Isoflurane protects against renal ischemia and reperfusion injury and modulates leukocyte infiltration in mice

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-infla...

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Published in:American journal of physiology. Renal physiology 2007-09, Vol.293 (3), p.F713-F722
Main Authors: Lee, H Thomas, Kim, Mihwa, Kim, Minjae, Kim, NaLa, Billings, 4th, Frederic T, D'Agati, Vivette D, Emala, Sr, Charles W
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Granulocyte Colony-Stimulating Factor
Inflammation - prevention & control
Interleukin-3
Isoflurane - pharmacology
Kidney - pathology
Kidney diseases
Kidney Diseases - prevention & control
Kidneys
Leukocytes
Leukocytes - drug effects
Mice
Necrosis - prevention & control
Nephrology
Recombinant Fusion Proteins
Recombinant Proteins
Reperfusion Injury - prevention & control
Rodents
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Summary: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 with 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 proinflammatory mRNAs (TNF-alpha, ICAM-1, KC, and IL-1beta) as well as reduced nuclear translocation of NF-kappaB 24 h 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 h after renal ischemia compared with pentobarbital anesthesia. However, only the differential reduction of NK1.1+ lymphocytes persisted 24 h 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.
ISSN:1931-857X
1522-1466
DOI:10.1152/ajprenal.00161.2007