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Effect of postischemic hypoperfusion on vasodilatory mechanisms in cats
N Clavier1, J R Kirsch, P D Hurn
1Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-4963.
The American Journal of Physiology
|November 1, 1994
Summary
Global cerebral ischemia impairs brain blood vessel response to muscarinic stimulation, suggesting a defect in nitric oxide (NO) synthesis or breakdown in the endothelium.
Area of Science:
- Neuroscience
- Vascular Biology
- Cerebrovascular Physiology
Background:
- Reduced cerebral blood flow (CBF) after ischemia can impair brain function.
- Pial vascular reactivity is crucial for regulating CBF.
- Muscarinic stimulation plays a role in regulating cerebral vascular tone.
Purpose of the Study:
- To investigate the mechanism of reduced pial vascular reactivity following global cerebral ischemia.
- To determine if the impairment involves receptor-dependent or independent pathways.
- To assess the role of nitric oxide (NO) in post-ischemic vascular dysfunction.
Main Methods:
- Cats were subjected to global cerebral ischemia or served as controls.
- Pial arteriolar diameters and CBF were measured using intravital microscopy and microspheres.
- Vascular responses to acetylcholine (ACh), A-23187, nitroprusside (NP), and oxotremorine were evaluated.
Main Results:
- Post-ischemic hypoperfusion was observed.
- Pial arteries showed attenuated dilation to ACh and A-23187 after ischemia.
- Dilation to the NO donor NP remained intact.
- CBF response to oxotremorine was decreased post-ischemia.
Conclusions:
- Endothelium-dependent vasodilation is impaired during post-ischemic hypoperfusion.
- Vascular smooth muscle responsiveness to nitric oxide is preserved.
- The defect in signal transduction likely involves abnormalities in NO synthesis or degradation within the endothelium.