scholarly journals Inhibitory Effects of Verapamil and Nitroglycerin on Contraction and Cytosolic Ca2+ Levels in Cerebrovascular Smooth Muscle During Chronic Cerebral Vasospasm.

2001 ◽  
Vol 41 (5) ◽  
pp. 238-245 ◽  
Author(s):  
Yuichi TANAKA ◽  
Toshio MASUZAWA ◽  
Mitsuru SAITO ◽  
Takeshi YAMADA
1998 ◽  
Vol 38 (8) ◽  
pp. 459-463 ◽  
Author(s):  
Yuichi TANAKA ◽  
Toshio MASUZAWA ◽  
Mitsuru SAITO ◽  
Takeshi YAMADA ◽  
Kiyoshige FUJIMOTO

1983 ◽  
Vol 59 (6) ◽  
pp. 925-932 ◽  
Author(s):  
Douglas Chyatte ◽  
Nancy Rusch ◽  
Thoralf M. Sundt

✓ 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.


1994 ◽  
Vol 56 (2) ◽  
pp. 275-279 ◽  
Author(s):  
Kimihiko SATOH ◽  
Toshio OHTA ◽  
Shigeo ITO ◽  
Yoshikazu NAKAZATO

1997 ◽  
Vol 3 (4) ◽  
pp. E7
Author(s):  
Charles C. Park ◽  
Moon L. Shin ◽  
J. Marc Simard

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.


1984 ◽  
Vol 36 ◽  
pp. 186
Author(s):  
K. Murakami ◽  
H. Karaki ◽  
N. Urakawa

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