Premium
Elevated arterial wall calcium in small diameter cerebral arteries from rabbit model of subarachnoid hemorrhage
Author(s) -
Nystoriak Matthew A.,
Wellman George C.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1151.22
Subject(s) - cerebral arteries , subarachnoid hemorrhage , medicine , vasospasm , arterial wall , anesthesia , cardiology , constriction , anatomy
Cytosolic Ca 2+ in cerebral artery smooth muscle is a critical determinant of blood vessel diameter and cerebral blood flow. Cerebral vasospasm associated with subarachnoid hemorrhage (SAH) results from complex mechanisms that may involve increased Ca 2+ influx via voltage dependent Ca 2+ channels (VDCCs). However, intracellular Ca 2+ levels in small diameter cerebral arteries following SAH are currently unknown. Here, the objective was to measure arterial wall [Ca 2+ ] of intact pressurized small diameter cerebral arteries from a rabbit model of SAH. Cerebral arteries were mounted in an arteriograph chamber and loaded with Ca 2+ indicator dye, Fura‐2. Under basal conditions (6 mM K + & 20 mmHg), arteries from SAH animals exhibited elevated wall [Ca 2+ ] compared with arteries from control animals. Further, membrane potential depolarization due to elevated extracellular K + (60 mM) or increased intravascular pressure caused a greater increase in arterial wall Ca 2+ in arteries from SAH animals. Elevated arterial wall [Ca 2+ ] corresponded to enhanced constriction at 80 and 110 mmHg and was abolished by VDCC blockers. These results suggest elevated arterial wall [Ca 2+ ] due to increased VDCC activity contributes to enhanced arterial constriction following SAH. This work is supported by the Totman Medical Research Trust Fund, the Peter Martin Brain Aneurysm Endowment, the AHA and the NIH.