Selective accumulation of monoclonal antibodies against neurospecific enolase in brain tissue of rats with middle cerebral artery occlusion

Local CBF (LCBF) was compared with the corresponding local tissue concentration of ATP, phosphocreatine (PCr), and lactate in anaesthetized baboons subjected to focal ischaemia produced by middle cerebral artery occlusion (MCAO). LCBF hydrogen electrodes were implanted in cortical regions where MCAO had been previously shown to produce severe and penumbral ischaemia and in posterior regions where blood flow is not altered. Metabolites were assayed in small tissue samples collected either by cryoprobe biopsy in the regions where LCBFs were measured (series 1) or by sampling appropriate regions of the rapidly frozen brain (series 2). Subsequent topographical study of brain tissue pH with umbelliferone was performed in this latter series. The results from these two series are compared and discussed in terms of the more appropriate way to perform simultaneous electrode measurements and analysis of tissue samples for studying focal ischaemia in the primate brain. They confirm that the concentrations of ATP and PCr decrease, and that lactate level increases, with decreasing blood flow. These metabolites tended to change more rapidly below a blood flow threshold, rather than showing a steady decrease as the blood flow was reduced, although the variability of the data precluded us from establishing this with confidence. Topographical study of tissue pH often showed sharp boundaries between zones of very low pH and regions with normal pH.

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Effect of Sevoflurane postconditioning on gene expression in brain tissue of the middle cerebral artery occlusion rat model

Molecular Biology Reports ◽

10.1007/s11033-012-1935-y ◽

2012 ◽

Vol 39 (12) ◽

pp. 10505-10513 ◽

Cited By ~ 16

Author(s):

Hai-Gen Liu ◽

Zhen Hua ◽

Yan Zhang ◽

Ya-Xin Wang ◽

Chun Meng ◽

...

Keyword(s):

Gene Expression ◽

Middle Cerebral Artery ◽

Middle Cerebral Artery Occlusion ◽

Brain Tissue ◽

Cerebral Artery ◽

Rat Model ◽

Artery Occlusion ◽

Cerebral Artery Occlusion ◽

Sevoflurane Postconditioning

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Brain tissue osmolality after middle cerebral artery occlusion in cats

Experimental Neurology ◽

10.1016/0014-4886(82)90231-x ◽

1982 ◽

Vol 77 (3) ◽

pp. 599-611 ◽

Cited By ~ 26

Author(s):

Y. Matsuoka ◽

K.-A. Hossmann

Keyword(s):

Middle Cerebral Artery ◽

Middle Cerebral Artery Occlusion ◽

Brain Tissue ◽

Cerebral Artery ◽

Artery Occlusion ◽

Cerebral Artery Occlusion ◽

Tissue Osmolality

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Reperfusion-Induced Temporary Appearance of Therapeutic Window in Penumbra after 2 h of Photothrombotic Middle Cerebral Artery Occlusion in Rats

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2008.147 ◽

2008 ◽

Vol 29 (3) ◽

pp. 565-574 ◽

Cited By ~ 10

Author(s):

Hiroshi Yao ◽

Narihiko Yoshii ◽

Toshiaki Akira ◽

Tatsuo Nakahara

Keyword(s):

Middle Cerebral Artery ◽

Water Content ◽

Middle Cerebral Artery Occlusion ◽

Brain Tissue ◽

Cerebral Artery ◽

Ischemic Injury ◽

Artery Occlusion ◽

Male Rats ◽

Ischemic Core ◽

Cerebral Artery Occlusion

To explore the effects of reperfusion on evolution of focal ischemic injury, spontaneously hypertensive male rats were subjected to photothrombotic distal middle cerebral artery occlusion (MCAO) with or without YAG laser-induced reperfusion. The volume of fodrin breakdown zone, water content, and brain tissue levels of sodium (Na+) and potassium (K+) were measured in the ischemic core and penumbra. Reperfusion attenuated fodrin breakdown, and the volume containing fodrin breakdown product at 3 h after reperfusion (5 h after MCAO) (30±7 mm3) was significantly smaller than the 42±3 mm3 of the permanent occlusion group. After 3 to 6 h of ischemia, Na+ increased, and K+ decreased in the ischemic core. Reperfusion after 2 h of MCA occlusion did not mitigate the ischemia-induced changes in brain tissue electrolytes and water content at 3 to 6 h of ischemia. Even in reperfusion after comparatively long periods of occlusion where brain infarction size, assessed 3 days after MCAO, was not significantly reduced by reperfusion, and the precipitating indicators of the ischemic core (Na+, K+, water content) did not improve, temporary improvement or a delay in progression of ischemic injury was discernible in the penumbra. These results indicate the possibility that treatment with reperfusion is permissive to the effects of neuroprotection.

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Comparison of the Effect of Etomidate and Desflurane on Brain Tissue Gases and pH during Prolonged Middle Cerebral Artery Occlusion

Anesthesiology ◽

10.1097/00000542-199805000-00008 ◽

1998 ◽

Vol 88 (5) ◽

pp. 1188-1194 ◽

Cited By ~ 57

Author(s):

William E. Hoffman ◽

Fady T. Charbel ◽

Guy Edelman ◽

Mukesh Misra ◽

James I. Ausman

Keyword(s):

Middle Cerebral Artery ◽

Middle Cerebral Artery Occlusion ◽

Brain Tissue ◽

Cerebral Artery ◽

Artery Occlusion ◽

Tissue Po2 ◽

Brain Tissue Oxygen Pressure ◽

Carbon Dioxide Pressure ◽

End Tidal ◽

Cerebral Artery Occlusion

Background The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in patients who had middle cerebral artery occlusion for > 15 min. Methods After a craniotomy, a probe that measures PO2, PCO2, and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. Results During baseline conditions, tissue PO2, PCO2, and pH were similar between the two groups (PO2 = 15 mmHg, PCO2 = 60 mmHg, pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue PO2 decreased in five of six patients without a change in PCO2 or pH. During administration of 9% desflurane, tissue PO2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). Conclusion These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue PO2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.

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