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CAN inhNO ATTENUATE INFLAMMATION AND APOPTOSIS IN PIG LUNGS AFTER CPB

^* Department of anaesthesia, Hospital Notre-Dame, 1560, Sherbrooke street east, Montreal, Quebec H2L 4M1,
^** Department of anesthesia and reanimation, Centre Hospitalier Universitaire de liège, Domaine Universitaire du Sart Tilman, 4000 Liège, Belgium

INTRODUCTION

The occurrence of the systemic and pulmonary inflammation reaction during cardiac surgery with cardiopulmonary bypass^1,2 (CPB) has been established. This leads to tissue injury and apoptosis. Apoptosis is a process of programmed cell death that deletes individual cells in the course of development or cell turn over. Nitric oxide have been shown to inhibit inflammation and apoptosis in several type of cells. The aim of this study was to test whether inhaled NO can modulate inflammation and apoptosis in the lung.

MATERIEL AND METHODS

Twenty pigs weighing 30 to 40 kg were randomized in 4 groups. Two groups were subjected to a sternotomy (without CPB) while the two other groups were subjected to 90 minutes CPB with cardiac arrest and aortic clamping for 75 min. Half of all the groups were exposed to 20ppm of inhaled NO. After 24h of treatment, all animals were sacrificed and their lungs were harvested, perfused, embedded in paraffin, cutted and mounted on immunological slides. The samples were enzymaticaly labeled (TUNEL) for detection of apoptosis. All slides were visualized under fluorescent microscopy and analysed with the Metamorph 4.6 software. Il-8 concentrations were measured, on broncho-alveolar lavage (BAL), using ELISA Kit (Biosource, Nivelles, Belgium). A neutrophil count was also made on BAL.

RESULTS

After 24hours, the percentage of neutrophils was (11.0 ± 11.73 )% and (13.6 ± 20.77)% in sham group and sham NO group respectively. In CPB groups, pigs exposed to nitric oxide had (9.0 ± 10.10)% of neutrophils while the CPB group without inhaled NO had greater values of neutrophils (18.4 ± 23.64)%. No statistical difference was found between groups.

CONCLUSION

Inhaled NO seems to reduce inflammation by decreasing cytokines synthesis, and can have both antiapoptotic and proapoptotic role depending of physiological and pathophysiological conditions respectively.

REFERENCES

1 Ann Thorac Surg 1996, 61:1714–1720[Abstract/Free Full Text]

2 Chest 2001, 119:31–36[Abstract/Free Full Text]

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