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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the dynamics of pathomorphologic alterations in the development of acute pancreatitis (AP) and the corresponding changes of the patterns of pancreatic enzymes in rats AP was induced by: 1) combination of a pancreatic juice edema and temporary pancreatic ischemia, ii) by intraductal instillation of trypsin, and iii) by trypsin instillation in combination with ischemia. At 4, 8 and 24 h postoperatively the histologic findings and the activities of lipase and alpha-amylase in the pancreas and the serum were analyzed. The histologic sum score of the individual rats did not correlate with their enzymic patterns in pancreas and in serum. In all three models there was a development of parenchymal necrosis independent of the existence of pancreatic fat necrosis. Therefore, it is not probable that fat necrosis represents an obligatory precondition for the initiation of autodigestion.
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PMID:Experimental acute pancreatitis--a quantification of dynamics at enzymic and histomorphologic levels. 281 89

The biochemical characterization of experimental acute pancreatitis was performed by determination of the secretory enzymes lipase and alpha-amylase, of the cytoplasmic ALAT (alanine aminotransferase), of total protein and calcium concentration in serum of rats. The moderate and protracted course of the pathological process in the small animal model presented allowed to study the initial phase from 1-24 h. In the first 4-8 h most massive enzyme release into the intravasal space was observed. The level of enzyme activities was correlating with the severity of assault. One noxa alone (ischemia or juice edema) resulted in a moderate enzyme release (lipase : 2-2.5 fold of control). The action of both noxae caused a drastical increase in enzyme activities in the initial phase lipase : 8-20 fold, ALAT: 7 fold, alpha-Amylase: 2.5 fold). 24 h postoperatively the serum enzyme activities were at distinct pathological level. At this time acute pancreatitis provoked already a decreased serum protein content. A hypocalcemia was not observed.
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PMID:Contribution of pancreatic edema and short-term ischemia to experimental acute pancreatitis in the rat. II. Behaviour of serum parameters. 349 93

Acute pancreatitis was produced in rats by a combination of dyschylic edema and short-term ischemia of the pancreas. The incidence of acute pancreatitis, reflected by peri- and extra-pancreatic fat necrosis, was found to be dependent on the duration of ischemia. Under most conditions there were no significant differences in enzyme activities between the animals with macroscopic signs and those without these. The time course of alpha-amylase and lipase release was investigated within 24 hours postoperatively. Additionally the quantitative correlation was estimated of the enzyme activities released from the pancreatic tissue and the activities determined in rat serum. The data show that the serum enzymes represent only a small and variable portion of the total amount of enzymes effused from the pancreas.
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PMID:Influence of pancreatic edema and short-term ischemia of rat pancreas on lipase- and alpha-amylase-activities in the serum and in the pancreas. 349 5

For investigations of cell injury during pathogenesis of acute pancreatitis antisera to pancreatic acinar cells were used as experimental tool. Within one hour after intraductal injection of antiserum a strong pancreatic edema was developed. Within 24 h this edema receded to a large extent but at this time there were inflammatory cells scattered in the intra- and periductal region. As a sequel of application of antiserum pancreatic enzymes were released. At 24 h after this application serum activities of alpha-amylase and lipase were significantly increased in comparison to the control and reached that level which was found in a model of acute pancreatitis provoked by pancreatic edema plus short-term ischemia.
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PMID:Influence of antisera to pancreatic acinar cells on rat pancreas in situ. 355 41

The influence of a short-term ischemia of the pancreas for the pathogenesis of a hemorrhagic necrotising pancreatitis was investigated in 28 mongrel dogs. Ischemia of the pancreas in 20 minute intervals repeated three times did not leave any macroscopic, histologic or electron microscopic changes and no alterations of the level of the alpha-amylase, the lipase, and the glucose in the serum. An ischemia of 20 minutes' duration by starvation of the celiac artery and the superior mesenteric artery produces a hemorrhagic necrotising pancreatitis under the precondition of a following pancreatic edema by ligature of the pancreatic duct and secretomotoring with secretin and pancreozymin. The necrosis starts histologically in the perilobular adipose and affects the parenchyma later. Whether the lipase is the starting enzyme for the acute pancreatitis or only conditions the early adipose necrosis should be discussed after these findings. Already a fugitive pancreatic edema produces a hemorrhagic necrotising pancreatitis after previous ischemic damage.
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PMID:[Animal experiment studies on the role of ischemia in the pathogenesis of acute pancreatitis]. 633 88

