Change in Ca2+ Sensitivity of Cerebrovascular Smooth Muscle in Experimental Chronic Cerebral Vasospasm.

1998 ◽  
Vol 38 (8) ◽  
pp. 459-463 ◽  
Author(s):  
Yuichi TANAKA ◽  
Toshio MASUZAWA ◽  
Mitsuru SAITO ◽  
Takeshi YAMADA ◽  
Kiyoshige FUJIMOTO
Keyword(s):  
Smooth Muscle ◽  
Cerebral Vasospasm ◽  
Chronic Cerebral Vasospasm

Prevention of chronic experimental cerebral vasospasm with ibuprofen and high-dose methylprednisolone

1983 ◽  
Vol 59 (6) ◽  
pp. 925-932 ◽  
Author(s):  
Douglas Chyatte ◽  
Nancy Rusch ◽  
Thoralf M. Sundt
Keyword(s):  
Smooth Muscle ◽  
Cerebral Vasospasm ◽  
Autologous Blood ◽  
Barium Chloride ◽  
High Dose ◽  
Content Type ◽  
High Dose Methylprednisolone ◽  
Prostaglandin F ◽  
Basilar Arteries ◽  
Chronic Cerebral Vasospasm

✓ Severe chronic cerebral vasospasm was reliably induced in dogs by two injections, 2 days apart, of autologous blood into the cisterna magna. Treatment with ibuprofen or high-dose methylprednisolone after the first injection prevented or reduced vasospasm. Both drugs reduced meningismus and accelerated the rate of neurological recovery. Compared with specimens from normal dogs, rings of basilar arteries obtained from untreated dogs contracted weakly in response to 5-hydroxytryptamine, prostaglandin F2α, potassium chloride, and barium chloride. Rings of arteries from dogs who received ibuprofen or methylprednisolone contracted more strongly. Electron micrographs of basilar arteries from untreated dogs showed degeneration of smooth muscle, whereas those from treated dogs did not. Thus, what is termed “chronic cerebral vasospasm” probably represents a structural derangement of the blood vessel wall leading to its narrowing, rather than a sustained contraction of the vascular smooth muscle. Administration of high-dose methylprednisolone and ibuprofen can prevent its occurrence.

The complement membrane attack complex and the bystander effect in cerebral vasospasm

1997 ◽  
Vol 3 (4) ◽  
pp. E7
Author(s):  
Charles C. Park ◽  
Moon L. Shin ◽  
J. Marc Simard
Keyword(s):  
Smooth Muscle ◽  
Cerebral Vasospasm ◽  
Complement Activation ◽  
Bystander Effect ◽  
Cell Damage ◽  
Membrane Attack Complex ◽  
Membrane Conductance ◽  
Autologous Serum ◽  
Innocent Bystander ◽  
Patch Clamp Technique

Activation of complement results in formation of membrane attack complexes (MACs) that can insert themselves either into cells that initiate complement activation or into nearby (“innocent bystander”) cells. The MACs form large-conductance, nonspecific ion channels that can cause lytic or sublytic cell damage. The authors used a highly sensitive patch clamp technique to assess the contribution of the bystander effect to the pathophysiology of cerebral vasospasm. They compared the effect of complement activation by autologous aged versus fresh erythrocytes on the membrane conductance of freshly isolated rat cerebral artery smooth-muscle cells. In the presence of autologous serum, aged, but not fresh, erythrocytes caused a large increase in membrane conductance, an effect that was prevented by heat-inactivating the serum. Ethyleneglycol tetraacetic acid in the presence of Mg++ attenuated the effect, indicating that complement activation was taking place via the classic pathway. The effect was reproduced by zymosan-activated autologous serum, suggesting that such changes in conductance could result from insertion of MACs secondary to a bystander effect. Both C8- and C9-depleted heterologous sera produced minimal effects that were converted to full effect by addition of the missing complement component. Superoxide dismutase plus catalase did not attenuate the conductance changes produced by autologous serum plus aged erythrocytes. Autologous serum plus aged erythrocyte membrane ghosts that were free of lysate caused a typical increase in conductance. This study demonstrates that complement activation by aged erythrocytes can result in MAC insertion into innocent bystander smooth-muscle cell membranes and that this mechanism, heretofore undescribed, may contribute to development of vasospasm after subarachnoid hemorrhage.

scholarly journals Mechanism of Cerebral Vasospasm Following Subarachnoid Hemorrhage in Monkeys

