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Canadian Journal of Anesthesia 48:A38 (2001)
© Canadian Anesthesiologists' Society, 2001


Abstracts - Monday June 11 15:45 p.m. - 17:45 p.m.

PREVENTION OF THE PULMONARY INFLAMMATION FOLLOWING CARIOPULMONARY BYPASS WITH INHALED NO

Bernard Hubert, MD, Paolo M Renzi, MD, Marek Radomski, PhD and Gilbert Blaise, MD

Laboratoire d'anesthésie Hopital Notre-Dam, rue Sherbrooke Est 1560 Montréal, Québec H2L 4M1.

INTRODUCTION

Cardiopulmonary bypass (CPB) is associated with a systemic inflammatory response consisting of humoral inflammatory cascade and cellular activation.

Inflammation is triggered off by the contact of blood cells with CPB synthetics surfaces, by ischemia -reperfusion injury and by bacteria translocation from the gut.

Inflammation involves the lung inducing an acute lung injury syndrome(ALI) but can also induce a SIRS.

The aim of the study is to evaluate the efficiency of inhaled NO (inhNO) given perioperatively in prévention of ALI syndrome following CPB in pigs.

MÉTHODS

After receiving a premédication (atropine, ketamine, azaperone) pigs were anaesthetized with thiopenthal and fentanyl and maintened with continous infusion of thiopenthal(5 mg/kg) and fentanyl(10 mg/kg).

Pigs were submitted to three differents inflammatory levels (sternotmy, CPB, CPB+LPS administration) and submitted during 24 hours to three inhNO concentrations(0 ppm, 5 ppm, 20 ppm).

Anesthésia technique, monitoring, reanimation, CPB and postoperative treatement were identical to the treatment applies in human. Respiratory, hemodynamic parameters, matrix metalloproteinases 2 and 9 (MMP 2 and MMP 9) on BAL, cytokines on blood were mesured.

RESULTS

Preliminary results show that in this pig model CPB produced only a moderate inflammatory state with systemic vascular resistance reduction. This inflammation process is equivalent to the inflammatory state induced by CPB in human having localized arteriosclerosis or valve dysfunction.

The inflammatory response post CPB is enhanced by LPS. This late inflammatory process is similar to the one seen in human suffers from severe arthériosclerosis or from other extracardiac pathology (pulmonary, renal).

InhNO reduces pulmonary arterial pressure and improves oxygenation after CPB and LPS administration.

InhNO inhibits MMP-2 and MMP-9 and TNFa production induced by mechanical ventilation and CPB.

CONCLUSION

InhNO delivery perioperatively reduces ventilation induce lung injury (VILI) and ALI syndrome prevention following CPB. As this model is relevant to the human situation, we think that preventive InhNO could be particulary useful in human prone to developps ALI post CPB (older patient with extracardiac pathology).





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