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Kimberly S Kirkwood - One of the best experts on this subject based on the ideXlab platform.
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substance p is a determinant of lethality in diet induced Hemorrhagic Pancreatitis in mice
Surgery, 2000Co-Authors: Eileen F Grady, Shandra K Yoshimi, Todd E Drasin, Matthew M Hutter, Nigel W Bunnett, Kimberly S KirkwoodAbstract:Abstract Background: The neuropeptide substance P (SP) induces plasma extravasation and neutrophil infiltration by activating the neurokinin 1-receptor (NK1-R). SP-induced neurogenic inflammation is terminated by the cell surface enzyme neutral endopeptidase (NEP), which degrades SP. We determined whether genetic deletion of the NK1-R reduces mortality and, conversely, whether genetic deletion of NEP increases mortality in a lethal model of Hemorrhagic Pancreatitis. Methods: Necrotizing Pancreatitis was induced by feeding mice a diet deficient in choline and supplemented with ethionine. We determined the length of survival, the severity of Pancreatitis (by measuring the neutrophil enzyme myeloperoxidase [MPO] and by histologic evaluation), and the severity of Pancreatitis-associated lung injury (lung MPO and histology) in NK1-R (+/+)/(-/-) and NEP (+/+)/(-/-) mice. Results: Genetic deletion of the NK1-R significantly improved survival (100% vs 8% at 120 hours, P P Conclusions: Substance P is an important determinant of lethality in this model of necrotizing Pancreatitis. Defects in NEP expression could lead to uncontrolled inflammation. (Surgery 2000;128:232-9.)
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Substance P is a determinant of lethality in diet-induced Hemorrhagic Pancreatitis in mice * **
Surgery, 2000Co-Authors: Eileen F Grady, Shandra K Yoshimi, Todd E Drasin, Matthew M Hutter, Nigel W Bunnett, Kimberly S KirkwoodAbstract:Abstract Background: The neuropeptide substance P (SP) induces plasma extravasation and neutrophil infiltration by activating the neurokinin 1-receptor (NK1-R). SP-induced neurogenic inflammation is terminated by the cell surface enzyme neutral endopeptidase (NEP), which degrades SP. We determined whether genetic deletion of the NK1-R reduces mortality and, conversely, whether genetic deletion of NEP increases mortality in a lethal model of Hemorrhagic Pancreatitis. Methods: Necrotizing Pancreatitis was induced by feeding mice a diet deficient in choline and supplemented with ethionine. We determined the length of survival, the severity of Pancreatitis (by measuring the neutrophil enzyme myeloperoxidase [MPO] and by histologic evaluation), and the severity of Pancreatitis-associated lung injury (lung MPO and histology) in NK1-R (+/+)/(-/-) and NEP (+/+)/(-/-) mice. Results: Genetic deletion of the NK1-R significantly improved survival (100% vs 8% at 120 hours, P P Conclusions: Substance P is an important determinant of lethality in this model of necrotizing Pancreatitis. Defects in NEP expression could lead to uncontrolled inflammation. (Surgery 2000;128:232-9.)
Timo J Nevalainen - One of the best experts on this subject based on the ideXlab platform.
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phospholipase a2 in sodium taurocholate induced experimental Hemorrhagic Pancreatitis in the rat
Journal of Surgical Research, 1995Co-Authors: Antti J Hietaranta, Heikki Peuravuori, Timo J NevalainenAbstract: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 taurocholate. The contribution of pancreas to the CA-PLA2 in plasma was studied by removing pancreatic PLA2 by absorbing plasma samples with a polyclonal antibody raised in a rabbit against rat pancreatic PLA2. Sodium taurocholate injected into the pancreatic duct produced Hemorrhagic Pancreatitis with necrosis and inflammatory cell invasion within 8 hr. Saline injection caused edematous Pancreatitis, but sham operation did not alter pancreatic morphology from normal. The concentration of pan-PLA2 increased rapidly in plasma in all animals, but significantly more in sodium taurocholate-injected animals than in saline-injected or sham-operated animals. The level of CA-PLA2 in plasma increased in sodium taurocholate-injected animals only. There was no correlation between pan-PLA2 and CA-PLA2 values in plasma in sodium taurocholate-injected animals. The CA-PLA2 was marginally increased in pancreatic tissue of sodium taurocholate-injected animals compared to that of saline-injected and sham-operated animals at 8 hr. Treatment by the anti-pan-PLA2 antibody effectively removed pan-PLA2 from plasma and peritoneal fluid samples in sodium taurocholate-injected animals. The level of CA-PLA2 in plasma was similar before and after antibody treatment. It was concluded that the concentrations of pancreatic PLA2 and the catalytic activity of PLA2 increase in rat plasma during experimental Hemorrhagic acute Pancreatitis. The catalytically active PLA2 in plasma is derived from a nonpancreatic source(s).
