pictures which we tend to label as complications. A few examples by way of explanation: shock, adult respiratory distress syndrome (ARDS), stress ulcer, acute post-traumatic cholecystitis, haemorrhagic pancreatitis, and problems caused by resolving the hypovolaemia-ischaemia situation and by implementing reperfusion (oxygen radicals). Trauma favours - and surgeons concerned with organ transplants are well aware of this - the only possibility of death which, perhaps with a grain of excessive optimism, we may even accept as fruitful, in that it occurs without all the destructive deterioration involved in the process of dying. The above consideration probably plays a major role in our attitudes of almost fatalistic resignation towards the youthful victims of trauma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Biomechanico-clinical study of gunshot wounds (general problems--II)]. 304 29

Therapeutic use of the perfluorochemical emulsion, Fluosol DA, in acute pancreatitis was experimentally discussed in view of maintaining the local blood flow and oxygen supply in the pancreas to avoid further aggravation of pancreatitis. Acute pancreatitis was induced by deoxycholate injection into the pancreatic duct in adult mongrel dogs. Fluosol DA or 6% hydroxyethylstarch (HES) solution as control was transfused at 20 ml/kg/hour for the first 3 hours. Fluosol DA and HES solution improved the depressed cardiac output and pancreatic blood flow to normal levels. Compared with HES solution, Fluosol DA administration revealed a prominent increase in oxygen tension in the pancreatic tissue, which had decreased severely from onset of pancreatitis. Fluosol DA administration brought about better preservation of pancreatic mitochondrial functions. Despite no significant differences in blood levels of other pancreatic enzymes between Fluosol DA and HES solution, the sharp decrease in plasma postheparin phospholipase A2 suggested the protection of involved systemic organs including pancreas. Thus, maintaining pancreatic blood flow and increasing the oxygen transport by Fluosol DA administration seemed to play a positive role in inhibiting the progress of pancreatitis, though improvement of survival rate in acute pancreatitis was incomplete by Fluosol DA administration alone.
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PMID:Experimental studies on fluosol DA administration in acute pancreatitis. 317 91

Conscious rats were treated with a supramaximal dose of 5.10(-6)g.kg-1.h-1 of cerulein for periods of 3 and 12 h. In both groups of animals typical features of acute oedematous pancreatitis were proved by biochemical and histologic examinations. The most important finding of our study was the decrease of superoxide dismutase (SOD) activity in pancreatic tissue, accompanied by a slight increase of this scavenger enzyme in serum of rats stimulated with cerulein during 3 h. Parallelly, evident elevation of malondialdehyde (MDA) concentration in pancreatic tissue was noted. After the 12-h infusion of cerulein we were not able to detect any SOD activity in pancreatic tissue, whereas this activity appeared in ascitic fluid of tested animals. Further increase of MDA concentration in pancreatic tissue, in comparison with 3-h pancreatitis, was found. These data suggest that in 3-h and 12-h cerulein-induced pancreatitis the oxygen-derived free radicals mediate the increased lipid peroxidation in pancreatic tissue. We think that the depletion of the scavenger enzyme SOD may be responsible for such a disturbance of lipid metabolism.
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PMID:Oxygen-derived free radicals in cerulein-induced acute pancreatitis. 324 21

Acute pancreatitis is often associated with impaired cardiovascular function. This study examined the systemic cardiovascular effect of acute pancreatitis induced by injection of autologous bile (0.5 ml/kg) into the canine pancreatic duct. After acute pancreatitis was induced, eight dogs were given no resuscitation (group 1, untreated pancreatitis), and lactated Ringer's solution was infused in 11 dogs (group II, treated pancreatitis) to maintain mean arterial pressure and pulmonary wedge pressure at control values. In the untreated pancreatitis group, mean arterial pressure, cardiac output, stroke volume, and stroke work values decreased (mean arterial pressure from 101 +/- 4 to 74 +/- 12 mm Hg, cardiac output from 118 +/- 7 to 56.2 +/- 1.1 ml/min/kg; stroke volume from 0.93 +/- 0.08 to 0.22 +/- 0.07 ml/beat/kg; p less than 0.05), whereas heart rate and peripheral resistance increased (heart rate from 125 +/- 7 to 185 +/- 10 beats/min, peripheral vascular resistance from 3130 +/- 410 to 4436 +/- 610 dynes/sec/cm5; p less than 0.05). Although coronary blood flow, endocardial-epicardial flow ratio, and myocardial oxygen delivery values decreased progressively in group I after induction of pancreatitis, these changes did not achieve statistical significance. All indices of cardiovascular function and coronary blood flow remained unchanged in group II. Neither dP/dt max, the maximal rate of left ventricular pressure increase, nor dP/dt at a developed pressure of 40 mm Hg (an index of myocardial contractility minimally affected by changes in preload and afterload) were depressed by bile-induced acute canine pancreatitis in either group. Our data indicate that the detrimental effects of acute pancreatitis on cardiovascular function are related solely to hypovolemia and reduced cardiac filling and not to humoral or reflex effects induced by the disease.
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PMID:Hemodynamic function in acute pancreatitis. 328 79

