Tanaka Y, Masuzawa T, Saito M, Yamada T, Fujimoto K
Department of Surgical Neurology, Jichi Medical School, Tochigi, Japan.
Neurol Med Chir (Tokyo). 1998 Aug;38(8):459-63. doi: 10.2176/nmc.38.459.
The mechanism of chronic cerebral vasospasm was investigated by examining the relation between cytosolic Ca2+ level ([Ca2+]i) and muscle contraction in vascular smooth muscle after experimental vasospasm produced by the two-hemorrhage method in the canine basilar artery. [Ca2+]i and tension were recorded simultaneously with a fluorimeter using the arterial strips with a Ca2+ indicator, fura-2. High K+ concentration (72.4 mM) and U-46619 (thromboxane A2 analogue, 10(-8) M) were used as stimulants. The increase in contractile tension per [Ca2+]i per unit cross-sectional area was calculated, and compared for the vasospasm and the control groups. The increase in [Ca2+]i in the vasospasm group was smaller than that in the control group, so the increase in tension per [Ca2+]i per unit sectional area was larger in the vasospasm group. This value was much larger for the contraction induced by U-46619 than that induced by high K+ concentration in both groups. These results suggest that there is an increase in the basal Ca2+ sensitivity of the contractile elements in vasospastic vessels. In addition, the U-46619-induced increase in Ca2+ sensitivity seemed to be augmented in the vasospasm group.
