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. Author manuscript; available in PMC: 2012 Feb 4.
Published in final edited form as: Exp Neurol. 2011 Dec 8;233(1):566–574. doi: 10.1016/j.expneurol.2011.11.044

Fig. 3.

Fig. 3

Comparative effects of glibenclamide and riluzole on progressive hemorrhagic necrosis, capillary fragmentation and neuron counts. A: Representative longitudinal sections of perfusion-cleared spinal cords through the epicenter of injury 16 h after impact, in rats administered vehicle (V), riluzole (R) or glibenclamide (G) within 2 min of impact; a millimeter scale is shown at left; the bar graph (right) depicts the average lesion areas in the 3 groups; 3 rats per group; *Pb 0.05; **Pb 0.01 with respect to control. B–D: Images at low (left panels) and at high (right panels) magnification of spinal cord sections in the region of the penumbra immunolabeled for laminin, from rats administered vehicle (B), riluzole (C) or glibenclamide (D); same tissues as above; the epicenter of injury is denoted by an asterisk; the region shown at high magnification in the panel on the right is indicated by an arrow in the panel on the left. E: Histograms of the lengths of penumbral microvessels in rats administered vehicle, riluzole or glibenclamide. F: Counts of NeuN-positive neurons in contralateral gray matter in rats administered vehicle, riluzole or glibenclamide; same tissues as above; *Pb 0.05; **Pb 0.01 with respect to control.