Using 14C- iodoantipyrine or -IMP to measure rCBF, the lowest rCBF was detected at day 3–7, returned to normal after day 14. In this study, we found rCBF in G3 and G4 groups decreased to the minimal value at 3 days of SAH and recovered to 50% at 7 days of SAH. Our results of -IMP was agree with the course vasospasm, which was observed by SRA. However, this CBF measurement only provided terminal evaluations. Surface CBF measured by LDF was deemed as an in vivo method. The CBF of MCA supplying area began to decrease immediately after SAH induction and reached the lowest CBF only in a few seconds, and it maintained at a steady low level up to 150 minutes. We drilled four holes to measure cortical CBF; we observed the lowest CBF at 30 minutes after SAH induction, which was in alignment with the results of Westermaier’s. The changes of surface CBF at 1 to 7 days of SAH were corroborated with rCBF changes at 1, 3, 5 and 7 days of SAH, but they did not match each other entirely. The positive correlation of SRA imaging and surface CBF supported the hypothesis that diameter changes of cerebral artery reflected the tendency of CBF changes. The limitation of SRA is that this performance is Ganoderic-acid-G an invasive and irradiative technique: a PE-10 tube has to be inserted into ECA; therefore, the catheterized ECA had to be sacrificed. In addition, the imaging window is currently limited to 45 mm62.5 mm, and it has to be scanned at least four frames to cover the whole hemispheric brain area. Finally, X-ray can damage brains. To limit the changes of blood vessels caused by radiation, we chose different groups of rats for SRA study after SAH. Using real time SRA to detect fine changes of cerebral vessels through accomplishment of intravenous cerebral angiography and low irradiation may be developed. We chose two injection models to perform this study instead of artery puncture model owing to the operated simplicity and clinical similarity. To exclude the flaws of these two injection models, we made an additional group of cerebral artery puncture SAH model according to the previous report. We found that the mortality in this model was 27%, which was similar with blood injection models. While neurological score in this model was higher,Ganoderic-acid-F suggesting the clinical symptom of this vessel puncture model was not so severe as that of injection models. There were many controversies of these two injection models. The advantage of prechiasmatic cistern injection model was its similarity to clinical rupture of aneurysm, but the mortality was high. The mortality of cisterna magna injection model was low ; however, whether this model could produce pronounced vasospasm of the circle of Willis, especially anterior circulation arteries, remained unfathomed. In our study, mortality of cisterna magna injection model was 23%, which was consistent with some studies, but it was much higher than our expectation. According to the intracranial pressure monitor, the mortality was probably not due to high ICP into cisterna magna. We considered the high mortality of cistern magna injection SAH model was on account of the subarachnoid base, at which we injected blood, being close to the juncture of medulla and spinal cord. Furthermore, one rat of saline cisterna magna injection died during operation, we believed the death might be the result of brain stem injury from the PE-10 tube or the little bulb for ICP measurement. It suggested that the technique used to induce cisterna magna injection might possibly result in brain stem injury. Mortality of prechiasmatic cistern injection model was 13%, which was lower than Prunell’s report and in accordance with another study. According to the results of LDF-CBF, -IMP CBF, histological outcomes and SRA, the course of anterior circulation arteries vasospasm in these two models appeared similar.