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Sevoflurane preconditioning induces rapid ischemic tolerance against spinal cord ischemia/reperfusion through activation of extracellular signal-regulated kinase in rabbits.
Anesth Analg. 2009 Oct; 109(4):1263-72.A&A

Abstract

BACKGROUND

The protective effect of sevoflurane preconditioning against spinal cord ischemia/reperfusion (I/R) is unclear. We designed this study to investigate whether sevoflurane preconditioning could induce rapid ischemic tolerance to the spinal cord in a rabbit model of transient spinal cord ischemia and how the role of extracellular signal-regulated kinase (ERK) is involved.

METHODS

To test whether preconditioning with sevoflurane induces rapid ischemic tolerance, New Zealand White male rabbits were randomly assigned to three groups. Animals in the Sev group received preconditioning with 3.7% sevoflurane (1.0 minimum alveolar anesthetic concentration) in 96% oxygen for 30 min, whereas animals in the O(2) group serving as controls inhaled only 96% oxygen for 30 min. The Sham group received the same anesthesia and surgical preparation but no preconditioning or spinal cord I/R. To evaluate the role of ERK activation in sevoflurane preconditioning, rabbits were randomly assigned to four groups. U0126, an ERK inhibitor, was administered IV 20 min before the beginning of preconditioning in the U0126 + O(2) and U0126 + Sev groups. Dimethylsulfoxide was administered IV at the same time in the vehicle + O(2) and vehicle + Sev groups. At 1 h after preconditioning, the animals were subjected to spinal cord I/R induced by infrarenal aorta occlusion. All animals were assessed at 48 h after reperfusion with modified Tarlov criteria, and the spinal cord segments (L5) were harvested for histopathological examination, TUNEL staining, and Western blot of phosphor-ERK1/2.

RESULTS

The animals in the Sev group had higher neurological scores and more normal motor neurons than those in the O(2) group (P < 0.01 for each comparison). Compared with vehicle + Sev group, the U0126 + Sev group had worse neurological outcomes, fewer viable neurons, more apoptotic neurons, and significantly decreased ERK1/2 phosphorylation (P <or= 0.01 for each comparison). There were no significant differences in the outcomes among vehicle + O(2), U0126 + O(2), and U0126 + Sev groups.

CONCLUSIONS

This study demonstrates that sevoflurane preconditioning induces rapid tolerance to spinal cord I/R in rabbits, and the tolerance is possibly mediated through the activation of ERK. These data suggest that sevoflurane preconditioning might provide a new practical method for protecting perioperative spinal cord I/R.

Authors+Show Affiliations

Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, Shaanxi Province, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19762756

Citation

Ding, Qian, et al. "Sevoflurane Preconditioning Induces Rapid Ischemic Tolerance Against Spinal Cord Ischemia/reperfusion Through Activation of Extracellular Signal-regulated Kinase in Rabbits." Anesthesia and Analgesia, vol. 109, no. 4, 2009, pp. 1263-72.
Ding Q, Wang Q, Deng J, et al. Sevoflurane preconditioning induces rapid ischemic tolerance against spinal cord ischemia/reperfusion through activation of extracellular signal-regulated kinase in rabbits. Anesth Analg. 2009;109(4):1263-72.
Ding, Q., Wang, Q., Deng, J., Gu, Q., Hu, S., Li, Y., Su, B., Zeng, Y., & Xiong, L. (2009). Sevoflurane preconditioning induces rapid ischemic tolerance against spinal cord ischemia/reperfusion through activation of extracellular signal-regulated kinase in rabbits. Anesthesia and Analgesia, 109(4), 1263-72. https://doi.org/10.1213/ane.0b013e3181b2214c
Ding Q, et al. Sevoflurane Preconditioning Induces Rapid Ischemic Tolerance Against Spinal Cord Ischemia/reperfusion Through Activation of Extracellular Signal-regulated Kinase in Rabbits. Anesth Analg. 2009;109(4):1263-72. PubMed PMID: 19762756.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sevoflurane preconditioning induces rapid ischemic tolerance against spinal cord ischemia/reperfusion through activation of extracellular signal-regulated kinase in rabbits. AU - Ding,Qian, AU - Wang,Qiang, AU - Deng,Jiao, AU - Gu,Qiuhan, AU - Hu,Sheng, AU - Li,Yang, AU - Su,Binxiao, AU - Zeng,Yi, AU - Xiong,Lize, PY - 2009/9/19/entrez PY - 2009/9/19/pubmed PY - 2009/10/2/medline SP - 1263 EP - 72 JF - Anesthesia and analgesia JO - Anesth. Analg. VL - 109 IS - 4 N2 - BACKGROUND: The protective effect of sevoflurane preconditioning against spinal cord ischemia/reperfusion (I/R) is unclear. We designed this study to investigate whether sevoflurane preconditioning could induce rapid ischemic tolerance to the spinal cord in a rabbit model of transient spinal cord ischemia and how the role of extracellular signal-regulated kinase (ERK) is involved. METHODS: To test whether preconditioning with sevoflurane induces rapid ischemic tolerance, New Zealand White male rabbits were randomly assigned to three groups. Animals in the Sev group received preconditioning with 3.7% sevoflurane (1.0 minimum alveolar anesthetic concentration) in 96% oxygen for 30 min, whereas animals in the O(2) group serving as controls inhaled only 96% oxygen for 30 min. The Sham group received the same anesthesia and surgical preparation but no preconditioning or spinal cord I/R. To evaluate the role of ERK activation in sevoflurane preconditioning, rabbits were randomly assigned to four groups. U0126, an ERK inhibitor, was administered IV 20 min before the beginning of preconditioning in the U0126 + O(2) and U0126 + Sev groups. Dimethylsulfoxide was administered IV at the same time in the vehicle + O(2) and vehicle + Sev groups. At 1 h after preconditioning, the animals were subjected to spinal cord I/R induced by infrarenal aorta occlusion. All animals were assessed at 48 h after reperfusion with modified Tarlov criteria, and the spinal cord segments (L5) were harvested for histopathological examination, TUNEL staining, and Western blot of phosphor-ERK1/2. RESULTS: The animals in the Sev group had higher neurological scores and more normal motor neurons than those in the O(2) group (P < 0.01 for each comparison). Compared with vehicle + Sev group, the U0126 + Sev group had worse neurological outcomes, fewer viable neurons, more apoptotic neurons, and significantly decreased ERK1/2 phosphorylation (P <or= 0.01 for each comparison). There were no significant differences in the outcomes among vehicle + O(2), U0126 + O(2), and U0126 + Sev groups. CONCLUSIONS: This study demonstrates that sevoflurane preconditioning induces rapid tolerance to spinal cord I/R in rabbits, and the tolerance is possibly mediated through the activation of ERK. These data suggest that sevoflurane preconditioning might provide a new practical method for protecting perioperative spinal cord I/R. SN - 1526-7598 UR - https://www.unboundmedicine.com/medline/citation/19762756/Sevoflurane_preconditioning_induces_rapid_ischemic_tolerance_against_spinal_cord_ischemia/reperfusion_through_activation_of_extracellular_signal_regulated_kinase_in_rabbits_ L2 - http://dx.doi.org/10.1213/ane.0b013e3181b2214c DB - PRIME DP - Unbound Medicine ER -