Relationship between Regional Calcium Content and Energy Metabolism during Recovery from Prolonged Cerebral Ischemia

Author(s):  
B. Grosse Ophoff ◽  
K. -A. Hossmann ◽  
W. Bodsch ◽  
W. Paschen
2001 ◽  
Vol 21 (4) ◽  
pp. 430-439 ◽  
Author(s):  
Laszlo Olah ◽  
Stefan Wecker ◽  
Mathias Hoehn

Changes in apparent diffusion coefficients (ADC) were compared with alterations of adenosine triphosphate (ATP) concentration and pH in different phases of transient focal cerebral ischemia to study the ADC threshold for breakdown of energy metabolism and tissue acidosis during ischemia and reperfusion. Male Wistar rats underwent 1 hour of middle cerebral artery occlusion without recirculation (n = 3) or with 1 hour (n = 4) or 10 hours of reperfusion (n = 5) inside the magnet, using a remotely controlled thread occlusion model. ADC maps were calculated from diffusion-weighted images and normalized to the preischemic value to obtain relative ADC maps. Hemispheric lesion volume (HLV) was determined on the last relative ADC maps at different relative ADC thresholds and was compared to the HLV measured by ATP depletion and by tissue acidosis. The HLVs, defined by ATP depletion and tissue acidosis, were 26.0% ± 10.6% and 38.1% ± 6.5% at the end of ischemia, 3.3% ± 2.4% and 4.8% ± 3.5% after 1 hour of reperfusion, and 11.2% ± 4.7% and 10.9% ± 5.2% after 10 hours of recirculation, respectively. The relative ADC thresholds for energy failure were consistently approximately 77% of the control value in the three different groups. The threshold for tissue acidosis was higher at the end of ischemia (86% of control) but was similar to the results obtained for ATP depletion after 1 hour (78% of control) and 10 hours (76% of control) of recirculation. These results indicate that the described relative ADC threshold of approximately 77% of control provides a good estimate for the breakdown of energy metabolism not only during middle cerebral artery occlusion but also at the early phase of reperfusion, when recovery of energy metabolism is expected to occur, or some hours later, when development of secondary energy failure was described.


Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 35-42 ◽  
Author(s):  
KMA Welch ◽  
JA Helpern ◽  
JR Ewing ◽  
WM Robertson ◽  
G D'Andrea

Although decreased CBF has now been reported during the prodrome of migraine, the cause of the decreased flow is still unknown. It is particularly unclear whether these phenomena are related to vasospasm and “steal” between the extracranial and intracranial circulation or to the spreading depression of Leao and the accompanying metabolic depression. In the present paper, metabolic changes in the brain during ischemia and reperfusion are reviewed and compared with CNS biochemical changes during migraine attack. In addition, the technique of Topical Magnetic Resonance (TMR) as applied to the in vivo study of energy phosphate metabolism in extracranial tissues and brain is described and the potential of this technique to evaluate shifts in energy metabolism and pH in stroke and migraine is discussed.


1997 ◽  
Vol 85 (3) ◽  
pp. 593-599 ◽  
Author(s):  
Yoshiki Nakajima ◽  
Goroku Moriwaki ◽  
Kazuyuki Ikeda ◽  
Yutaka Fujise

2002 ◽  
Vol 333 (2) ◽  
pp. 91-94 ◽  
Author(s):  
Jun Yang ◽  
Lori K Klaidman ◽  
Artak Nalbandian ◽  
Jasmine Oliver ◽  
Mei L Chang ◽  
...  

1988 ◽  
Vol 8 (4) ◽  
pp. 462-473 ◽  
Author(s):  
J.-P. Nowicki ◽  
C. Assumel-Lurdin ◽  
D. Duverger ◽  
E. T. MacKenzie

Focal cerebral ischemia in the rat was induced by occlusion of the left middle cerebral artery. The temporal evolution of regional energy metabolism was studied over the 14 days consequent to the induction of ischemia in the frontal, cingulate, parietal, and occipital cortices as well as in the striatum. Regional concentrations of adenosine triphosphate (ATP), phosphocreatine, and lactate and, in addition, glucose and the cerebral/plasma glucose ratio (C/P) were measured in the hemispheres both ipsilateral and contralateral to the occlusion. Two hours after middle cerebral artery occlusion, the biochemical changes were severe in the striatum and moderate in cortical regions. Later on (at 24 and 48 h), an overall aggravated metabolic status was noted while lactate declined and glucose markedly increased. These latter biochemical changes likely indicate a marked inhibition of the rate of glucose utilization. At 48 h, the energy reserves (ATP, phosphocreatine) of parietal cortex no longer equaled those of other cortical regions, but abruptly fell to the levels found in the striatum without any increase in lactate level. Finally, at 7 and 14 days, the levels of the various metabolites in most cortical regions returned toward control values, although signs of a depressed glucose metabolism remained. However, in both striatum and parietal cortex, ATP and phosphocreatine concentrations, although higher than those observed at 48 h, remained significantly decreased. Our present biochemical study permits the classification of these selected brain regions into three categories. First there are those that are outside the area of infarction: the frontal, cingulate, and occipital cortices. These regions show little temporal evolution of brain energy metabolism but, notwithstanding, they are regions in which glucose use would appear to be greatly depressed. Second is a region considered to be the focus of infarction: the striatum. The caudate-putamen is a region with early and profound metabolic disturbances with no final restitution. Last is the region of metabolic penumbra—the parietal cortex, in which there is a time-related exacerbation of the consequences of middle cerebral occlusion in the rat.


2000 ◽  
Vol 47 (4) ◽  
pp. 485-492 ◽  
Author(s):  
Tobias Back ◽  
Mathias Hoehn ◽  
G�nter Mies ◽  
Elmar Busch ◽  
Bernd Schmitz ◽  
...  

Nosotchu ◽  
1986 ◽  
Vol 8 (5) ◽  
pp. 433-439 ◽  
Author(s):  
Toshihiro Higuchi ◽  
Shoji Naruse ◽  
Yoshiharu Horikawa ◽  
Chuzo Tanaka ◽  
Kimiyoshi Hirakawa

Sign in / Sign up

Export Citation Format

Share Document