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Titolo:
Inhibition of p38 mitogen activate kinase attenuates the severity of pancreatitis-induced adult respiratory distress syndrome
Autore:
Denham, W; Yang, J; Wang, HC; Botchkina, G; Tracey, KJ; Norman, J;
Indirizzi:
Univ S Florida, Dept Surg, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 Florida, Dept Surg, Tampa, FL 33612 USA N Shore Univ Hosp, Picower Inst Med Res, Dept Surg, Manhasset, NY 11030 USA N Shore Univ Hosp Manhasset NY USA 11030 pt Surg, Manhasset, NY 11030 USA
Titolo Testata:
CRITICAL CARE MEDICINE
fascicolo: 7, volume: 28, anno: 2000,
pagine: 2567 - 2572
SICI:
0090-3493(200007)28:7<2567:IOPMAK>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE; LUNG INJURY; CYTOKINE PRODUCTION; INTERLEUKIN-1; EXPRESSION; RAT; ENDOTOXIN; MECHANISM; MEDIATORS;
Keywords:
CNI-1493; rat; ascites; tumor necrosis factor; nitric oxide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Denham, W Univ S Florida, Dept Surg, MDC Box 16,12901 Bruce B Downs Blvd, Tampa, FL 33612 USA Univ S Florida MDC Box 16,12901 Bruce B Downs Blvd Tampa FL USA 33612
Citazione:
W. Denham et al., "Inhibition of p38 mitogen activate kinase attenuates the severity of pancreatitis-induced adult respiratory distress syndrome", CRIT CARE M, 28(7), 2000, pp. 2567-2572

Abstract

Objective: Adult respiratory distress syndrome (ARDS) is responsible for asignificant portion of the morbidity and mortality during severe acute pancreatitis, Because inflammatory mediators such as tumor necrosis factor (TNF)-alpha and nitric oxide (NO) produced within the lungs have been implicated in sepsis-induced ARDS, we aimed to determine the role of these mediators in pancreatitis-induced ARDS using a model whereby ascites from animals with pancreatitis is transferred to otherwise healthy animals resulting in pulmonary injury. Design: Prospective, randomized, controlled trial. Setting: Research laboratory at a university medical school. Subjects: Pathogen-free Sprague-Dawley rats weighing 225-250 g. Interventions: Sterile, endotoxin- and cytokine-free pancreatic ascites tested for interleukin (IL)-1 beta, TNF-alpha, interferon-gamma, and IL-6 wasobtained from rats 18 hrs after the induction of severe, acute pancreatitis. Ascites was subsequently administered intravenously (20 mL/kg) to healthy rats. Sham animals were administered intravenous saline. Healthy animals administered intravenous ascites were randomized to receive a single intraperitoneal injection of the p38 mitogen activated kinase inhibitor CNI-1493 (1 mg/kg) or vehicle. Measurements: Pulmonary injury was assessed at 24 hrs by histology and leukocyte and protein concentrations via bronchoalveolar lavage, Pulmonary TNF-alpha protein was detected by immunohistochemistry. Serum nitrite, as a measure of NO production, was measured utilizing the Griess reaction. Main Results:After the intravenous administration of pancreatic ascites, the number of leukocytes and the protein concentration within the bronchoalveolar fluid were increased and pulmonary histology was worsened consistent with acute lung injury (all p < .001 vs. sham), Each of these variables of pulmonary injury was lessened in animals receiving CNI-1493 and intravenousascites (p < .05 vs. vehicle). Pulmonary TNF-alpha protein and serum nitrites were decreased with the administration of CNI-1493 (p < .005 vs. vehicle). Conclusions: A component of pancreatic ascites other than endotoxin, bacteria, or cytokines (IL-1 beta, TNF, interferon-gamma, or IL-6) is capable ofinducing ARDS in healthy animals, Inhibition of p38 mitogen activated kinase decreases the pulmonary injury through attenuated production of TNF-alpha and NO suggesting a primary role for these mediators in pancreatitis-induced ARDS.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 20:10:56