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Dmitriy N. Atochin, Annie Wang, Victor W.T. Liu, Jeffrey D. Critchlow, Ana Paula V. Dantas, Robin Looft-Wilson, Takahisa Murata, Salvatore Salomone, Hwa Kyoung Shin, Cenk Ayata, Michael A. Moskowitz, Thomas Michel, William C. Sessa, Paul L. Huang
Published in Volume 117, Issue 7
J Clin Invest. 2007; 117(7):1961–1967 doi:10.1172/JCI29877
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Figure 5
Effect of S1179A and S1179D eNOS mutations on cerebral infarct size.

Mice were subjected to the filament model of MCA occlusion for 1 hour, followed by 23 hours of reperfusion. The brains were cut into 2-mm coronal sections and stained using 2,3,5-triphenyltetrazolium chloride. (A) Rostral to caudal distribution of infarct areas (mm2) in coronal sections. Abscissa shows the distance (mm) from the rostral surface of the brain. n = 7 mice for each group. *P < 0.05 versus corresponding sections from S1179A/eNOS KO mice; P < 0.05 versus corresponding sections from eNOS KO mice using 1-way ANOVA. (B) Infarct volumes were determined by integrating the infarct areas in each section over the entire brain, using the indirect method, which corrects for edema. *P < 0.05 versus infarct volume from S1179A/eNOS and from eNOS KO mice using ANOVA. Neurologic scores for each group of mice are as follows: eNOS KO, 2.5; S1179A/eNOS KO, 2.67; S1179D/eNOS KO, 1.57; WT, 1.86. Kruskal-Wallis 1-way ANOVA on ranks showed a statistically significant difference between eNOS KO and S1179A/eNOS KO mice and WT and S1179D/eNOS KO mice (P < 0.05).