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Conference Paper: Post-ischemic conditioning decreases apoptosis after retinal ischemia

TitlePost-ischemic conditioning decreases apoptosis after retinal ischemia
Authors
Issue Date2010
PublisherAmerican Society Anesthesiologists (ASA).
Citation
The 2010 Annual Meeting of the American Society Anesthesiologists (ASA), San Diego, CA., 16-20 October 2010. In Conference Proceedings, 2010, abstract no. A1030 How to Cite?
AbstractIschemic preconditioning (IPC) protects the rat retina against the deleterious effects of severe ischemia. Ischemic post-conditioning (Post-C) involves a brief ischemic stimulus delivered after ischemia. We studied the impact of Post-C on apoptosis following ischemia and the impact of combining IPC and Post-C. A second purpose of the study was analyze the effect of Post-C on inflammation following ischemia. METHODS: IPC and ischemia were induced in rats as previously described (1). IPC was 8 min ligation of the central retinal artery ([start_en]201C;ligation PC”) 24 h prior to ischemia, while post conditioning ([start_en]201C;Post-C') was increased intraocular pressure (IOP) for 5 min, beginning 10 min after the end of 55 min ischemia. Ketamine-xylazine anesthetized rats breathed spontaneously with temperature held constant at 36-37 C, whilst monitoring systemic blood pressure, and pulse oximetry. At 24 h after ischemia, when apoptotic injury peaks, retinas were removed and 7 micron frozen sections prepared, and stained using TUNEL. % TUNEL retinal ganglion cells (RGCs) was calculated using simultaneous staining with the nuclear dye, DAPI. Identity of the TUNEL-positive RGCs was confirmed by double labeling with RGC-specific anti-thy1 antibody. Inflammation was assessed on frozen retinal sections using antibodies specific for infiltrating macrophages (anti-MIP1), monocytes (anti-MCP), and leukocytes (anti-CD45). Data were quantitated using NIH Image. Data were analyzed as previously described (1). RESULTS: Figure 1 shows that TUNEL cells were thy-1 positive, identifying them as RGCs.[figure1]There was a significant reduction in TUNEL positivity with Post-C; previous application of IPC blocked the anti-apoptotic effect of Post-C (Table 1).[table1]There was no significant leukocyte infiltration, but both macrophages and monocytes infiltrated retinas after ischemia, with Post-C decreasing the macrophage infiltation (Figure 2).[figure2]CONCLUSIONS: Post-C and IPC are not additive in decreasing apoptosis, suggesting that IPC alters the post-ischemic environment that prevents the post-C protection effect. Post-ischemic inflammation as reflected by inflammatory cell infiltration was decreased by Post-C.
DescriptionTopic: Experimental Neurosciences
Persistent Identifierhttp://hdl.handle.net/10722/141238

 

DC FieldValueLanguage
dc.contributor.authorRoth, Sen_US
dc.contributor.authorDreixler, JCen_US
dc.contributor.authorShaikh, ARen_US
dc.contributor.authorAlexander, Men_US
dc.contributor.authorMarcet, Men_US
dc.date.accessioned2011-09-23T06:28:51Z-
dc.date.available2011-09-23T06:28:51Z-
dc.date.issued2010en_US
dc.identifier.citationThe 2010 Annual Meeting of the American Society Anesthesiologists (ASA), San Diego, CA., 16-20 October 2010. In Conference Proceedings, 2010, abstract no. A1030en_US
dc.identifier.urihttp://hdl.handle.net/10722/141238-
dc.descriptionTopic: Experimental Neurosciences-
dc.description.abstractIschemic preconditioning (IPC) protects the rat retina against the deleterious effects of severe ischemia. Ischemic post-conditioning (Post-C) involves a brief ischemic stimulus delivered after ischemia. We studied the impact of Post-C on apoptosis following ischemia and the impact of combining IPC and Post-C. A second purpose of the study was analyze the effect of Post-C on inflammation following ischemia. METHODS: IPC and ischemia were induced in rats as previously described (1). IPC was 8 min ligation of the central retinal artery ([start_en]201C;ligation PC”) 24 h prior to ischemia, while post conditioning ([start_en]201C;Post-C') was increased intraocular pressure (IOP) for 5 min, beginning 10 min after the end of 55 min ischemia. Ketamine-xylazine anesthetized rats breathed spontaneously with temperature held constant at 36-37 C, whilst monitoring systemic blood pressure, and pulse oximetry. At 24 h after ischemia, when apoptotic injury peaks, retinas were removed and 7 micron frozen sections prepared, and stained using TUNEL. % TUNEL retinal ganglion cells (RGCs) was calculated using simultaneous staining with the nuclear dye, DAPI. Identity of the TUNEL-positive RGCs was confirmed by double labeling with RGC-specific anti-thy1 antibody. Inflammation was assessed on frozen retinal sections using antibodies specific for infiltrating macrophages (anti-MIP1), monocytes (anti-MCP), and leukocytes (anti-CD45). Data were quantitated using NIH Image. Data were analyzed as previously described (1). RESULTS: Figure 1 shows that TUNEL cells were thy-1 positive, identifying them as RGCs.[figure1]There was a significant reduction in TUNEL positivity with Post-C; previous application of IPC blocked the anti-apoptotic effect of Post-C (Table 1).[table1]There was no significant leukocyte infiltration, but both macrophages and monocytes infiltrated retinas after ischemia, with Post-C decreasing the macrophage infiltation (Figure 2).[figure2]CONCLUSIONS: Post-C and IPC are not additive in decreasing apoptosis, suggesting that IPC alters the post-ischemic environment that prevents the post-C protection effect. Post-ischemic inflammation as reflected by inflammatory cell infiltration was decreased by Post-C.-
dc.languageengen_US
dc.publisherAmerican Society Anesthesiologists (ASA).-
dc.relation.ispartofAnnual Meeting of the American Society Anesthesiologists, ASA 2010 Proceedingsen_US
dc.titlePost-ischemic conditioning decreases apoptosis after retinal ischemiaen_US
dc.typeConference_Paperen_US
dc.identifier.emailMarcet, M: marcet@hku.hken_US
dc.identifier.authorityMarcet, M=rp01363en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros194467en_US
dc.publisher.placeUnited States-

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