Eileen F Grady - One of the best experts on this subject based on the ideXlab platform.
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substance p is a determinant of lethality in diet induced Hemorrhagic Pancreatitis in mice
Surgery, 2000Co-Authors: Eileen F Grady, Shandra K Yoshimi, Todd E Drasin, Matthew M Hutter, Nigel W Bunnett, Kimberly S KirkwoodAbstract:Abstract Background: The neuropeptide substance P (SP) induces plasma extravasation and neutrophil infiltration by activating the neurokinin 1-receptor (NK1-R). SP-induced neurogenic inflammation is terminated by the cell surface enzyme neutral endopeptidase (NEP), which degrades SP. We determined whether genetic deletion of the NK1-R reduces mortality and, conversely, whether genetic deletion of NEP increases mortality in a lethal model of Hemorrhagic Pancreatitis. Methods: Necrotizing Pancreatitis was induced by feeding mice a diet deficient in choline and supplemented with ethionine. We determined the length of survival, the severity of Pancreatitis (by measuring the neutrophil enzyme myeloperoxidase [MPO] and by histologic evaluation), and the severity of Pancreatitis-associated lung injury (lung MPO and histology) in NK1-R (+/+)/(-/-) and NEP (+/+)/(-/-) mice. Results: Genetic deletion of the NK1-R significantly improved survival (100% vs 8% at 120 hours, P P Conclusions: Substance P is an important determinant of lethality in this model of necrotizing Pancreatitis. Defects in NEP expression could lead to uncontrolled inflammation. (Surgery 2000;128:232-9.)
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Substance P is a determinant of lethality in diet-induced Hemorrhagic Pancreatitis in mice * **
Surgery, 2000Co-Authors: Eileen F Grady, Shandra K Yoshimi, Todd E Drasin, Matthew M Hutter, Nigel W Bunnett, Kimberly S KirkwoodAbstract:Abstract Background: The neuropeptide substance P (SP) induces plasma extravasation and neutrophil infiltration by activating the neurokinin 1-receptor (NK1-R). SP-induced neurogenic inflammation is terminated by the cell surface enzyme neutral endopeptidase (NEP), which degrades SP. We determined whether genetic deletion of the NK1-R reduces mortality and, conversely, whether genetic deletion of NEP increases mortality in a lethal model of Hemorrhagic Pancreatitis. Methods: Necrotizing Pancreatitis was induced by feeding mice a diet deficient in choline and supplemented with ethionine. We determined the length of survival, the severity of Pancreatitis (by measuring the neutrophil enzyme myeloperoxidase [MPO] and by histologic evaluation), and the severity of Pancreatitis-associated lung injury (lung MPO and histology) in NK1-R (+/+)/(-/-) and NEP (+/+)/(-/-) mice. Results: Genetic deletion of the NK1-R significantly improved survival (100% vs 8% at 120 hours, P P Conclusions: Substance P is an important determinant of lethality in this model of necrotizing Pancreatitis. Defects in NEP expression could lead to uncontrolled inflammation. (Surgery 2000;128:232-9.)
Howard A. Reber - One of the best experts on this subject based on the ideXlab platform.
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The effect of dopamine in a model of biliary acute Hemorrhagic Pancreatitis
Pancreas, 1991Co-Authors: Nariman D. Karanjia, A. L. Widdison, Frank J. Lutrin, Howard A. ReberAbstract:Perfusion of the main pancreatic duct in cats with a dilute solution of bile salts increases ductal permeability. Subsequent perfusion of a permeable duct with activated pancreatic enzymes results in acute edematous Pancreatitis. Simultaneous infusion of 16-16 dimethyl-PgE2 converts edematous Pancreatitis to acute Hemorrhagic Pancreatitis (AHP). AHP may be associated with a reduction in pancreatic blood flow; it is certainly associated with increases in microvascular permeability. Low dose dopamine is a splanchnic vasodilator and may also reduce pancreatic microvascular permeability through beta agonist effects. In these studies, we investigated the effect of dopamine in an established feline model of biliary AHP. We also studied its effect on blood flow in both normal pancreas and after induction of AHP. We found that dopamine significantly reduced the degree of pancreatic inflammation, even when administered up to 12 h after onset of biliary AHP. However, the drug had no significant effect on blood flow either in normal pancreas or in the gland affected by Hemorrhagic Pancreatitis. We concluded that the effect of dopamine was most likely due to its ability to reduce pancreatic microvascular permeability.
