Poly(adenosine diphosphate ribose) polymerase inhibition modulates spinal cord dysfunction after thoracoabdominal aortic ischemia-reperfusion Patrick.

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Poly(adenosine diphosphate ribose) polymerase inhibition modulates spinal cord dysfunction after thoracoabdominal aortic ischemia-reperfusion Patrick J. Casey, MD, James H. Black, MD, Csaba Szabo, MD, PhD, Matthew Frosch, MD, PhD, Hassan Albadawi, MD, Min Chen, MD, PhD, Richard P. Cambria, MD, Michael T. Watkins, MD Journal of Vascular Surgery Volume 41, Issue 1, Pages 99-107 (January 2005) DOI: 10.1016/j.jvs.2004.10.040 Copyright © 2005 The Society for Vascular Surgery Terms and Conditions

Fig 1 Pathways to PARP activation. PARP is activated by DNA single strand breaks, which develop in response to intracellular/extracellular generation of reactive oxygen and/or nitrogen species. PARP activation exacerbates underlying energy crisis brought on by pre-existing ischemia or mitochondrial dysfunction during tissue reperfusion. Depletion of reduced nicotinamide adenine dinucleotide and ATP contributes to tissue injury, cell necrosis, and endothelial dysfunction. Journal of Vascular Surgery 2005 41, 99-107DOI: (10.1016/j.jvs.2004.10.040) Copyright © 2005 The Society for Vascular Surgery Terms and Conditions

Fig 2 Paralysis scoring after thoracic aortic ischemia-reperfusion. PS was markedly decreased in the PARP −/− (KO) vs untreated (UN) animals (*P < .001), but not PJ mice on awakening. After awakening, the PS in the PJ mice was markedly less than in UN mice (**P < .001). The KO mice were normal after 6 hours of reperfusion. Journal of Vascular Surgery 2005 41, 99-107DOI: (10.1016/j.jvs.2004.10.040) Copyright © 2005 The Society for Vascular Surgery Terms and Conditions

Fig 3 Cross-sectional spinal cord anatomy of an untreated mouse (original magnification, ×10). Forty-eight hours after TAR, global depletion of anterior motor neuron cells (A) with preservation of the sensory posterior columns (P) is demonstrated in this photomicrograph of the thoracolumbar spine. The dorsal sensory nuclei were preserved (D). Journal of Vascular Surgery 2005 41, 99-107DOI: (10.1016/j.jvs.2004.10.040) Copyright © 2005 The Society for Vascular Surgery Terms and Conditions

Fig 4 High power photomicrographs of the thoracolumbar spinal cord (original magnification, ×40). A, Evidence of chromalytic Nissl bodies in an anterior motor neuron of an untreated mouse 48 hr after TAR (black solid arrows). B, Evidence of preserved motor nuclei in a Sham animal (white solid arrows). C, Axonal spherocytosis in an untreated animal 48 hr after TAR (dotted black arrows). Journal of Vascular Surgery 2005 41, 99-107DOI: (10.1016/j.jvs.2004.10.040) Copyright © 2005 The Society for Vascular Surgery Terms and Conditions

Fig 5 Distal thoracic spinal cord photomicrographs (original magnification, ×10). Untreated mice show widespread depletion of anterior motor neuron cells, whereas PJ and PARP −/− (KO) mice exhibit preserved anterior motor neurons. Journal of Vascular Surgery 2005 41, 99-107DOI: (10.1016/j.jvs.2004.10.040) Copyright © 2005 The Society for Vascular Surgery Terms and Conditions

Fig 6 PAR immunohistochemistry murine spinal cord at 48 hr (original magnification, ×40). A, Sham mouse cord demonstrating many anterior motor neurons and no intense PAR staining. B, PJ mouse with abundant anterior motor nuclei and sparse PAR staining. C, Untreated mouse cord demonstrating few anterior motor nuclei and focal intense PARS staining. Journal of Vascular Surgery 2005 41, 99-107DOI: (10.1016/j.jvs.2004.10.040) Copyright © 2005 The Society for Vascular Surgery Terms and Conditions