Global increase in cerebral metabolism and blood flow produced by focal electrical stimulation of dorsal medullary reticular formation in rat. Academic Article uri icon

Overview

abstract

  • We sought to determine whether the increases in local cerebral blood flow (LCBF) elicited by focal electrical stimulation within the dorsal medullary reticular formation (DMRF), are secondary to or independent of, increased local cerebral glucose utilization (LCGU). Rats were anesthetized (chloralose), paralyzed, artificially ventilated and arterial pressure and blood gases controlled. LCBF and LCGU were determined in two separate groups of animals, using the autoradiographic [14C]iodoantipyrine and [14C]2-deoxyglucose methods, respectively. In unstimulated controls, LCBF (n = 5) and LCGU (n = 5) were linearly related (r = 0.780; P less than 0.001) in the 27 brain regions studied. During DMRF stimulation LCGU increased significantly in 21 of the 27 regions, including cerebral cortex (up to 168% of control), thalamic nuclei (up to 161%) and selected ponto-medullary regions (e.g. parabrachial complex: 212%; vestibular complex: 147%). Along with LCGU, LCBF rose significantly in 25 regions (sensory motor cortex: 163%; anterior thalamus: 161%; parabrachial complex: 186%). Correlation analysis demonstrated that, during DMRF stimulation, the close relationship between LCBF and LCGU is preserved (r = 0.845; P less than 0.001) and that, in addition, the increase in LCBF (delta LCBF) is proportional to the increase in LCGU (delta LCGU) (delta LCBF = 2.18 delta LCGU + 6.92; r = 0.7729; P less than 0.001). Excitation of neurons or fibers within DMRF increases brain metabolism globally and blood flow secondarily. The DMRF appears to modulate cerebral metabolism globally, by as yet undefined pathways.

publication date

  • August 1, 1983

Research

keywords

  • Blood Glucose
  • Cerebrovascular Circulation
  • Medulla Oblongata
  • Reticular Formation

Identity

Scopus Document Identifier

  • 0020626205

Digital Object Identifier (DOI)

  • 10.1016/0006-8993(83)90367-0

PubMed ID

  • 6616188

Additional Document Info

volume

  • 272

issue

  • 1