OBJECTIVE: Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) has been hypothesized to occur because of both inflammation-mediated sustained contraction of smooth muscle cells and vascular remodeling. As our recent study showed that tenascin-C (TN-C), an extracellular matrix glycoprotein which is up-regulated in inflammatory states and is associated with tissue remodeling, causes vasospasm-like changes in arterial walls, we examined whether TN-C might be induced in relation to the occurrence of cerebral vasospasm experimentally and clinically. METHODS: First, rat models were produced by means of a single cisternal injection of either autologous arterial blood or saline. Immunostaining for TN-C was performed with basilar arteries obtained from non-operated rats (n=3) and on days 1-4 in SAH (n=18) or saline-injected (n=12) rats. Second, levels of TN-C were prospectively measured in serum in 31 consecutive patients diagnosed with aneurysmal SAH on days 1-12 and compared between those with and without subsequent cerebral vasospasm. RESULTS: In SAH rats, marked induction of TN-C immunoreactivity was shown throughout the vasospastic arterial wall, especially in the smooth muscle cell layers, in comparison with control rats. In a clinical study, serum TN-C levels increased transiently, the extent being significantly greater in patients with subsequent vasospasm; the peak occurred 2.4 days before an increase in the mean transcranial Doppler velocity to > or =120 cm/s and 3.6 days before the onset of symptomatic vasospasm (n=14). DISCUSSION: This is the first study suggesting TN-C increases with close linkage to the occurrence of vasospasm after SAH.
OBJECTIVE:Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) has been hypothesized to occur because of both inflammation-mediated sustained contraction of smooth muscle cells and vascular remodeling. As our recent study showed that tenascin-C (TN-C), an extracellular matrix glycoprotein which is up-regulated in inflammatory states and is associated with tissue remodeling, causes vasospasm-like changes in arterial walls, we examined whether TN-C might be induced in relation to the occurrence of cerebral vasospasm experimentally and clinically. METHODS: First, rat models were produced by means of a single cisternal injection of either autologous arterial blood or saline. Immunostaining for TN-C was performed with basilar arteries obtained from non-operated rats (n=3) and on days 1-4 in SAH (n=18) or saline-injected (n=12) rats. Second, levels of TN-C were prospectively measured in serum in 31 consecutive patients diagnosed with aneurysmalSAH on days 1-12 and compared between those with and without subsequent cerebral vasospasm. RESULTS: In SAHrats, marked induction of TN-C immunoreactivity was shown throughout the vasospastic arterial wall, especially in the smooth muscle cell layers, in comparison with control rats. In a clinical study, serum TN-C levels increased transiently, the extent being significantly greater in patients with subsequent vasospasm; the peak occurred 2.4 days before an increase in the mean transcranial Doppler velocity to > or =120 cm/s and 3.6 days before the onset of symptomatic vasospasm (n=14). DISCUSSION: This is the first study suggesting TN-C increases with close linkage to the occurrence of vasospasm after SAH.