Jeanwan Kang, MD, Hassan Albadawi, MD, Patrick J. Casey, MD, Thomas A

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The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion Jeanwan Kang, MD, Hassan Albadawi, MD, Patrick J. Casey, MD, Thomas A. Abbruzzese, MD, Virendra I. Patel, MD, Hyung-Jin Yoo, MS, Richard P. Cambria, MD, Michael T. Watkins, MD Journal of Vascular Surgery Volume 52, Issue 2, Pages 435-443 (August 2010) DOI: 10.1016/j.jvs.2010.03.021 Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 1 Temporal paralysis scores (A) through 48 hours after thoracic aortic ischemia-reperfusion (TAR) and (B) at 24 and 48 hours after TAR. The 38 TAR mice uniformly displayed dense neurologic deficit throughout the 48 hours of normothermic reperfusion (A and B). A, Mice subjected to systemic hypothermia (34 TAR) had much milder neurologic deficit upon recovery from anesthesia and had normal neurologic function by 1 hour reperfusion (*P < .0001 vs 38 TAR). B, Between 24 and 48 hours after reperfusion, about half of these mice had delayed paralysis (34 DP), whereas the other half remained with intact neurologic function (34 NP) (**P < .001 vs 38 TAR, +P < .001 vs 38 TAR and 34 DP). The data are presented with the standard error of the mean. Journal of Vascular Surgery 2010 52, 435-443DOI: (10.1016/j.jvs.2010.03.021) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 2 Photomicrographs show spinal cord histology results at 48 hours after thoracic aortic ischemia-reperfusion (TAR). Spinal cord sections stained with hematoxylin and eosin (H&E) from (A and B) 38 TAR mice demonstrate significant degree of injury, as indicated by replacement of normal architecture with vacuoles and paucity of motoneurons in the anterior half of the spinal cord. Spinal cords from (C and D) 34 DP mice also demonstrate evidence of injury; however, injury is limited to the periphery of the anterior horns compared with the spinal cords from 38 TAR mice. Finally, spinal cords from (E and F) 34 NP mice show no evidence of vacuolization or destruction of cord tissue (original magnification ×200). Journal of Vascular Surgery 2010 52, 435-443DOI: (10.1016/j.jvs.2010.03.021) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 3 The degree of injury to the spinal cord was quantified by looking at the number of viable motoneurons at (A) 24 and (B) 48 hours after thoracic aortic ischemia-reperfusion (TAR). A, At 24 hours, 38 TAR mice had a marked decrease in number of motoneurons (*P < .0001) compared with 34 TAR mice. There was no difference in the number of motoneurons between 34 TAR and sham mice. B, At 48 hours, 38 TAR mice had a significantly lower number of motoneurons than 34 DP (+P < .05) and 34 NP mice (++P < .001). In addition, 34 DP mice had a significantly lower number of motoneurons compared with 34 NP mice (**P < .001). The data are presented with the standard error of the mean. Journal of Vascular Surgery 2010 52, 435-443DOI: (10.1016/j.jvs.2010.03.021) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 4 Lung tissue levels at 24 and 48 hours' reperfusion are shown, respectively, for (A and B) keratinocyte chemokine (KC), (C and D) interleukin-6 (IL-6), and (E and F) myeloperoxidase (MPO). E, At 24 hours, MPO was the only marker of inflammation with significantly different levels between 34 and 38 TAR mice (**P = .01). At 48 hours, there was no difference in (B) lung KC, (D) IL-6, or (F) MPO levels among the experimental groups. There were two instances where 34 and 38 sham mice had significantly different levels of inflammatory markers: (A) KC at 24 hours (*P = .03) and (F) MPO at 48 hours (+P = .02). The data are presented with the standard error of the mean. Journal of Vascular Surgery 2010 52, 435-443DOI: (10.1016/j.jvs.2010.03.021) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 5 Liver levels at 24 and 48 hours' reperfusion are shown, respectively, for (A and B) keratinocyte chemokine (KC), (C and D) interleukin-6 (IL-6), and (E and F) myeloperoxidase (MPO). There was no difference in KC, IL-6, or MPO levels at either time point among any groups. The data are presented with the standard error of the mean. Journal of Vascular Surgery 2010 52, 435-443DOI: (10.1016/j.jvs.2010.03.021) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 6 Kidney levels at 24 and 48 hours' reperfusion are shown, respectively, for (A and B) keratinocyte chemokine (KC), (C and D) interleukin-6 (IL-6), and (E and F) myeloperoxidase (MPO). A, At 24 hours, there was a significantly higher level of KC in 38 TAR mice compared with 34 TAR mice (*P = .02). At 48 hours, there was significant difference in all three markers in the kidney among the experimental groups (B, **P = .02; D, ++P = .01; E, #P = .03). In addition, there was a significant difference in IL-6 levels between 34 sham and 38 sham mice at 24 hours (C, +P = .04). The data are presented with the standard error of the mean. Journal of Vascular Surgery 2010 52, 435-443DOI: (10.1016/j.jvs.2010.03.021) Copyright © 2010 Society for Vascular Surgery Terms and Conditions