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R. Loch Macdonald, Bryce K. A. Weir, Tim D. Runzer, Michael G. A. Grace, J. Max Findlay, Kenichi Saito, David A. Cook, Bruce W. Mielke and Kenji Kanamaru

–326, 1977 (Jpn) 10. Findlay JM , Weir BKA , Steinke D , et al : Effect of intrathecal thrombolytic therapy on subarachnoid clot and chronic vasospasm in a primate model of SAH. J Neurosurg 69 : 723 – 735 , 1988 Findlay JM, Weir BKA, Steinke D, et al: Effect of intrathecal thrombolytic therapy on subarachnoid clot and chronic vasospasm in a primate model of SAH. J Neurosurg 69: 723–735, 1988 11. Fujii S , Fujitsu K : Experimental vasospasm in cultured arterial smooth-muscle cells. Part I

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J. Max Findlay, R. Loch Macdonald, Bryce K. A. Weir and Michael G. A. Grace

ruptured intracranial aneurysms. J Cereb Blood Flow Metab ( Suppl 1 ) 1 : 518 – 519 , 1981 Ferguson GG, Farrar JK, Meguro K, et al: Serial measurements of CBF as a guide to patients with ruptured intracranial aneurysms. J Cereb Blood Flow Metab (Suppl 1) 1: 518–519, 1981 5. Findlay JM , Weir BKA , Steinke D , et al : Effect of intrathecal thrombolytic therapy on subarachnoid clot and chronic vasospasm in a primate model of SAH. J Neurosurg 69 : 723 – 735 , 1988 Findlay JM, Weir BKA, Steinke D, et al

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R. Loch Macdonald, Bryce K. A. Weir, James D. Young and Michael G. A. Grace

vessel wall damage and that these changes are more important than vascular smooth-muscle contraction in generating and maintaining vasospasm. Bevan and coworkers 1, 2, 41 proposed that vasospasm begins as smooth-muscle contraction but that other processes, including inflammation and collagen deposition, are responsible for more chronic narrowing. A third theory invokes proliferation of cells and connective tissue within vasospastic arterial walls, resulting in increased wall mass which then contributes primarily to lumen narrowing. 5 The timing of such changes

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are derived from medial smooth muscle. 2 Smith and Bernanke believe human cerebral arteries in vasospasm generate a distinct cell, the myofibroblast. Clearly, cells do appear in the intima, even in monkeys. The exact nature of these cells, and their contribution to vasospasm, remains to be determined. This work will involve studies in humans and in animal models. References 1. Handa Y , Weir BKA , Nosko M , et al : The effect of timing of clot removal on chronic vasospasm in a primate model. J Neurosurg 67 : 558

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Bozena A. M. Vollrath, Bryce K. A. Weir, R. Loch Macdonald and David A. Cook

membrane lipids and proteins and initiate lipid peroxidation and activation of phospholipase A 2 , thus releasing products of the arachidonic acid cascade. 27, 31 Lipid peroxidation associated with lysis of the subarachnoid clot may be involved in the genesis of chronic vasospasm after SAH, 9, 31 and the lipid peroxide 15-hydroperoxyarachidonic acid has been shown to produce a constriction of cerebral arteries in vivo and in vitro , profound vascular damage, and enhanced synthesis of lipoxygenase products. 32 Most of the eicosanoids activate phospholipase C through

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Akihiko Hino, Bryce K. A. Weir, R. Loch Macdonald, Ronald A. Thisted, Chul-Jin Kim and Lydia M. Johns

cerebral vasospasm. J Cardiovasc Pharmacol 22 (Suppl 8): S332–S335, 1993 9. Findlay JM , Weir BKA , Steinke D , et al : Effect of intrathecal thrombolytic therapy on subarachnoid clot and chronic vasospasm in a primate model of SAH. J Neurosurg 69 : 723 – 735 , 1988 Findlay JM, Weir BKA, Steinke D, et al: Effect of intrathecal thrombolytic therapy on subarachnoid clot and chronic vasospasm in a primate model of SAH. J Neurosurg 69: 723–735, 1988 10. Foley PL , Caner HH , Kassell NF , et al

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Yong-Yuan Guan, Bryce K. A. Weir, Linda S. Marton, R. Loch Macdonald and He Zhang

C erebral artery spasm is a major complication in patients with subarachnoid hemorrhage (SAH) and is both slow to develop and long lasting. 16 Despite numerous studies, the mechanism of the prolonged cerebral vasoconstriction is unclear. It is generally accepted that cerebral vasospasm is closely related to the release of breakdown products from the blood clot. Among these products, hemoglobin has been the focus of investigation in part because the occurrence of chronic cerebral vasoconstriction in the absence of hemoglobin is extraordinarily rare. 28

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Marcus Stoodley, R. Loch Macdonald, Bryce Weir, Linda S. Marton, Lydia Johns, Zhen Du Zhang and Andrew Kowalczuk

. For example, vasospastic arteries and those remodeled by chronic reductions in blood flow display an early papaverine-sensitive contraction that is followed by a papaverine-insensitive phase. 15, 23, 29 The second remodeling phase is similar to vasospasm in that it is not associated with changes in artery composition, as measured by cell number or biochemical content. 15, 20, 22 Langille 14 noted that it is not known to what extent the second phase of remodeling is a consequence of chronic constriction as opposed to being a response to shear stress. The finding

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Hoang Le, Ilyas Munshi, R. Loch Macdonald, Robert Wollmann and Jeffrey Frank

artery (ACA) immediately underneath the twist-drill hole ( Fig. 1 right; arrow ). The aneurysm was excised via a small craniotomy, and the hematoma was evacuated. Histopathological examination of the aneurysm revealed complete disruption of all three layers of the arterial wall and a false aneurysm (the wall of which consisted of fibrous tissue) arising from the torn edges and blending into a large hematoma with chronic inflammation, hemosiderin-laden macrophages, and decaying blood products ( Fig. 2 ). The degree of fibrous tissue formation was consistent with the

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Shigeki Ono, Taro Komuro and R. Loch Macdonald

induction of HO-1 due to inflammation would be less in this group. 6 We observed no differences in the degree of inflammation associated with each virus. In our previous study we did not find dilation of the BA in dogs 7 days after intracisternal injection of Ad-βGal. One possibility is that the dilatory effects of inflammation induced by Ad-βGal are transient. The CBF is elevated in the acute stages of meningitis, and when inflammation becomes chronic the CBF is reduced. 24 Furthermore, inhibition of inflammation 7 days after SAH reduced vasospasm. 36 The duration of