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Postischemic cerebral blood flow and neuroeffector mechanisms
R Macfarlane1, M A Moskowitz, E Tasdemiroglu
1Stroke Research Laboratory, Neurology and Neurosurgery Services, Massachusetts General Hospital, Harvard Medical School, Boston.
Blood Vessels
|January 1, 1991
Summary
Trigeminal ganglionectomy reduced post-ischemic cerebral hyperemia by impairing neuroeffector mechanisms. Endothelium-dependent vasodilation was also impaired after cerebral ischemia, suggesting a role in regulating cerebral blood flow.
Area of Science:
- Neuroscience
- Cerebrovascular Physiology
- Neuropeptide Signaling
Background:
- Regulation of cerebral blood flow after ischemia is crucial for recovery.
- Neuroeffector mechanisms, involving neuropeptides like substance P, play a role in vascular responses.
- Endothelium-dependent vasodilation is a key factor in maintaining blood flow.
Purpose of the Study:
- To investigate the role of neuroeffector mechanisms in regulating post-ischemic cerebral blood flow.
- To determine the extent to which endothelium-dependent mechanisms contribute to hyperemia following global cerebral ischemia.
Main Methods:
- Microsphere determination in cats after unilateral trigeminal ganglionectomy.
- Induction of global cerebral ischemia followed by reperfusion.
- Topical application of acetylcholine to pial arterioles using a closed cranial window technique.
Main Results:
- Cortical hyperemia was significantly attenuated ipsilateral to trigeminal ganglionectomy.
- Acetylcholine, an endothelium-dependent vasodilator, induced vasoconstriction in pial arterioles during early reperfusion.
- Restoration of acetylcholine-induced vasodilation was delayed and incomplete after ischemia.
Conclusions:
- Neuroeffector mechanisms, particularly those involving the trigeminal nerve, are important for regulating post-ischemic cerebral blood flow.
- Endothelium-dependent vasodilation is impaired following cerebral ischemia, contributing to altered cerebral blood flow regulation.
- These findings highlight the complex interplay of neural and endothelial factors in cerebrovascular recovery.
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