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Capillary patency after transient middle cerebral artery occlusion of 2 h duration
1Center for the Study of Neurological Diseases, The Neuroscience Institute, Queen's Medical Center, Honolulu, HI 96813, USA. pingan@www.cns.queens.org
Abstract:
Reperfusion after transient focal ischemia of 2 h duration is followed by secondary bioenergetic failure after 4 h of reperfusion. The objective of the present study was to explore whether or not this secondary deterioration is due to secondary microcirculatory compromise. Normal fasted rats were subjected to 2 h of MCA occlusion and allowed reperfusion for 2, 4, 6 and 8 h. At predetermined reperfusion times, rats were injected with Evans blue and decapitated. Capillary patency was determined using a fluorescent double-staining technique. No capillary perfusion deficits were detected in the ischemic neocortical penumbra, neocortical focus or striatal focus. We concluded that the secondary deterioration of bioenergetic state is not due to microcirculatory compromise. Since hyperglycemic animals show pan-necrotic lesions, a hyperglycemic group was added at 8 h of reperfusion to test if the adverse effect of hyperglycemia on ischemic damage is related to capillary compromise. The results showed that, in hyperglycemic rats, capillary perfusion in the striatal focus was compromised after 8 h of recirculation following 2 h of MCA occlusion. It is concluded that when normoglycemic rats are subjected to 2 h of MCA occlusion, capillary patency is not affected during the first 4-6 h of reflow. At 8 h of reflow, though, particularly in hyperglycemic rats, microcirculation is compromised in the caudoputamenal focus, probably reflecting infarction.
Insights
Secondary bioenergetic failure after stroke reperfusion is not caused by microcirculatory compromise in normoglycemic rats. However, hyperglycemia exacerbates this damage by impairing capillary patency.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Ischemic Stroke
Background:
- Transient focal ischemia can lead to secondary bioenergetic failure during reperfusion.
- The underlying cause of this secondary deterioration remains unclear.
Purpose of the Study:
- To investigate if secondary microcirculatory compromise contributes to bioenergetic failure after focal cerebral ischemia.
- To examine the role of hyperglycemia in exacerbating ischemic damage and its relation to microcirculation.
Main Methods:
- Rats underwent 2-hour middle cerebral artery (MCA) occlusion followed by 2, 4, 6, or 8 hours of reperfusion.
- Capillary patency was assessed using fluorescent double-staining and Evans blue injection.
- Hyperglycemic rats were included to evaluate the effect of high blood glucose on microcirculation.
Main Results:
- No capillary perfusion deficits were observed in normoglycemic rats during the first 4-6 hours of reperfusion.
- In hyperglycemic rats, capillary perfusion was compromised in the striatal focus at 8 hours of reperfusion.
- Microcirculatory compromise was noted in the caudoputamenal focus at 8 hours of reperfusion, particularly in hyperglycemic conditions.
Conclusions:
- Secondary bioenergetic failure after focal ischemia in normoglycemic rats is not attributed to microcirculatory compromise.
- Hyperglycemia significantly impairs capillary patency during reperfusion, potentially contributing to increased ischemic damage.
- Microcirculatory compromise may play a role in later stages of infarction, especially under hyperglycemic conditions.