Reperfusion-induced temporary appearance of therapeutic window in penumbra after 2 h of photothrombotic middle cerebral artery occlusion in rats

• Published in: Journal of cerebral blood flow and metabolism 2009-03, Vol.29 (3), p.565-574
• Main Authors: Yao, Hiroshi, Yoshii, Narihiko, Akira, Toshiaki, Nakahara, Tatsuo
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Flow Velocity - physiology; Brain Edema - etiology; Brain Edema - pathology; Brain Edema - prevention & control; Carrier Proteins - metabolism; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges; Cerebral Cortex - blood supply; Cerebral Cortex - pathology; Cerebrovascular Circulation - physiology; Disease Models, Animal; Electrolytes - metabolism; Fluorescent Dyes - administration & dosage; Fundamental and applied biological sciences. Psychology; Infarction, Middle Cerebral Artery - etiology; Infarction, Middle Cerebral Artery - metabolism; Infarction, Middle Cerebral Artery - pathology; Infarction, Middle Cerebral Artery - therapy; Laser Therapy; Lasers - adverse effects; Male; Medical sciences; Microfilament Proteins - metabolism; Neurology; Neuroprotective Agents - administration & dosage; Rats; Rats, Inbred SHR; Reperfusion - instrumentation; Reperfusion - methods; Rose Bengal - administration & dosage; Time Factors; Vascular diseases and vascular malformations of the nervous system; Vertebrates: nervous system and sense organs
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.2008.147

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.