- Meeting abstract
- Open Access
Progesterone and interleukin-8 during and after cardiopulmonary bypass in infants and children
© Current Science Ltd 1999
- Published: 2 March 1999
- Heart Disease
- Proinflammatory Cytokine
- Congenital Heart Disease
It has been shown that proinflammatory cytokines are suppressed by progesterone (P). cardiopulmonary bypass (CPB) leads to the release of pro- and anti-inflammatory cytokines. Because sex steroids have the ability to adsorb extensively to synthetic surfaces a decrease of P during the contact with the CPB circuit is conceivable. If P concentrations would decrease the inflammatory response to CPB could be effected. The purpose of the study was to look for the course of P in relation to the proinflammatory cytokine interleukin-8 (IL-8) during and after CPB.
Twelve infants and children (age 2 months to 15 years, median 2.4 years, four females) were operated on CPB for congenital heart disease (2 ASD, 5 VSD, 3 Fallot, subaortic stenosis, aortopulmonary window). Blood samples were taken before, during (10 min after onset) and after (disconnection, 6 and 24 h, 3 and 7 days) CPB. Plasma concentrations of P and IL-8 were determined using a RIA- and an ELISA-kit, respectively.
P concentrations before CPB were 0,21 ng/ml (median, 0.012-0.72). They increased to a maximum of 5.59 ng/ml (0.13-35.4) at 6 h after CPB. The pre-CPB concentrations were reached on the 7th day post-CPB. This course of P concentrations was similar in female and male infants of every age. The maximum IL-8 concentrations were found at 6 h after CPB. The decline of IL-8 from 6 to 24 h after CPB was correlated to the P concentration at 6 h (r = 0.77).
The results were in contrast to our expectation because P increased with CPB. However, the significant increase with a maximum at 6 h after CPB needs further explanation. The maximal P concentrations coincided with the peak of the IL-8 response and correlated to the following decrease of IL-8. We speculate that the release of P during and after CPB could be of benefit in terminating the associated proinflammatory response. Further studies are needed to clarify the physiology and role of the P increase in the setting of CPB.