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low dose dopamine protects against Hemorrhagic Pancreatitis in cats
Journal of Surgical Research, 1990Co-Authors: Nariman D. Karanjia, Frank J. Lutrin, Yibin Chang, Howard A. ReberAbstract:Abstract Acute Hemorrhagic Pancreatitis (HP) is probably associated with decreased blood flow in its early phases, as well as with an increase in microvascular permeability. Dopamine (DOP; 5 μg/kg-min) is a splanchnic vasodilator, and also has β-adrenergic effects that can prevent increases in microvascular permeability. We hypothesized that low dose dopamine might have beneficial effects on both blood flow and microvascular permeability, thus ameliorating the severity of the disease. We studied its actions in an animal model of HP. In anesthetized cats, intragastric ethanol (20 ml/40% solution) rendered the main pancreatic duct permeable to pancreatic enzymes. Then the duct was perfused from tail to head with 0.5 ml of activated pancreatic enzymes for 1 hr. To create HP, 16,16-dimethyl prostaglandin E2 (2 μg/kg-hr, iv) was given for 2 hr to increase blood flow and microvascular permeability. Seven of eight cats developed HP in 24 hr. Control cats received no additional drugs. Two experimental groups received DOP (6 hr infusion) begun either (1) at the onset of enzyme perfusion or (2) 12 hr later. Each pancreas was examined after 24 hr and graded (1–4) histologically for edema, hemorrhage, polymorphonuclear cell infiltrate, and architectural loss. An inflammatory score (IS) from 0 to 16 was thus created (higher scores = greater damage). The results showed an IS of 10.9 ± 1.8 for the controls, 3.3 ± 0.5 for the immediate treatment group, and 7.2 ± 1.8 for the delayed treatment group. Both treated groups had a significantly better IS (t tests, P
Kou Kaneko - One of the best experts on this subject based on the ideXlab platform.
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acute fatt liver of pregnanc with h perlipidemia acute Hemorrhagic Pancreatitis and disseminated intravascular coagulation
Asia-Oceania journal of obstetrics and gynaecology, 2010Co-Authors: Hisanori Minakami, K Kimura, Takashi Kanazawa, Taro Tamada, Kou KanekoAbstract:An autops- case of a 32-ear old nulliparous woman who died of acute fatt- liver of pregnanc- (AFLP) associated with h-perlipidemia, acute Hemorrhagic Pancreatitis and disseminated intravascular coagulation (DIC) is reported. Although acute Pancreatitis has been reported as one of the major complications of AFLP, their interrelationships are poorl- understood because of the rarit- and the fulminating nature of this disease. H-perlipidemia has been interpreted as the etiological factor in acute Pancreatitis. It is also known that an increase in circulating lipids occurs during pregnanc- ph-siologicall-. AFLP presents itself onl- in the last trimester of pregnanc-. The intention of the following report is to document a case of AFLP with evidence of supra-ph-siologic h-perlipidemia and to discuss the pathogenesis of AFLP and acute Pancreatitis.
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Acute Fatt‐ Liver of Pregnanc‐ with H‐perlipidemia, Acute Hemorrhagic Pancreatitis and Disseminated Intravascular Coagulation
Asia-Oceania journal of obstetrics and gynaecology, 2010Co-Authors: Hisanori Minakami, K Kimura, Takashi Kanazawa, Taro Tamada, Kou KanekoAbstract:An autops- case of a 32-ear old nulliparous woman who died of acute fatt- liver of pregnanc- (AFLP) associated with h-perlipidemia, acute Hemorrhagic Pancreatitis and disseminated intravascular coagulation (DIC) is reported. Although acute Pancreatitis has been reported as one of the major complications of AFLP, their interrelationships are poorl- understood because of the rarit- and the fulminating nature of this disease. H-perlipidemia has been interpreted as the etiological factor in acute Pancreatitis. It is also known that an increase in circulating lipids occurs during pregnanc- ph-siologicall-. AFLP presents itself onl- in the last trimester of pregnanc-. The intention of the following report is to document a case of AFLP with evidence of supra-ph-siologic h-perlipidemia and to discuss the pathogenesis of AFLP and acute Pancreatitis.