Our group has developed percutaneous extracorporeal Arterio Venous CO2 Removal (AVCO2R) utilizing a low-resistance membrane gas exchanger. AVCO2R may improve survival in respiratory distress syndrome (RDS) by reducing the barotrauma and volutrauma afforded by mechanical ventilation, while providing near-total CO2 removal. Alternatively, use of this device may decrease inflammation through effects of improved CO2 homeostasis or other mechanisms. To test this later hypothesis, we measured mRNA for two molecular markers, aquaporin-1 (AQP-1) and inducible nitric oxide synthase (iNOS), in a clinically relevant model of RDS produced by combined smoke inhalation and 40% full-thickness burn injury. Both AQP-1 and iNOS may be involved in the characteristic large increase in lung transvascular fluid flux observed after this injury. AQP-1 and iNOS mRNA were quantitated by a reverse transcriptase - polymerase chain reaction technique (RT-PCR) that utilized an internal, competitive standard engineered to adhere to the same primers as AQP-1 or iNOS. AQP-1 mRNA was 53,500 ± 15,373 at 48 h in ventilator treated animals and 20,520 ± 6,938 at 96 h after injury and 48 h of AVCO2R in AVCO2R treated animals (copies/μg total RNA, means ± S.E.M.) (p=0.07) while iNOS mRNA was 17,178 ± 3,095 at 48 h in ventilator treated animals and 7,853 ± 2,229 at 96 h after injury and 48 h of AVCO2R in AVCO2R treated animals (copies/μg total RNA, means ± S.E.M.) (p=0.008). These findings suggest that AVCO2R device may be associated with decreasing expression of AQP-1 and iNOS, two molecules that may be important in the pathogenesis of RDS.
ASJC Scopus subject areas
- Biomedical Engineering