Ischemia as a causative factor for acute pancreatitis has been discussed for decades but has only recently gained wider acceptance. Chronic pancreatitis, however, has rarely been attributed to ischemic injury. While experimental evidence is available for the ischemic pathogenesis of acute pancreatitis, no studies have been reported about pancreatic ischemia as a single cause of chronic pancreatitis. Also, the progression from acute to chronic pancreatitis has been a very controversial issue. To address both questions we have injected polystyrene microspheres of 20-microns diameter into the pancreatic branches of the splenic artery of 36 rats. Thirteen more rats were sham operated and injected with saline. The animals were killed at 1, 2, 3, and 9 weeks after operation and macroscopically and histologically examined, and serum alpha-amylase and weight gain were determined. For the pancreas the following parameters were assessed using a score from 0 (no change) to 4 (severe change): atrophy, hemorrhage, edema, fat necrosis, acinar necrosis, polymorphonuclear infiltration, mononuclear infiltration, interstitial fibrosis, and ductal changes. While no difference between control and experiment was observed for serum alpha-amylase, weight gain, edema, and hemorrhage, persistent differences were evident for the parameters characteristic of chronic pancreatitis, most significantly for interstitial fibrosis, ductal changes, mononuclear infiltration, acinar necrosis, and atrophy. No spontaneous deaths occurred. The severity of the lesions remained stationary after the first week. Our work shows for the first time that pancreatic ischemia by microvascular hypoperfusion can cause histopathologic changes characteristic of chronic pancreatitis and that these changes follow acute necrotizing pancreatitis.
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PMID:Does acute pancreatitis progress to chronic pancreatitis? A microvascular pancreatitis model in the rat. 853 54

We aimed to evaluate early pancreas transplant graft function after histidine-tryptophan-ketoglutarate (HTK) versus University of Wisconsin (UW) perfusion. Prospective randomized multicenter study including 68 pancreas transplantations stratified according to preservation fluid used (27 HTK vs. 41 UW). Primary endpoint was pancreas graft survival at 6 months. Serum alpha-amylase, lipase, C-peptide, HbA1C and exogenous insulin requirement were compared at several time points. Mean pancreas cold ischemia time was 10.8 +/- 3.7 (HTK) vs. 11.8 +/- 3.4 h (UW) (P = 0.247). Simultaneous pancreas-kidney transplantation was performed in 95.6% of the patients, pancreas transplantation alone in 2.9%, and pancreas after kidney transplantation in 1.5%. Six months graft survival was 85.2% (HTK) vs. 90.2% (UW) (P = 0.703). Serum amylase and lipase values did not differ between both the groups during the observation period. C-peptide levels were elevated in both the groups without significant differences at each time point. Higher exogenous insulin requirement early after transplantation in the UW group had resolved at 3 months. Six month patient survival was 96.3% (HTK) vs. 100% (UW) (P = 0.397). With a mean cold ischemia time of 10 h in this study, HTK and UW solutions appear to be equally suitable for perfusion and organ preservation in clinical pancreas transplantation.
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PMID:A prospective randomized multicenter trial comparing histidine-tryptophane-ketoglutarate versus University of Wisconsin perfusion solution in clinical pancreas transplantation. 1895 63

Generalized anxiety disorder (GAD) is the most commonly occurring anxiety disorder and has been related to cardiovascular morbidity such as cardiac ischemia, sudden cardiac death, and myocardial infarction. Both GAD and its cardinal symptom - worry - have been shown to promote muted physiological reactivity in response to laboratory and ecological stressors. Importantly, no study to date has examined the concurrent and relative contributions of trait and state worry within healthy controls, (non-clinical) high trait-worry controls, and GAD participants. The present study examined heart rate (HR), respiratory sinus arrhythmia (RSA), and salivary alpha-amylase (sAA) responses to laboratory stress during and following the experimental induction of worry versus relaxation in healthy controls (n=42), high trait worriers (n=33) and participants with GAD (n=76). All groups exhibited increased HR and decreased RSA in response to the stressor, with no differences by condition. Baseline sAA significantly moderated HR and RSA reactivity, such that higher sAA predicted greater increases in HR and decreases in RSA. There was a significant group by baseline sAA interaction such that in GAD, higher baseline sAA predicted decreased change in sAA during stress, whereas higher baseline sAA predicted greater sAA change in healthy controls. High-worry controls fell non-significantly between these groups. The present study provides additional evidence for the effect of worry on diminished HR stress response and points to possible suppression of adrenergic sympathetic stress responses in GAD.
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PMID:Heart rate and autonomic response to stress after experimental induction of worry versus relaxation in healthy, high-worry, and generalized anxiety disorder individuals. 2338 13