Pial arterial pressure in cats following middle cerebral artery occlusion. II. Relationship to regional disturbance of energy metabolism.


Journal Article

Focal cerebral ischemia was produced in 16 cats by occluding the left middle cerebral artery (MCA) for 120 min. Cortical blood flow and pial artery pressure were determined prior to vascular occlusion and after 15, 60 and 120 min. At the end of the experiments (after 120 min MCA occlusion) heads were frozen in situ with liquid nitrogen. Cooled brains were cut into 0.5 cm thick slices. From these slices twenty-micron sections passing through the territory of the MCA were prepared in a cryostat and used in the pictorial presentation of glucose and ATP. NADH-fluorescence was recorded from the tissue slice, immersed in liquid nitrogen. In addition, tissue samples were taken from regions of interest and used for quantitative determination of biochemical substrates. In all but two animals permanent MCA occlusion led to disturbances in the energy-producing metabolism, as indicated by reduction in glucose and ATP, and increase in lactate. The regions exhibiting bright NADH-fluorescence were much smaller than those in which ATP was absent. In 6 animals NADH-fluorescence was not increased but even decreased in areas with disturbed energy-producing metabolism. A close correlation was obtained after comparing cortical blood flow measured 15 min after MCA occlusion with the area of ATP-depletion at the end of the experiments. However, the size of ATP-depletion did not correlate with flow measured 60 or 120 min after MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Full Text

Cited Authors

  • Paschen, W; Shima, T; Hossmann, KA

Published Date

  • July 1, 1984

Published In

Volume / Issue

  • 15 / 4

Start / End Page

  • 686 - 690

PubMed ID

  • 6464061

Pubmed Central ID

  • 6464061

Electronic International Standard Serial Number (EISSN)

  • 1524-4628

International Standard Serial Number (ISSN)

  • 0039-2499

Digital Object Identifier (DOI)

  • 10.1161/01.str.15.4.686


  • eng