1992 ◽  
Vol 19 (4) ◽  
pp. 419-427 ◽  
Author(s):  
R.L. Macdonald ◽  
B.K.A. Weir ◽  
M.G.A. Grace ◽  
M.H. Chen ◽  
T.P. Martin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Structural Changes ◽  
Arterial Wall ◽  
Smooth Muscle Contraction ◽  
Wall Area ◽  
Angiographic Vasospasm ◽  
Vascular Smooth Muscle Contraction ◽  
Scanning Electron

ABSTRACT:This paper reviews our recent studies on the mechanism of cerebral vasospasm following subarachnoid hemorrhage (SAH) in monkeys. Middle cerebral artery (MCA) vasospasm was maximal at 7 days, resolving by 14 days, and absent at 28 days after SAH. Arterial fibrosis was not detected during vasospasm, although there was intimal hyperplasia with fibrosis 28 days after SAH. On scanning electron microscopy, smooth muscle cells from vasospastic arteries had corrugated cell membranes and appeared similar to cells contracted pharmacologically, suggesting that vasospastic smooth muscle is contracted. Morphometric analysis of arteries obtained 7 days after SAH showed no significant increases in arterial wall area of vasospastic arteries compared with normal MCAs. The results suggest vasospasm in monkeys is not due to hypertrophy, hyperplasia, or fibrosis in the arterial wall. Vasospasm may be mainly vascular smooth muscle contraction, which damages the arterial wall, leading to secondary structural changes in the arterial wall which occur after angiographic vasospasm.

Increase of metabolic activity and disruption of normal contractile protein distribution by bilirubin oxidation products in vascular smooth-muscle cells

2004 ◽  
Vol 100 (3) ◽  
pp. 505-511 ◽  
Author(s):  
Melissa A. Lyons ◽  
Rakesh Shukla ◽  
Kejun Zhang ◽  
Gail J. Pyne ◽  
Meha Singh ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cerebral Vasospasm ◽  
Metabolic Activity ◽  
Oxidative Metabolism ◽  
Vascular Remodeling ◽  
Oxidation Products ◽  
Content Type ◽  
Ldh Release ◽  
Fine Print

Object. Cerebral vasospasm is a common cause of morbidity and death following aneurysmal subarachnoid hemorrhage (SAH). Previous research has shown that bilirubin oxidation products (BOXes) are present in the cerebral spinal fluid in patients with SAH-induced cerebral vasospasm and can contribute to vasoconstriction and vasospasm in vitro and in vivo. The events leading to cerebral vasospasm are not understood; however, one component of the occlusion may be due to vascular remodeling. In this study the authors have investigated the actions of BOXes, okadaic acid ([OA], a phosphatase inhibitor), and phorbol-12 myristate-13 acetate ([PMA], a protein kinase activator) on vascular smooth-muscle cell (VSMC) morphology and metabolism. Methods. Immunohistochemical analysis was performed to assess VSMC morphology and α–smooth-muscle actin (αSMA) distribution following the application of BOXes, OA, or PMA. Changes in the level of lactate dehydrogenase (LDH) release and oxidative metabolism were also measured. The BOXes, OA, or PMA caused VSMCs to change their shape and exhibit altered αSMA distribution. These treatments increased LDH release (p < 0.05), which is an index of increased cell stress. Oxidative metabolism significantly increased at low and high doses of BOXes, that is, 143 ± 8.5% and 180 ± 11.8%, respectively (p < 0.0001). Both PMA and OA also caused a significant increase in metabolism. Conclusions. The authors concluded that BOXes, OA, and PMA alter VSMC morphology and metabolic activity, events that have been observed during vascular remodeling. Although the mechanism remains unclear, the results indicate that BOXes may play a role in the vascular remodeling that occurs following aneurysmal SAH.

Intrathecal Nimodipine Therapy in a Primate Model of Chronic Cerebral Vasospasm

Neurosurgery ◽  
1988 ◽  
Vol 22 (3) ◽  
pp. 492-500 ◽  
Author(s):  
Jeffrey P. Lewis ◽  
Bryce K. A. Weir ◽  
Michael G. Nosko ◽  
Takamaru Tanabe ◽  
Michael G. Grace
Keyword(s):  
Cerebral Vasospasm ◽  
Primate Model ◽  
Chronic Cerebral Vasospasm

A trial of the 21-aminosteroid U74006F in a primate model of chronic cerebral vasospasm

Neurosurgery ◽  
1989 ◽  
Vol 24 (2) ◽  
pp. 179???86 ◽  
Author(s):  
D E Steinke ◽  
B K Weir ◽  
J M Findlay ◽  
T Tanabe ◽  
M Grace ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Primate Model ◽  
Chronic Cerebral Vasospasm
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