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Role of Nitric Oxide in Variations of the Response of Cerebral Blood Flow to Hypotension and Focal Ischemia

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Ischemic Blood Flow in the Brain

Summary

We contend that there are similarities between the vasoregulatory mechanisms near the lower limit of autoregulation and the region surrounding the ischemic core in focal cerebral ischemia. Cortical nitric oxide synthase (NOS) inhibition raises the lower limit of autoregulation and is thus at least partially responsible for the vasodilation that maintains cerebral blood flow as blood pressure falls from 100 mmHg to 60 mmHg. There are wide variations among animals in the pattern of autoregulation that cannot be explained by damaged vessels or nonphysiological factors. Specific neuronal NOS inhibition does not change the lower limit, suggesting that endothelial NOS mediates the vasodilation near the lower limit. Endothelial NOS immunolocalization in focal ischemia parallels these findings.

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© 2001 Springer Japan

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Jones, S.C., Kharlamov, A., Radinsky, C.R., Qu, Y., Easley, K.A. (2001). Role of Nitric Oxide in Variations of the Response of Cerebral Blood Flow to Hypotension and Focal Ischemia. In: Fukuuchi, Y., Tomita, M., Koto, A. (eds) Ischemic Blood Flow in the Brain. Keio University Symposia for Life Science and Medicine, vol 6. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67899-1_33

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  • DOI: https://doi.org/10.1007/978-4-431-67899-1_33

  • Publisher Name: Springer, Tokyo

  • Print ISBN: 978-4-431-67990-5

  • Online ISBN: 978-4-431-67899-1

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