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Stroke involves cerebral infarction and hemorrhaging and is associated with very high mortality. Previous reports have indicated that ischemic stimulation such as the reoxygenation that occurs after hypoxia produces a large quantity of reactive oxygen species (ROS) that strongly induces neuronal death in vivo and in vitro (Negishi et al., 2001). Indeed, this is considered to be the factor that most strongly induces cell death in cerebral ischemia. In recent years, apoptosis has been suggested to be the mechanism responsible for ischemic neuronal death in animal stroke models (Tagami et al., 1998). Stroke-prone spontaneously hypertensive rats (SHRSP) are widely used as a model of human stroke (Yamori et al., 1974). In this model, blood pressure is elevated as age increases, as is found in humans; and the rats eventually die of stroke. One feature of this model is that strokes develop spontaneously following severe hypertension (more than 150 mmHg). Therefore, in SHRSP, because strokes develop after the onset of elevated blood pressure, elevated blood pressure is considered to be the most critical factor for stroke induction. However, interestingly, the neuronal cells of this model exhibit a great vulnerability compared with normal control WKY/Izm rats during the reoxygenation conditions following hypoxia (Tagami et al., 1998; Yamagata et al., 2010c). In addition to the influence of blood pressure in SHRSP/Izm rats, the neuronal vulnerability of this model strongly contributes to stroke development. SHRSP/Izm rats are susceptible to apoptosis under conditions of hypoxia and reoxygenation (H/R) (Tagami et al., 1998). The expression of antioxidant enzymes in SHRSP/Izm rats is attenuated in comparison with that in WKY/Izm rats. We highlight that this attenuation of antioxidant enzymes is related to the vulnerability of neuronal cells (Yamagata et al., 2000b). Furthermore, an altered susceptibility to apoptosis was detected in the astrocytes of SHRSP/Izm rats compared with those of WKY/Izm rats (Yamagata et al., 2010a).

Ischemic Neurodegeneration in Stroke-Prone Spontaneously Hypertensive Rats and Its Prevention with Antioxidants Such as Polyphenols