Abstract Body (Do not enter title and authors here): Background: Extracorporeal membrane oxygenation(ECMO) is a critical intervention for treating critically ill patients, Kidney injury is a common occurrence during ECMO therapy, and studies indicate that Veno-Arterial ECMO (VA-ECMO) is linked to more severe kidney damage compared to Veno-Venous ECMO (VV-ECMO). This study aims to compare the impact of VV-ECMO and VA-ECMO on the kidneys and explore their potential underlying mechanisms.
Methods: Based on our prior research, we established rat models for both VV-ECMO and VA-ECMO. Subsequently, we conducted a comparative analysis to assess the impact of VV-ECMO and VA-ECMO on renal injury. This analysis involved the examination of various data points such as blood urea nitrogen (BUN), creatinine (CR), cystatin C, and Kidney Injury Molecule-1 (KIM-1). Histopathological analysis using HE staining was performed to evaluate the extent of pathological damage. Additionally, we placed particular emphasis on monitoring the pulsatility index in both groups.Furthermore, we employed RNA-Seq on both the VV-ECMO and VA-ECMO rat groups to investigate potential underlying mechanisms.
Results: The study demonstrated lower levels of renal injury indicators (e.g., BUN, CR, cystatin C, KIM-1) in the VV-ECMO group compared to the VA-ECMO group. Furthermore, HE staining revealed less severe pathological damage in the VV-ECMO group. VV-ECMO also displayed a higher pulsatility index. Transcriptomic analysis highlighted differentially expressed genes between the VV-ECMO and VA-ECMO groups, primarily associated with angiotensin II. Concurrently, the omics data indicated a milder inflammatory response in the VV-ECMO group. We further validated the more pronounced inflammatory response of VA-ECMO through Western blot and RT-PCR experiments. This suggests that VA-ECMO might activate angiotensin II, inducing inflammation due to the absence of cardiac pulsation.
Conclusion: Compared to VA-ECMO, VV-ECMO demonstrates a more favorable effect in mitigating renal injury. The potential mechanism may involve the rhythmic cardiac pulsation provided by VV-ECMO, effectively suppressing angiotensin II and thereby reducing inflammatory responses. This study offers crucial insights for developing rational strategies in the clinical selection of combined cardiopulmonary support systems.