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1 Anesthesiology, Columbia University, New York, New York, United States
2 Pathology, Columbia University, New York, New York, United States
* To whom correspondence should be addressed. E-mail: tl128{at}columbia.edu.
Inflammation after renal ischemia reperfusion (IR) injury is a major contributor to renal cell death. We previously demonstrated that several volatile anesthetics protect against renal IR injury and necrosis in rats in vivo. We subsequently showed that volatile anesthetics produced direct anti-inflammatory and anti-necrotic effects in cultured proximal tubule cells in vitro. In this study, we wanted to determine whether the volatile anesthetic isoflurane protects against renal IR injury by producing anti-inflammatory effects in mice. C57BL/6 mice subjected to renal IR under isoflurane anesthesia demonstrated improved renal function and reduced necrosis compared to mice subjected to renal IR under pentobarbital anesthesia. Mice subjected to renal IR under isoflurane anesthesia also showed a reduction in inflammation evidenced by a reduced renal influx of neutrophils and macrophages, reduced ICAM-1 expression, less upregulation of pro-inflammatory mRNAs (TNF-
, ICAM-1, KC and IL-1
) as well as reduced nuclear translocation of NF
B 24 hrs after renal IR injury. Analysis of specific lymphocyte subset trafficking to the kidney using flow cytometry demonstrated that isoflurane anesthesia reduced intrarenal influx of CD3+, CD4+, CD8+ and NK1.1+ lymphocytes at 3 hr after renal ischemia compared to pentobarbital anesthesia. However, only the differential reduction of NK1.1+ lymphocytes persisted 24 hr after renal ischemia. Therefore, we conclude that isoflurane anesthesia significantly attenuated renal IR injury in mice by reducing inflammation and modulating leukocyte influx. In particular, neutrophil, macrophage and NK1.1+ lymphocyte cell modulation may play a significant role in renal protection by isoflurane anesthesia.
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