Nitric Oxide in Brain Glucose Retention after Carotid Body Receptors Stimulation with Cyanide in Rats
In contrast to most other tissues, which exhibit considerable flexibility with respect to the nature of the substrates for their energy metabolism, the normal brain is restricted almost exclusively to glucose due to its distinguishing characteristics in vivo. Actual glucose utilization is 31 μmol/100 g tissue/min, in the normal, conscious human brain, indicating that glucose consumption is in excess for total oxygen consumption (Sokoloff, 1991). Although present in low concentration in brain (3.3 mmol/kg in rat), glycogen is a unique energy reserve for initiation of its metabolism. However, if glycogen concentration in the brain were the sole supply, normal energetic requirements would be maintained for less than 5 min (Sokoloff, 1991).
KeywordsNitric Oxide Nitric Oxide Carotid Body Saline Injection Carotid Sinus
Unable to display preview. Download preview PDF.
- Buerk D.G., Lahiri S. Evidence that nitric oxide plays a role in O2 sensing from tissue NO and PO2 measurements in cat carotid body. Adv. Exp. Med. Biol 2000; 475: 337–347.Google Scholar
- Hudson L.C., Hughes C.S., Bold-Fletcher N.O., Vaden, S.L. (1994). Cerebrospinal fluid collection in rats: modification of a previous technique. Lab Animal Sci, 44: 358–361.Google Scholar
- Kadekaro M., Terrell M. L., Liu H., Gestl S., Bui V., Summy-Long, J.Y. Effects of L-NAME on cerebral metabolic, vasopressin, oxytocin, and blood pressure responses in hemorrhaged rats. American Journal of Physiology 1998; 274: 1070–1077.Google Scholar
- Sokoloff, Louis. “Measurement of local cerebral glucose utilization and its relation to local functional activity in the brain.” In Fuel Homeostasis and the Nervous System, M. Vranic and et al. eds. New York: Plenum Press, 1991; pp. 21–42Google Scholar
- Uemura K., Tamagawa T., Chen Y., Maeda N., Yoshioka S., Itoh K., Miura H., Iguchi A., Hotta N. NG-methyl-L-arginine, an inhibitor of nitric oxide synthase, affects the central nervous system to produce peripheral hyperglycemia in conscious rats. Neuroendocrinol 1997; 66: 136–144.Google Scholar