These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Protective mechanism of ultrafiltration against cardiopulmonary bypass-induced lung injury. Author: Koike T, Tsuchida M, Saitoh M, Haga M, Satoh K, Aoki T, Toyabe SI, Hayashi JI. Journal: Transplant Proc; 2009 Nov; 41(9):3845-8. PubMed ID: 19917399. Abstract: BACKGROUND: We previously demonstrated a negative effect of cardiopulmonary bypass (CPB) in a canine model of single-lung graft function and an improved effect with ultrafiltration during CPB. OBJECTIVE: To investigate the mechanism of these effects, focusing on cytokines and pulmonary surfactants using real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). MATERIALS AND METHODS: Fifteen left-sided single-lung transplant procedures were performed in pairs of dogs. The animals were divided into 3 groups. In one group, transplantation was performed without CPB (non-CPB group); in a second group, transplantation was performed with CPB and CPB flow was decreased slowly and pulmonary artery pressure was controlled (CPB group; and in the third group, transplantation was performed with CPB and ultrafiltration (CPB+UF group). Grafted lung specimens were harvested for RT-PCR of cytokines (IL-6, IL-8, and IL-10) and surfactant proteins (SP-A, SP-B, and SP-C). RESULTS: Real-time quantitative RT-PCR demonstrated increased IL-6 expression in the CPB group compared with the non-CPB group. IL-6 gene expression was suppressed and pulmonary surfactant restored using ultrafiltration. Gene expression of surfactant protein (SP)-A, SP-B, and SP-C was decreased in the CPB group compared with normal lung and ultrafiltration groups, which demonstrated sustained gene expression of SP-A and SP-B. CONCLUSION: Cardiopulmonary bypass has negative effects on grafts; however, ultrafiltration attenuates acute lung dysfunction by decreasing the inflammatory response and increasing pulmonary surfactant.[Abstract] [Full Text] [Related] [New Search]