phospholipase/hemorrhage

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Experimental pancreatitis in the rat. The role of phospholipase A in sodium taurocholate-induced acute haemorrhagic pancreatitis.

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Acute haemorrhagic pancreatitis was induced in rats by injecting 0.2 ml of 5% (92.9 mmol/l) aqueous solution of sodium taurocholate into the common biliopancreatic duct. Lysolecithin was separated from the pancreatic homogenate by thin-layer chromatography and quantified by phosphorus determination.

Evidence for the role of phosphatidylcholine-specific phospholipase in experimental subarachnoid hemorrhage in rats.

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Neuron apoptosis and inflammatory responses contribute to subarachnoid hemorrhage (SAH)-induced early brain injury (EBI), which is the main aspect that affects patients' outcome. Previous research has demonstrated that phosphatidylcholine-specific phospholipase C (PC-PLC) plays critical roles in

Group VIB Ca(2+)-independent phospholipase A(2γ) is associated with acute lung injury following trauma and hemorrhagic shock.

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BACKGROUND Gut-derived mediators are carried via mesenteric lymph duct into systemic circulation after trauma/hemorrhagic shock (T/HS), thus leading to acute lung injury (ALI)/multiple-organ dysfunction syndrome. Phospholipase A2 (PLA(2)) is a key enzyme for the production of lipid mediators in

Is Admission Lipoprotein-Associated Phospholipase A2 a Novel Predictor of Vasospasm and Outcome in Patients With Aneurysmal Subarachnoid Hemorrhage?

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The relationships between lipoprotein-associated phospholipase A2 (Lp-PLA2) level, vasospasm, and clinical outcome of patients with aneurysmal subarachnoid hemorrhage (aSAH) are still unclear.To identify the associations between admission Lp-PLA2 and

Analysis of phospholipase C gene in patients with subarachnoid hemorrhage due to ruptured intracranial saccular aneurysm.

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This study is designed to determine whether patients with aneurysmal subarachnoid hemorrhage have mutations in the phospholipase C-delta 1 (PLC-delta 1) gene, which was identified as a gene responsible for hypertension in spontaneously hypertensive rats. Seventy-two cases (31 male and 41 female)

Post-hemorrhagic shock mesenteric lymph lipids prime neutrophils for enhanced cytotoxicity via phospholipase A2.

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Hemorrhagic shock induced mesenteric hypoperfusion has long been implicated as a key event in the pathogenesis of the adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF). Previous work links post-hemorrhagic shock mesenteric lymph (PHSML) lipids and neutrophil (PMN) priming

Neutralizing properties of Musa paradisiaca L. (Musaceae) juice on phospholipase A2, myotoxic, hemorrhagic and lethal activities of crotalidae venoms.

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The use of plants as medicine has been referred to since ancient peoples, perhaps as early as Neanderthal man. Plants are a source of many biologically active products and nowadays they are of great interest to the pharmaceutical industry. The study of how people of different culture use plants in

Calcium and phospholipase A2 appear to be involved in the pathogenesis of hemorrhagic shock-induced mucosal injury and bacterial translocation.

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OBJECTIVE The mechanism by which hemorrhagic shock injures the gut and leads to the translocation of bacteria remains incompletely determined. Since increased free cellular calcium levels and phospholipase A2 activity can lead to cellular injury and both have been documented in certain shock states,

Phospholipase C activity in cerebrospinal fluid following subarachnoid hemorrhage related to brain damage.

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Phosphoinositide-specific phospholipase C (PLC) activities were measured in CSF from patients after subarachnoid hemorrhage (SAH). Their PLC activities were significantly higher than those in control CSF. Moreover, there was an obvious correlation between the PLC activity in CSF collected on day 3

Defective signal transduction induced by thromboxane A2 in a patient with a mild bleeding disorder: impaired phospholipase C activation despite normal phospholipase A2 activation.

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A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A2 (TXA2) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in shape change, aggregation, and release reaction in response to synthetic TXA2 mimetic (STA2).

The role of phospholipase A2 in the pathogenesis of respiratory damage in hemorrhagic necrotizing pancreatitis--assessment of a new experimental model.

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The new experimental model has been set as a standard with the purpose to explore and analyze the role of phospholipase A2 in predicting the severity of acute pancreatitis with specific interest for the onset of hemorrhagic necrotizing pancreatitis and pleuropulmonary complications. The experiments

Phospholipase A2 in sodium taurocholate-induced experimental hemorrhagic pancreatitis in the rat.

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We investigated the concentration of immunoreactive pancreatic phospholipase A2 (pan-PLA2) and the catalytic activity of phospholipase A2 (CA-PLA2) in plasma, peritoneal fluid, and pancreas of rats in which acute hemorrhagic pancreatitis was induced by an intraductal injection of sodium

Can admission lipoprotein-associated phospholipase A2 predict the symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage?

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Background: Inflammation has been believed to be related to the development of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (aSAH). A potential biomarker for vascular inflammation that is well recognized is the

Assessment of lipoprotein-associated phospholipase A2 level and its changes in the early stages as predictors of delayed cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage.

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OBJECTIVE:The relationship between lipoprotein-associated phospholipase A2 (Lp-PLA2) and various cardiovascular and cerebrovascular diseases is inconsistent. However, the connection between Lp-PLA2 level and delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) remains

Phospholipase A2 in serum and ascitic exudate in experimental acute haemorrhagic pancreatitis in pigs.

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We have developed a model of experimental haemorrhagic pancreatitis in pigs with a 100% mortality within 24 h without treatment. In this model we have studied the production of peritioneal exudate and compared the concentrations of amylase, lipase and phospholipase A2 in the ascitic exudate and

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