ISSN:
1432-1238
Keywords:
Key words Nitric oxide
;
Leukocyte sequestration
;
Sepsis
;
Endotoxin
;
Shock
;
Lung
;
Oxygenation
;
Pulmonary vasoconstriction
;
Blood volume
;
Circulation
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Objective: Sequestration and migration of activated neutrophils plays a major role in the pulmonary injury typical of septic shock and the adult respiratory distress syndrome. Inhaled NO may counteract alveolar-capillary damage attributed to activated neutrophils. The present study describes a method to directly demonstrate the effects of NO inhalation on endotoxin-induced sequestration of 99 mTc-labelled leukocytes [As(t)] in the lungs of pigs.¶Design: Prospective controlled study.¶Setting: Laboratory for experimental surgery at a university medical centre.¶Subjects: Anaesthetised and ventilated pigs.¶Interventions: To induce inflammatory shock 26 animals received a continuous endotoxin infusion. Thirteen animals inhaled NO from the start of the experiments, while 13 served as controls. In 13 animals from both groups, leukocytes were labelled in vitro and reinjected, while in the 13 others erythrocytes were labelled in vivo to provide corrections for changes in blood volume.¶Measurements and results: The pulmonary distribution of 99 mTc-labelled leukocytes or erythrocytes was studied dynamically for 180 min. After correction for changes in pulmonary and heart blood volume (PBV, HBV), leukocyte sequestration curves were generated. Endotoxin induced pulmonary vasoconstriction, reduced PBV, impaired oxygenation, and caused a maximum increase in As(t) of 30 % in the lungs. NO inhalation attenuated pulmonary vasoconstriction and the reduction in PBV. The maximum increase in As(t) was reduced to 15 % of baseline.¶Conclusions: Inhaled NO exerts its main vascular effects in the pulmonary microvasculature, the primary site of physiological neutrophil margination and pathological adhesion of activated leukocytes. Early use of NO inhalation may offer protection against the development of more lasting pulmonary failure in septic shock by reducing leukocyte sequestration in the lungs.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s001340051159
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