AI Article Synopsis
- Postischemic delayed hypoperfusion (PDH) arises from an imbalance of vasodilators and vasoconstrictors in the brain after ischemia.
- In a study with gerbils, PDH was observed 45 minutes post-reperfusion, leading to increased cerebral edema over time, although local blood flow recovered within 24 hours.
- The findings indicate that PDH contributes to the development of cerebral edema rather than the other way around, suggesting a complex interaction between these two processes.
Article Abstract
Postischemic delayed hypoperfusion (PDH) is based on the imbalance between local vasodilators and vasoconstrictors. We evaluated the time course of cerebral blood flow and cerebral specific gravity representing cerebral edema after transient forebrain ischemia induced by bilateral occlusion of the common carotid arteries in anesthetized gerbils to determine whether PDH is a significant factor in development of cerebral edema. PDH appeared 45 minutes after reperfusion followed by the increase of cerebral edema. Thereafter, the local cerebral blood flow recovered from PDH 24 hours after reperfusion in spite of the stable cerebral specific gravity. Furthermore, cerebral specific gravity established a linear correlation with the local cerebral blood flow 120 minutes after reperfusion in the 3 different durations of cerebral ischemia (30, 60, and 90 minutes). It is suggested that cerebral edema is not the cause in PDH development, but PDH may cause cerebral edema.
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| http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2006.12.001 | DOI Listing |
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