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Fig. 1 | BMC Neuroscience

Fig. 1

From: Thrombin contributes to the injury development and neurological deficit after acute subdural hemorrhage in rats only in collaboration with additional blood-derived factors

Fig. 1

Argatroban treatment does not affect the cerebral blood flow (CBF, Graph A) during the acute phase of ASDH. Two minutes after start of subdural infusion CBF dropped in all rats with a ASDH significant beneath the sham-operated animals and stayed there until end of recording (second minute: sham 32.6 ± 0.9 LDU, vehicle 20.5 ± 1.3 LDU, Argatroban 18.7 ± 1.7 LDU; Argatroban vs. vehicle n.s., **Argatroban vs. sham P < 0.001; **vehicle vs. sham P < 0.001, mean ± SEM). The NDS could not distinguish between vehicle or Argatroban treatment. Graph B presents the mean of each group by three trials per animal. Similarly, treatment with Argatroban had no effect on beam balance (C) performance (maximum time on beam was 60 s). Bars present the mean of each group by three trials per animal (sham 51.6 ± 2.0 s, vehicle [saline] 43.7 ± 5.6 s, Argatroban 53.8 ± 4.1 s; vehicle vs. Argatroban P > 0.05). Direct inhibition of thrombin with Argatroban (600 µg Argatroban/300 µl subdural infused blood) leads to a discreetly improved functional result and a slight reduction in the histological lesion volume compared to vehicle solution. Graph D and E show lesion volumes induced by subdural infusion of 300 µl blood after 14 days (Argatroban vs. vehicle P > 0.05, vehicle vs. sham P < 0.001 and Argatroban vs. sham P < 0.001). Images show hematoxylin–eosin stained brain sections at 1.25- and 2.5 fold magnification

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