Regional assessment of energy-producing metabolism following prolonged complete ischemia of cat brain.


Journal Article

The regional content of biochemical substrates of energy-producing metabolism was assessed in cat brains following prolonged cerebral ischemia. Ischemia was produced by intrathoracic occlusion of the innominate, the left subclavian, and both mammarian arteries, and additional lowering of the systolic blood pressure to 80 mm Hg. After 60 min of global ischemia and 3 h of recirculation, the regional distribution of glucose, ATP, and NADH was evaluated on intact brain sections by bioluminescence and fluorescence techniques. Additionally, the content of different substrates related to energy and redox state was assessed in small tissue samples. Recirculation following global ischemia led to three different patterns of biochemical substrates: in 6 of 14 animals, regional distribution of glucose, ATP, and NADH was similar to that of control animals. These animals exhibited recovery of evoked potentials and reappearance of low-voltage EEG activity. In five animals, ATP was decreased in small circumscribed regions belonging to border zones of cerebral vessels. In these regions, glucose was high and NADH-fluorescence was low, indicating that glucose deficiency was not the limiting factor for ATP depletion. In this group, evoked potentials recovered, but the EEG did not. In three animals, glucose and ATP were low throughout the whole brain, and electrophysiological recovery was absent. The pattern and localization of biochemical lesions and the correlation with hemodynamic and electrophysiological parameters suggest that disturbances of energy-producing metabolism are caused by regional ischemic episodes during the recirculation period and can be prevented by the immediate and homogeneous blood reperfusion of the brain after cerebrocirculatory arrest.

Full Text

Cited Authors

  • Paschen, W; Hossmann, KA; van den Kerckhoff, W

Published Date

  • September 1, 1983

Published In

Volume / Issue

  • 3 / 3

Start / End Page

  • 321 - 329

PubMed ID

  • 6874741

Pubmed Central ID

  • 6874741

Electronic International Standard Serial Number (EISSN)

  • 1559-7016

International Standard Serial Number (ISSN)

  • 0271-678X

Digital Object Identifier (DOI)

  • 10.1038/jcbfm.1983.47


  • eng