title: Intracellular calcium, myosin light chain phosphorylation, and contractile force in experimental cerebral vasospasm.
abstract: It remains unknown what proportion of delayed arterial narrowing after subarachnoid hemorrhage depends on ongoing metabolic activity within arterial smooth muscle cells versus changes in the passive structural properties of the arterial wall. To determine this, vasospasm was induced by the double subarachnoid hemorrhage model. Anterior spinal artery segments were harvested from control dogs and from dogs with vasospasm. The segments were suspended in a force transducer and stretched to an optimal length for contraction. The difference in tension between 37 and 0 degrees C was defined as the intrinsic tone, and the residual tension at 0 degrees C was defined as the passive tension. The segments taken from dogs with vasospasm had increased intrinsic tone and passive tension (the differences were 3.8 kN/m2 [P < 0.05] and 14.8 kN/m2 [P < 0.025], respectively). Hence, the passive component accounted for 79.6% of the increased tension in vasospastic arterial segments. The intracellular calcium concentration was measured in these segments, using the luminescent calcium indicator, aequorin. The vasospastic segments had increased basal intracellular calcium concentration (398 versus 258 nmol/L, P < 0.025). In parallel experiments, control and vasospastic vessels were immediately excised when the animals were killed, and the vessels were quick-frozen. Subsequently, using two-dimensional gel electrophoresis to measure percent myosin light chain phosphorylation, vasospastic vessels were found to have increased myosin light chain phosphorylation (37 versus 2%, P < 0.05). The increased intracellular calcium concentration and increased percent myosin light chain phosphorylation in vasospastic segments implicate a role for the Ca(2+)-dependent pathway of smooth muscle cell contraction in vasospasm.
authors.affiliation: Neurosurgical Service, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
authors.forename: W E
authors.initials: WE
authors.lastname: Bulter
authors.forename: J W
authors.initials: JW
authors.lastname: Peterson
authors.forename: N T
authors.initials: NT
authors.lastname: Zervas
authors.forename: K G
authors.initials: KG
authors.lastname: Morgan
mesh_terms: D000818:Animals; D017301:Ca(2+) Mg(2+)-ATPase / Q000502:physiology; D002118:Calcium / Q000502:physiology*; D004285:Dogs; D004789:Enzyme Activation / Q000502:physiology; D007424:Intracellular Fluid / Q000502:physiology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008840:Microfilament Proteins / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D018994:Myosin Light Chains / Q000502:physiology*; D009219:Myosin-Light-Chain Kinase / Q000502:physiology; D010766:Phosphorylation; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D008840:Microfilament Proteins; D018994:Myosin Light Chains; D009219:Myosin-Light-Chain Kinase; D017301:Ca(2+) Mg(2+)-ATPase; D002118:Calcium