Effects of Indomethacin on Myogenic Contractile Activation and Responses to Changes in O2 and CO2 in Isolated Feline Cerebral Arteries
Author(s) -
Nan A. Norins,
Karen J. Wendelberger,
Raymond G. Hoffman,
Peter A. Keller,
Jane A. Madden
Publication year - 1992
Publication title -
journal of cerebral blood flow and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.167
H-Index - 193
eISSN - 1559-7016
pISSN - 0271-678X
DOI - 10.1038/jcbfm.1992.118
Subject(s) - myogenic contraction , cerebral arteries , contraction (grammar) , chemistry , anatomy , artery , prostaglandin , medicine , smooth muscle , biophysics , biology
We used an isolated, pressurized, and perfused feline middle cerebral artery preparation to measure how changes in intraluminal pressure and alterations in O 2 and CO 2 affect vessel diameter and myogenic contractile activation before and after treatment with indomethacin (IND). Vessel diameters were measured over the pressure range 60–140 mm Hg. The arteries were then exposed to low O 2 (50 torr) and/or high CO 2 (65 torr) and diameters remeasured over the same range. Under control conditions, the arteries exhibited myogenic contractile activation. Exposure to low O 2 , high CO 2 , or a mixture of low O 2 /high CO 2 , increased vessel diameter but did not change the vessels' myogenic contractile responsiveness to changes in pressure. Arteries exposed to IND decreased in diameter but retained myogenic contractile activity. In the presence of IND, vessels dilated to both low O 2 and a mixture of low O 2 /high CO 2 , but did not dilate to high CO 2 alone. Under all conditions, vessels retained myogenic contractile activity. Results obtained under control conditions and low O 2 confirm those of others using similar systems. Myogenic contractile activity in the presence of high CO 2 or a mixture of low O 2 /high CO 2 has not been previously reported. The dilation to low O 2 but not to high CO 2 in the presence of IND suggests that this drug's effects in cerebral arteries are not limited solely to inhibition of prostaglandin synthesis.
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