Preconditioning with volatile anaesthetic sevoflurane in ischemic retinal lesion in rats
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Volatile anaesthetic agents have been recognized for their neuroprotective properties since the 1960s. However, little is known regarding the potential retinoprotective effects of preconditioning by anaesthetic drugs. Retinal ischemia can be modeled by permanent bilateral common carotid artery occlusion (BCCAO). Here we studied the degree of ischemic injury with preconditioning by sevoflurane in the rat retina. During the BCCAO operation and preconditioning Wistar rats were anaesthetized with 1 MAC of sevoflurane. The oxygen, carbon dioxide, and anaesthetic vapor concentration in the anaesthetizing box was monitored with a gas analyzer. We examined 4 groups: non- and preconditioning groups in control and BCCAO animals. The duration of preconditioning period was 1 h and it was performed 1 day before BCCAO. The retinas were processed for histological evaluation after 2 weeks survival to determine the cell number in the ganglion cell layer and the thickness of the whole retina and that of all retinal layers. BCCAO-induced retinal ischemic injury was ameliorated by sevoflurane preconditioning. Retinal thickness and the cell number in the ganglion cell layer were more retained in preconditioned animals after BCCAO compared to non-preconditioned group. These results suggest that preconditioning using sevoflurane could provide a new perspective in retinoprotective strategies.
KeywordsRetina Sevoflurane preconditioning Ischemia Retinoprotection
- Frässdorf J, Borowski A, Ebel D, Feindt P, Hermes M, Meemann T, Weber R, Müllenheim J, Weber NC, Preckel B, Schlack W (2009) Impact of preconditioning protocol on anesthetic-induced cardioprotection in patients having coronary artery bypass surgery. J Thorac Cardiovasc Surg 137:1436–1442PubMedCrossRefGoogle Scholar
- Mester L, Szabo A, Atlasz T, Szabadfi K, Reglodi D, Kiss P, Racz B, Tamas A, Gallyas F Jr, Sumegi B, Hocsak E, Gabriel R, Kovacs K (2009) Protection against chronic hypoperfusion-induced retinal neurodegeneration by PARP inhibition via activation of PI3-kinase Akt pathway and suppression of JNK and p38 MAP kinases. Neurotox Res 18:68–76CrossRefGoogle Scholar