1. Age-dependent cerebral vasodilation induced by volatile anesthetics is mediated by NG2 + vascular mural cells.
- Author
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Zhou H, Neudecker V, Perez-Zoghbi JF, Brambrink AM, and Yang G
- Subjects
- Animals, Mice, Isoflurane pharmacology, Cerebrovascular Circulation drug effects, Male, Sevoflurane pharmacology, Mice, Inbred C57BL, Female, KATP Channels metabolism, KATP Channels genetics, Brain blood supply, Brain metabolism, Brain drug effects, Age Factors, Arterioles drug effects, Arterioles metabolism, Vasodilation drug effects, Anesthetics, Inhalation pharmacology
- Abstract
Anesthesia can influence cerebral blood flow by altering vessel diameter. Using in vivo two-photon imaging, we examined the effects of volatile anesthetics, sevoflurane and isoflurane, on vessel diameter in young and adult mice. Our results show that these anesthetics induce robust dilation of cortical arterioles and arteriole-proximate capillaries in adult mice, with milder effects in juveniles and no dilation in infants. This anesthesia-induced vasodilation correlates with decreased cytosolic Ca
2+ levels in NG2+ vascular mural cells. Optogenetic manipulation of these cells bidirectionally regulates vessel diameter, and their ablation abolishes the vasodilatory response to anesthetics. In immature brains, NG2+ mural cells are fewer in number and express lower levels of Kir6.1, a subunit of ATP-sensitive potassium channels. This likely contributes to the age-dependent differences in vasodilation, as Kir6.1 activation promotes, while its inhibition reduces, anesthesia-induced vasodilation. These findings highlight the essential role of NG2+ mural cells in mediating anesthesia-induced cerebral vasodilation., Competing Interests: Competing interests The authors declare no competing interests., (© 2024. The Author(s).)- Published
- 2024
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