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001-es BibID:	BIBFORM028387
Első szerző:	Kirov, Mikhail Y.
Cím:	Aerosolized linear polyethylenimine-nitric oxide/nucleophile adduct attenuates endotoxin-induced lung injury in sheep / Mikhail Y. Kirov, Oleg V. Evgenov, Vladimir N. Kuklin, László Virág, Pál Pacher, Garry J. Southan, Andrew L. Salzman, Csaba Szabó, Lars J. Bjertnaes
Dátum:	2002
ISSN:	1073-449X
Megjegyzések:	Pulmonary hypertension and edema are mainstays of acute lung injury (ALI). We synthesized linear polyethylenimine-nitric oxide/nucleophile adduct (DS-1), a water-soluble nitric oxide donor, and demonstrated that it is a potent relaxant of precontracted rat aortic rings without inducing desensitization. Moreover, DS-1 does not suppress the viability of human pulmonary epithelial cells in vitro. We also tested whether DS-1 counteracts ALI in endotoxemic sheep. Animals were instrumented for a chronic study. In 16 awake, spontaneously breathing sheep, Escherichia coli endotoxin (10 ng/kg/minute) was infused for 8 hours. From 2 hours of endotoxemia, sheep received either nebulized DS-1 (1 mg/kg/hour) or isotonic saline. DS-1 reduced endotoxin-induced rises in pulmonary arterial and microwedge pressures and vascular resistance index by 40-70%. In parallel, DS-1 decreased the accumulation of extravascular lung water by 60-70% and reduced the increment in right ventricle stroke work index and the falls in right ventricle ejection fraction, stroke volume, and left ventricle stroke work indices. Furthermore, DS-1 reduced venous admixture and improved arterial oxygen saturation. In four healthy animals, DS-1 alone slightly increased arterial oxygenation but had no other effects. Thus, aerosolized DS-1 attenuates endotoxin-induced ALI in sheep by reducing pulmonary hypertension and edema and improving myocardial function and gas exchange.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban acute lung injury pulmonary circulation extravascular lung water nitric oxide donor endotoxin külföldön készült közlemény
Megjelenés:	American Journal Of Respiratory And Critical Care Medicine 166 : 11 (2002), p. 1436-1442. -
További szerzők:	Evgenov, Oleg V. Kuklin, Vladimir N. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Pacher Pál Southan, Garry J. Salzman, Andrew L. Szabó Csaba (1967-) (orvos) Bjertnaes, Lars J.
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001-es BibID:	BIBFORM028378
Első szerző:	Liaudet, Lucas
Cím:	Activation of poly(ADP-Ribose) polymerase-1 is a central mechanism of lipopolysaccharide-induced acute lung inflammation / Lucas Liaudet, Pál Pacher, Jon G. Mabley, László Virág, Francisco G. Soriano, György Haskó, Csaba Szabó
Dátum:	2002
ISSN:	1073-449X
Megjegyzések:	Recent studies demonstrated that activation of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1) by oxidant-mediated DNA damage is an important pathway of tissue injury in conditions associated with oxidative stress. Using a dual approach of PARP-1 suppression, by genetic deletion or pharmacological inhibition with the phenanthridinone PARP inhibitor PJ-34, we now demonstrate an essential role of PARP-1 in the development of pulmonary inflammation induced by lipopolysaccharide (LPS). PARP-1+/+ and PARP-1-/- mice received an intratracheal instillation of LPS (50 microg), followed after 24 h by bronchoalveolar lavage to measure the cytokines TNF-alpha, IL-1beta, and IL-6, the chemokines MIP-1alpha and MIP-2, leukocyte counts and myeloperoxidase activity (neutrophil accumulation), protein content (high permeability edema), and nitrite/ nitrate (nitric oxide production). Malondialdehyde (an index of lipid peroxidation) was measured in lung tissue. Similar experiments were conducted in BALB/c mice treated with PJ-34 or vehicle. The absence of functional PARP-1 reduced LPS-induced increases of cytokines and chemokines, alveolar neutrophil accumulation, lung hyperpermeability, NO production, and lipid peroxidation. Histological analysis revealed attenuated lung damage after PARP inhibition. Our findings support a mechanistic role of PARP-1 in the regulation of LPS-induced lung inflammation. Pharmacological inhibition of PARP may be useful in clinical conditions associated with overwhelming lung inflammation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban lung ARDS lipopolysaccharide poly(ADP-ribose) polymerase chemokines külföldön készült közlemény
Megjelenés:	American Journal Of Respiratory And Critical Care Medicine 165 : 3 (2002), p. 372-377. -
További szerzők:	Pacher Pál Mabley, Jon G. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Soriano, Francisco Garcia Haskó György (1967-) (biokémikus) Szabó Csaba (1967-) (orvos)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM040070
Első szerző:	Soejima, Kazutaka
Cím:	Role of nitric oxide in vascular permeability after combined burns and smoke inhalation injury / Soejima, K., Traber, L. D., Scghmalstieg, F. C., Hawkins, H., Jodoin, J. M., Szabó, Cs., Szabó, É., Virag, L., Salzman, A., Traber, D. L.
Dátum:	2001
Megjegyzések:	Patients with severe burn and/or smoke inhalation injury suffer both systemic and pulmonary vascular hyperpermeability. We hypothesized that nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) plays a role in the changes in microvascular permeability seen with this injury. To test the hypothesis, we administered mercaptoethylguanidine (MEG), a selective iNOS inhibitor, to conscious sheep subjected to a combined smoke inhalation and third-degree burn injury to 40% of total body surface area. The sheep were surgically prepared for chronic study with lung and prefemoral lymph fistulas in order to estimate microvascular permeability. Both the groups and a control group of animals showed an increase in iNOS protein and message in their lungs. The control animals showed significant increases in either plasma or lymph NO2-/NO3- (NOx) concentration at 24 h after injury, with associated cardiac depression and hemoconcentration. The airway epithelium stained for nitrotyrosine. In the treatment group, NOx did not increase significantly in plasma or lymph throughout the experiment, there was no nitrotyrosine staining, hemodynamic depression was not observed, and the fluid requirement was significantly less than in the control group. Changes in pulmonary microvascular permeability were significantly suppressed by inhibition of iNOS. However, there was no significant difference between the two study groups in the microvascular permeability of burned tissue. These data suggest that NO produced by iNOS plays an important role in the changes in systemic and pulmonary microvascular permeability in combined smoke inhalation/third-degree burn injury, but does not affect the vascular permeability of third-degree-burned tissue in this type of injury.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	American Journal of Respiratory and Critical Care Medicine 163 : 3 Pt1 (2001), p. 745-752. -
További szerzők:	Traber, Lilliand D. Scghmalstieg, Frank C. Hawkins, Hal Jodoin, Jeffrey M. Szabó Cs. Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Salzman, Andrew L. Traber, Daniel L.
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