Wird die pulmonale Inflammationsreaktion beatmungsbedürftiger Frühgeborener durch moderate permissive Hyperkapnie beeinflusst?
Influence of moderate permissive hypercapnia on pulmonary inflammation in extremely low birthweight infants (ELBWI). Background and aims We tested the hypothesis that moderate permissive hypercapnia (PHC) results in less lung injury than mild hypercapnia (MHC) and therefore may reduce the concentration of proinflammatory cytokines and acid sphingomyelinase (ASMase) in tracheal aspirates. Methods Preterm infants (birthweight 400-1000 g, gestational age 23 0/7 - 28 6/7 weeks) requiring mechanical ventilation within the first 24 h after birth, were randomly assigned to receive either PHC (PaCO2 target area starting with 55 - 65 mm Hg at day 1 to 65 - 75 mm Hg at day 7) or MHC (PaCO2 target area starting with 40-50 mm Hg at day 1 to 50 - 60 mm Hg at day 7). Tracheal aspirates were collected and analysed for IL-1Beta, IL-6, IL-8, IL-10, MIP-1Alpha;, LTB4, TGF-Beta, NPY, albumin, nitrate, ASMase and the secretory component for IgA. The primary endpoint BPD or death was determined at a postmenstrual age of 36 weeks ± 1 day. Results 71 infants were enrolled, 35 received PHC and 36 MHC. Analyses of variance for the main effect of the PaCO2 targets did not detect significant differences: IL-1Beta; (p = 0,42), IL-6 (p = 0,44), IL-8 (p = 0,91), IL-10 (p = 0,87), MIP-Alpha; (p = 0,34), LTB4 (p = 0,87), TGF-Beta (p = 0,26), NPY (p = 0,47), albumin (p = 0,63), nitrate (p = 0,73), ASMase (p = 0,25). BPD or death occured in 9 (26 %) and in 10 (28 %) of infants receiving PHC or MHC. Conclusion PHC did not result in lower inflammatory activity than MHC in ventilated ELBWI.
Subject HeadingsFrühgeborenes [GND]
Inflammation mediators [LCSH]
Infant, premature [MeSH]
Sphingomyelin phosphodiesterase [MeSH]