Skip to main content
. 2016 Jan 1;37(8):2780–2794. doi: 10.1177/0271678X16675368

Figure 1.

Figure 1.

NKCC1 inhibitor BMT attenuates ischemic stroke-mediated exacerbation of infarction and improves sensorimotor deficits in SHR. (a) Experimental protocol and data collection. BMT: bumetanide; tMCAO: transient middle cerebral artery occlusion. (b) rCBF measurements during and after 2-h tMCAO were indistinguishable in SHR and WKY rats. (c) Representative TTC staining images in WKY and SHRs at 24-h reperfusion, with quantitative analysis of infarct volume (d) and percent hemisphere swelling (e). Saline or bumetanide (10 mg/kg body weight/day in saline) was administered via intra-peritoneal injection, with an initial BMT dose (5 mg/kg) at 3 h and the second dose (5 mg/kg) at 8-h reperfusion and followed by two daily injections (bid). Data are mean ± SD, n = 4, *p < 0.05. (f) Turning-in-alley test latency. Data are mean ± SD, n = 8, *p < 0.05. (g) Neurological deficit scores in WKY and SHRs. Data are mean ± SD, n = 8, *p < 0.05 vs. respective control.