Functional changes in human pial arteries (300 to 900 micrometer ID) within 48 hours of aneurysmal subarachnoid hemorrhage.
OBJECTIVE
Animal studies of cerebral arteries 2 to 3 days after experimental subarachnoid hemorrhage (SAH) provide evidence of arterial change such as hyperresponsiveness to contractile agonists. There is evidence that small arteries, as well as those large enough to be seen on angiography, may be involved. To directly test these possibilities, the contractile and dilator responses of pial artery segments taken from patients up to 48 hours after SAH were compared with those from patients having elective surgery for an aneurysm (Clip) and with those from normal brain vessels overlying tumors (controls).


METHODS
Segments were mounted on a resistance artery myograph for measurements of wall force changes.


RESULTS
There were no differences in maximum contractility (Emax) of the 3 groups of segments. The responses of the SAH segments to K+ (30 mmol/L) were 60.7+/-4.6% of Emax (n [number of vessels]=18), which was significantly greater than those of controls (29.9+/-5% Emax) (n=20). Clip responses were the same as control. Contractions of SAH segments to norepinephrine (1 micromol/L) were 54.3+/-7.9% Emax (n=12), and these were significantly greater than those of controls (15.1+/-6.2% Emax) (n=25). All SAH segments showed spontaneous contractile activity of varying patterns. Spontaneous activity did not occur in the Clip group and occurred in only 50% of control segments. Dilation to acetylcholine was numerically less in SAH and Clip segments than in controls, but differences were not statistically significant. The change in agonist responsiveness could result from exposure to agents that damage the blood vessel wall, resulting in partial depolarization of endothelial and smooth muscle cells.


CONCLUSIONS
Small human pial arteries are hyperresponsive to contractile agents and show spontaneous contractile activity within 48 hours of SAH. Such effects could result in narrowed resistance arteries and reduction in cerebral blood flow. These effects emphasize the wisdom of early therapeutic intervention.
Bevan
J A
JA
Totman Laboratory for Cerebrovascular Research, Department of Pharmacology, University of Vermont, College of Medicine, Burlington, Vermont, USA.
Bevan
R D
RD
Walters
C L
CL
Wellman
T
T
D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D000368:Aged; D002536:Cerebral Arteries / Q000187:drug effects / Q000503:physiopathology*; D002543:Cerebral Hemorrhage / Q000503:physiopathology*; D006801:Humans; D066298:In Vitro Techniques; D008875:Middle Aged; D009129:Muscle Tonus / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D009638:Norepinephrine / Q000494:pharmacology; D010507:Periodicity; D010841:Pia Mater / Q000098:blood supply*; D011188:Potassium / Q000494:pharmacology; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D013997:Time Factors; D014661:Vasoconstriction / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000109:Acetylcholine; D011188:Potassium; D009638:Norepinephrine