Phosphate-related energy compounds are not exhausted in chronically hypoperfused rat brain cortex after cortical spreading depression

White Matter Damage and Hippocampal Neurodegeneration Induced by Permanent Bilateral Occlusion of Common Carotid Artery in the Rat: Comparison between Wistar and Sprague-Dawley Strain

“…In the case of Wistar rats, researchers have reported mortality rates ranging between 19.2% and 25%, comparable to the 29% mortality observed in this study (Hirabayashi et al, 2004;Liu et al, 2005). For SD rats, Sopala et al (2001) reported a 7% (2/27) mortality rate following BCCAO, which agrees with our observed rate of 7% (1/15) at three weeks post BCCAO induction.…”

“…Wistar rats failed to attain the sham-operated animals' weight gain after three weeks of BCCAO, whereas SD rats did. Similarly, Hirabayashi et al (2004) reported that the weight gain in Wistar rats during four weeks of BCCAO was significantly lower than that of the sham group, which implies perturbed nutritional intake behavior in rats with BCCAO. However, further studies are required to address the mechanism underlying the observed difference between the two strains.…”

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

“…Once again, corresponding constrictions have been observed in pial arteries (407,421,512), and reduced CBV by MRI, nearinfrared spectroscopy, multispectral reflectance, and intravascular dye imaging (18,71,195,227,351,407).…”

“…Direct pial artery diameter measurements showed a corresponding dilation (25-120%) in most studies, which appeared to be more prominent in smaller caliber arterioles than larger ones (16, 38, 46, 59, 64, 65, 314, 315, 407, 419 -422, 439, 460, 461, 512, 513). Multispectral reflectance, near-infrared spectroscopy, light transmission, and intravascular fluorescence imaging studies also showed hyperemia during SD in rats and cats (FIG-URE 5A; component II) (18,81,163,195,227,351,407,474,528). Hyperemia was further confirmed by magnetic resonance imaging (MRI), where CBV increased by ϳ30% for 1-2 min with a latency of 15-20 s after the apparent diffusion coefficient (ADC) changes during the depolarization (71).…”

“…In the post-SD period, tissue O 2 availability remains significantly reduced for up to 2 h as a result of the post-SD oligemia that leads to a reduction in tissue PO 2 (18,54,131,185,195,371,532). Despite this reduction in supply, CMRO 2 is increased after an SD for up to 2 h. In summary, O 2 delivery and availability can be reduced during the DC shift because of reduced delivery (initial hypoperfusion) and/or increased capillary transit time heterogeneity, and after CSD because of a reduced delivery (post-SD oligemia).…”