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Titolo:
PRETREATMENT WITH INHALED NITRIC-OXIDE INHIBITS NEUTROPHIL MIGRATION AND OXIDATIVE ACTIVITY RESULTING IN ATTENUATED SEPSIS-INDUCED ACUTE LUNG INJURY
Autore:
BLOOMFIELD GL; HOLLOWAY S; RIDINGS PC; FISHER BJ; BLOCHER CR; SHOLLEY M; BUNCH T; SUGERMAN HJ; FOWLER AA;
Indirizzi:
VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT INTERNAL MED RICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT SURG RICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PEDIAT RICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT RESP CARE RICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT ANAT RICHMOND VA 23298
Titolo Testata:
Critical care medicine
fascicolo: 4, volume: 25, anno: 1997,
pagine: 584 - 593
SICI:
0090-3493(1997)25:4<584:PWININ>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY-DISTRESS-SYNDROME; HYPOXIC PULMONARY VASOCONSTRICTION; ENDOTHELIAL CELL RECOGNITION; GRAM-NEGATIVE SEPSIS; MONOCLONAL-ANTIBODY; LEUKOCYTE ADHESION; RELAXING FACTOR; PORCINE MODEL; GAS-EXCHANGE; ARDS;
Keywords:
NITRIC OXIDE; INHALATION; ACUTE LUNG INJURY; ADULT RESPIRATORY DISTRESS SYNDROME; SEPSIS; ALVEOLAR CAPILLARY MEMBRANE INJURY; NEUTROPHIL; ADHESION; TRANSMIGRATION; ENDOTHELIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
G.L. Bloomfield et al., "PRETREATMENT WITH INHALED NITRIC-OXIDE INHIBITS NEUTROPHIL MIGRATION AND OXIDATIVE ACTIVITY RESULTING IN ATTENUATED SEPSIS-INDUCED ACUTE LUNG INJURY", Critical care medicine, 25(4), 1997, pp. 584-593

Abstract

Objective: To determine if, and by what mechanisms, inhaled nitric oxide attenuates acute lung injury in a porcine model of adult respiratory distress syndrome induced by Gram-negative sepsis. Design: Nonrandomized, controlled study. Setting: Laboratory at a university medical center. Subjects: Thirty pathogen-free Yorkshire swine (15 to 20 kg), Interventions: Four groups of swine were anesthetized, mechanically ventilated, and studied for 5 hrs. Both control-nitric oxide and septic-nitric oxide animals received inhaled nitric oxide at 20 parts per million throughout the study, Control (n = 10) and control-nitric oxide (n= 5) animals received a 1-hr infusion of sterile saline, Sepsis was induced in septic (n = 10) and septic-nitric oxide (n = 5) animals witha 1-hr intravenous infusion of live Pseudomonas aeruginosa. Measurements and Main Results: Untreated septic animals developed a progressivedecrease in Pac, that was prevented in septic-nitric oxide animals (73 +/- 4 vs. 214 +/- 23 torr [9.7 +/- 0.5 vs. 28.5 +/- 3.1 kPa], respectively, at 5 hrs, p <.05), Untreated septic animals showed a significant increase in bronchoalveolar lavage protein and neutrophil count at 5 hrs, compared with the baseline value, indicating acute lung injury. Septic-nitric oxide animals showed no significant increase in these parameters. Peripheral blood neutraphils from untreated septic animals and septic-nitric oxide animals exhibited significant (p < .05) up-regulation of CD18 receptor expression and oxidant activity (10.5 +/- 0.9and 5.0 +/- 0.9 nmol of superoxide anion/10(6) neutrophils/10 mins, respectively) compared with both control and control nitric oxide animals (3.0 +/- 0.6 and 2.6 +/- 0.2 nmol of superoxide anion/10(6) neutrophils/10 mins, respectively), Also, priming for the oxidant burst at 5 hrs was decreased by 50% in septic-nitric oxide animals compared with untreated septic animals, Both untreated septic and septic-nitric oxide animals showed a significant increase in pulmonary arterial pressureat 30 mins (47.5 +/- 2.4 and 51.0 +/- 3.0 mm Hg, respectively), followed by a progressive decrease (32.8 +/- 2.6 and 31.3 +/- 5.4 mm Hg, respectively, at 5 hrs). Both of these changes were significant (p < .05) compared with baseline values and compared with the control groups, There was no significant difference in pulmonary arterial pressure or systemic arterial pressure at any time between untreated septic and septic-nitric oxide animals. Conclusions: These results demonstrate thatinhaled nitric oxide attenuates alveolar-capillary membrane injury inthis porcine model of Gram negative sepsis but does not adversely affect systemic hemodynamics, The data suggest that inhaled nitric oxide preserves alveolar-capillary membrane integrity by the following means: a) inhibiting transendothelial migration of activated, tightly adherent neutrophils; and b) possibly by attenuating the neutrophil oxidantburst.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 12:41:59