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ENOXIMONE MODULATES THE INFLAMMATORY IMMUNE RESPONSE DURING CARDIOPULMONARY BYPASS

Loick, H.M. MD; Berendes, E. MD; Van Aken, H. MD, PHD; Erren, M. MD; Schmid, C.; Mollhoff, T. MD

doi: 10.1097/00000539-199802001-00080
Abstracts of Posters Presented at the International Anesthesia Research Society; 72nd Clinical and Scientific Congress; Orlando, FL; March 7-11, 1998: Cardiovascular Anesthesia
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(Loick, Berendes, Van Aken, Mollhoff) Klinik u. Polikl. fur Anasth. u. op. Intensivmed., (Schmid) Klinik u. Polikl. fur Herz, Thorax- und GefaBchirurgie; (Erren) Klinik fur Laborat.-Med.; WWU Munster, Germany.

Abstract S80

Cardiopulmonary bypass (CPB) is associated with a release of endotoxin and proinflammatory cytokines [1]. It was investigated, whether the administration of the phosphodiesterase inhibitor enoximone modulates the CPB induced immune response through a cAMP-mediated metabolism [2].

Method: Informed consent of the study participants and institutional review board approval for the study were obtained. Twenty patients scheduled for elective coronary artery bypass grafting were enrolled in the study. Anesthesia was induced and maintained by midazolam, fentanyl, and pancuronium. In addition to a standard monitoring (radial artery and pulmonary artery catheter) a catheter was inserted into the hepatic vein via the jugular vein. In a randomized order ten patients (enoximone) received a bolus of 0.2 mg/kg enoximone, followed by 5 [micro sign]g/kg/min, during and 24 hours following the surgical procedure. The remaining patients received equal volumes of NaCl 0,9% (control). Before drug intervention (baseline), 20 min afterwards, 20 min after CPB initiation (CPB) and during the ICU stay the following parameter were determined: mixed-venous and liver-venous endotoxin, interleukin 6 (IL-6), serum amyloid A (SAA) and C-reactive protein (CRP) concentrations. Data are expressed as means +/- SD and analyzed by two way anova.

RESULTS: Liver-venous endotoxin levels increased during CPB in both groups, followed by a release of IL-6. However, the extent was attenuated in the enoximone group. SAA and CRP rose 8 hrs after ICU admission with a peak 24 hrs postoperatively. No effect of enoximone on SAA and CRP was observed. No difference was obtained between mixed-venous and liver-venous plasma level of the studied mediators. (Figure 1)

Figure 1

Figure 1

Conclusion: Enoximone diminished markedly the perioperative inflammatory response following CPB, as determined by lowered levels of endotoxin and the proinflammatory cytokine IL-6. This can be explained by less intestinal mucosal lessions with less translocation and a suppression of IL-6 release within the monocytes. The favorable effect of enoximone on systemic inflammation may have impact on patient's postoperative morbidity.

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REFERENCES

1. Eur J Cardiothorac Surg. 1995;9:22-29
2. Immunology 1992,76,30-34
© 1998 International Anesthesia Research Society