Corticosteroids are widely used as therapy for the adult respiratory distress syndrome (ARDS) without proof of efficacy. We conducted a prospective, randomized, double-blind, placebo-controlled trial of methylprednisolone therapy in 99 patients with refractory hypoxemia, diffuse bilateral infiltrates on chest radiography and absence of congestive heart failure documented by pulmonary-artery catheterization. The causes of ARDS included sepsis (27 percent), aspiration pneumonia (18 percent), pancreatitis (4 percent), shock (2 percent), fat emboli (1 percent), and miscellaneous causes or more than one cause (42 percent). Fifty patients received methylprednisolone (30 mg per kilogram of body weight every six hours for 24 hours), and 49 received placebo according to the same schedule. Serial measurements were made of pulmonary shunting, the ratio of partial pressure of arterial oxygen to partial pressure of alveolar oxygen, the chest radiograph severity score, total thoracic compliance, and pulmonary-artery pressure. We observed no statistical differences between groups in these characteristics upon entry or during the five days after entry. Forty-five days after entry there were no differences between the methylprednisolone and placebo groups in mortality (respectively, 30 of 50 [60 percent; 95 percent confidence interval, 46 to 74] and 31 of 49 [63 percent; 95 percent confidence interval, 49 to 77]; P = 0.74) or in the reversal of ARDS (18 of 50 [36 percent] vs. 19 of 49 [39 percent]; P = 0.77). However, the relatively wide confidence intervals in the mortality data make it impossible to exclude a small effect of treatment. Infectious complications were similar in the methylprednisolone group (8 of 50 [16 percent]) and the placebo group (5 of 49 [10 percent]; P = 0.60). Our data suggest that in patients with established ARDS due to sepsis, aspiration, or a mixed cause, high-dose methylprednisolone does not affect outcome.
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PMID:High-dose corticosteroids in patients with the adult respiratory distress syndrome. 331 54

The effect of methylprednisolone on hemodynamics and oxygen transport was investigated in acute hemorrhagic pancreatitis in 13 dogs randomly allocated to a fluid treatment group, a methylprednisolone prophylaxis (MPP) group and a methylprednisolone therapy (MP) group. Methylprednisolone (30 mg/kg) was given as a bolus dose, starting 30 min before induction of pancreatitis in the MPP group and 30 min after induction in the MP group. Acute hemorrhagic pancreatitis was induced with a mixture of trypsin and sodium taurocholate, and hemodynamics and blood gases were monitored for 4.5 hours. MPP improved cardiac output significantly and prevented the initial increase in the arteriovenous oxygen content difference. In the MP group there were no significant differences from the control group in hemodynamics or oxygen transport. Prophylactically administered methylprednisolone thus partially attenuated the hemodynamic changes caused by acute hemorrhagic pancreatitis. It seemed especially to improve cardiac performance, assessed from changes in cardiac output.
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PMID:Methylprednisolone in acute canine hemorrhagic pancreatitis. 335 81

Carbon-mineral sorbents successfully combine a high mechanical resistance of the mineral matrix and a high activity of carbons. It is possible to prepare a mineral matrix of the wanted structure and use it as the basis for producing carbon-mineral sorbents. SUMS-1 and SUMS-2 are the sorbents of mild action. In other words, they cause no thrombosis, they do not absorb oxygen and protein from blood, and they have almost no destructive effect on the blood cells. The sorbents are highly effective in adsorbing microorganisms and their toxins. Treatment of patients with different diseases (sepsis, meningitis, bronchial asthma, tuberculosis, pneumonia, thyrotoxicosis, pancreatitis, liver coma, different types of poisoning) with the SUMS-1 and SUMS-2 has given satisfactory results.
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PMID:Physicochemical properties and applications of carbon-mineral sorbents. 345 27


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