Our goal was to determine whether responses of cerebral arteries are altered after cerebral ischemia and reperfusion. We measured diameter of cerebral arteries (150-180 μm) in cats in response to topical application of acetylcholine (ACh) and serotonin, which release endothelium-derived relaxing factor (EDRF), and adenosine and angiotensin, which do not release EDRF. Diameter of arteries was measured before and after 10 or 30 min of cerebral ischemia, when base-line diameter had returned to control levels. Under control conditions, serotonin and angiotensin constricted cerebral arteries by 16 ± 2 and 23 ± 3% (means ± SE), respectively, and ACh and adenosine dilated cerebral arteries by 22 ± 2 and 23 ± 3%, respectively. During reperfusion after 10 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. Vasodilator responses of arteries to ACh after 10 min of ischemia were heterogeneous. In 6 of 15 cats, vasodilatation in response to ACh was preserved. In contrast, in 9 of 15 cats, vasodilatation in response to ACh was impaired (7 ± 3%). In both groups, vasodilatation in response to adenosine was not impaired after 10 min of ischemia. During reperfusion after 30 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. In contrast, dilatation of cerebral arteries in response to ACh and adenosine was impaired. We speculate that impaired cerebral vasodilatation after ischemia, with maintenance of vasoconstriction, may contribute to impaired reperfusion after cerebral ischemia.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - 1988|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)