ALTERATION OF THE NEONATAL PULMONARY PHYSIOLOGY AFTER TOTAL CARDIOPULMONARY BYPASS

Citation
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
Citations number
33
ISSN journal
00225223
Volume
114
Issue
6
Year of publication
1997
Pages
1061 - 1069
Database
ISI
SICI code
0022-5223(1997)114:6<1061:AOTNPP>2.0.ZU;2-3
Abstract
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.