2014 Volume 7 Issue 1 Pages 35
Purpose: Immediately after subarachnoid hemorrhage (SAH), brain injury begins and determines the acute phase mortality and the long-term prognosis, but its mechanism is not well understood. When SAH at the skull base induces platelet-leukocyte-endothelial cell interactions in venules, the cerebral blood flow is kept well at the cerebral surface1). We investigated cerebral microcirculation through a mouse cranial window using two-photon laser scanning microscopy at a depth of about 100µm2,3), after SAH was induced at the skull base.
Methods: Tracheotomy was performed and femoral artery was cannulated in mice (FVB/N-Tｇ (GFAP GFP) 14Mes/j). Q-dot 655 nanocrystal (Q21021MP; Invitrogen) or rhodamine-6G was injected from the cannulated femoral vein, after a craniotomy at the parietal bone without cutting dura matter. SAH was induced at a prone position by using the endovascular perforation model4). Immediately and one hour after SAH, blood cell velocities were measured with a line scan method in precapillary and capillary using two-photon laser scanning microscopy.
Results: A penetrating arteriole branched into a precapillary arteriole at the depth of 85.9 +/- 21.0µm (n=7). Arterioles dilated immediately after SAH and then gradually constricted (n=5/7) and the blood flow disappeared immediately after SAH in the others (n=2/7). The blood cell velocity of the precapillary arteriole decreased from 10.7 +/- 3.0 mm/s before SAH to 0.9 +/- 0.4 mm/s after SAH. The capillary-velocities of blood cells (red blood cells, platelets and leukocytes) also decreased, and rolling and adherent leukocytes prevented blood cells from flowing in capillaries.
Conclusion: The cerebral blood flow decreases in arterioles and capillaries, when the SAH is induced.