May 1, 1986Stroke
Endothelial dependent relaxation demonstrated in vivo in cerebral arterioles.
Key result
Endothelial injury in mouse pial arterioles abolished dilation to acetylcholine and bradykinin, converting the response to constriction, demonstrating in vivo endothelial dependence.
Why the study?
Does endothelial injury alter the relaxation response to acetylcholine or bradykinin in mouse pial arterioles?
Population
Mouse pial arterioles
Comparison
Endothelial injury in situ with a light/dye… vs Before injury (baseline) and uninjured vessels
Design
Preclinical
Authors
Discussion
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Implication
May reverse vasodilator responses after cerebral endothelial injury; leaves open human stroke relevance.
Key Points
- This research aims to investigate how endothelial injury affects the relaxation response of cerebral arterioles to acetylcholine and bradykinin.
- Mouse pial arterioles were injured in situ using a light/dye technique.
- The vasodilatory responses to acetylcholine and bradykinin were compared before and after the injury.
- Responses to papaverine were also measured as a control for dilation capability.
- After endothelial injury, arterioles failed to dilate to acetylcholine and bradykinin and instead constricted.
- Uninjured vessels continued to dilate normally to acetylcholine and bradykinin.
- The results confirm that endothelial health is crucial for the dilation response in cerebral arterioles.
Structured PICO
Does endothelial injury alter the relaxation response to acetylcholine or bradykinin in mouse pial arterioles?
P
Population
Mouse pial arterioles
I
Intervention
Endothelial injury in situ with a light/dye technique
C
Comparator
Before injury (baseline) and uninjured vessels
O
Outcome
Arteriolar response (dilation or constriction) to acetylcholine or bradykininsurrogate
Endothelial injury in cerebral microcirculation eliminates dilating influences and converts them to constricting forces, demonstrating the in vivo dependence of relaxation on a normal endothelium.
Cite This Study
William I. Rosenblum (1986) studied this question. Endothelial injury (light/dye technique) vs. Before injury / uninjured vessels was evaluated on Arteriole response to acetylcholine or bradykinin. Endothelial injury in mouse pial arterioles abolished dilation to acetylcholine and bradykinin, converting the response to constriction, demonstrating in vivo endothelial dependence.