A. Serraf et al., ALTERATION OF THE NEONATAL PULMONARY PHYSIOLOGY AFTER TOTAL CARDIOPULMONARY BYPASS, Journal of thoracic and cardiovascular surgery, 114(6), 1997, pp. 1061-1069
Objectives: The purpose of this study was to analyze the mechanisms as
sociated with lung injury after cardiopulmonary bypass and to propose
strategies of prevention. Methods: Thirty-two neonatal piglets underwe
nt 90 minutes of hypothermic cardiopulmonary bypass without aortic cro
ssclamping. Five experimental groups were defined: group I had standar
d cardiopulmonary bypass (control), group II received continuous low-f
low lung perfusion during cardiopulmonary bypass, group III treatment
was similar to that of group I with maintenance of ventilation, group
IV received pneumoplegia, and group V received nitric oxide ventilatio
n (30 ppm) after cardiopulmonary bypass. Data drawn from hemadynamic a
nd gas exchange values and muscular and pulmonary tissular levels of a
denosine triphosphate (in micromoles per gram) and myeloperoxidase (in
international units per 100 mg) were used for comparisons before and
30 and 60 minutes after cardiopulmonary bypass. Pulmonary and systemic
vascular endothelial functions were assessed in vitro after cardiopul
monary bypass on isolated rings of pulmonary and iliac arteries. Resul
ts: Pulmonary vascular resistance index, cardiac index, and oxygen ten
sion were better preserved in groups II, IV, and V. All groups disclos
ed a significant decrease in lung adenosine triphosphate levels and an
increase in myeloperoxidase activity whereas these levels stayed with
in pre-cardiopulmonary bypass ranges in muscular beds. Endothelium-dep
endent relaxation was preserved in systemic arteries but was strongly
affected in pulmonary arteries after cardiopulmonary bypass. None of t
he methods that aimed to protect the pulmonary vascular bed demonstrat
ed any preservation of pulmonary endothelial function. Conclusion: Car
diopulmonary bypass results in ischemia-reperfusion injury of the pulm
onary vascular bed. Lung protection by continuous perfusion, pneumople
gia, or nitric oxide ventilation can prevent hemodynamic alterations a
fter cardiopulmonary bypass but failed to prevent any of the biochemic
al disturbances.