Pathological changes in cerebral arteries following experimental subarachnoid hemorrhage: Role of blood platelets

1988 ◽  
Vol 220 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Ben R. Clower ◽  
Junji Yoshioka ◽  
Yutaka Honma ◽  
Robert R. Smith
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Blood Platelets ◽  
Cerebral Arteries ◽  
Pathological Changes ◽  
Experimental Subarachnoid Hemorrhage

scholarly journals Upregulation of Relaxin after Experimental Subarachnoid Hemorrhage in Rabbits

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yuichiro Kikkawa ◽  
Satoshi Matsuo ◽  
Ryota Kurogi ◽  
Akira Nakamizo ◽  
Masahiro Mizoguchi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Messenger Rna ◽  
Cerebral Arteries ◽  
Enzyme Linked Immunosorbent Assay ◽  
Endothelin 1 ◽  
Basilar Arteries ◽  
Experimental Subarachnoid Hemorrhage

Background. Although relaxin causes vasodilatation in systemic arteries, little is known about its role in cerebral arteries. We investigated the expression and role of relaxin in basilar arteries after subarachnoid hemorrhage (SAH) in rabbits.Methods. Microarray analysis with rabbit basilar artery RNA was performed. Messenger RNA expression of relaxin-1 and relaxin/insulin-like family peptide receptor 1 (RXFP1) was investigated with quantitative RT-PCR. RXFP1 expression in the basilar artery was investigated with immunohistochemistry. Relaxin concentrations in cerebrospinal fluid (CSF) and serum were investigated with an enzyme-linked immunosorbent assay. Using human brain vascular smooth muscle cells (HBVSMC) preincubated with relaxin, myosin light chain phosphorylation (MLC) was investigated with immunoblotting after endothelin-1 stimulation.Results. After SAH, RXFP1 mRNA and protein were significantly downregulated on day 3, whereas relaxin-1 mRNA was significantly upregulated on day 7. The relaxin concentration in CSF was significantly elevated on days 5 and 7. Pretreatment with relaxin reduced sustained MLC phosphorylation induced by endothelin-1 in HBVSMC.Conclusion. Upregulation of relaxin and downregulation of RXFP1 after SAH may participate in development of cerebral vasospasm. Downregulation of RXFP1 may induce a functional decrease in relaxin activity during vasospasm. Understanding the role of relaxin may provide further insight into the mechanisms of cerebral vasospasm.

Ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage

1986 ◽  
Vol 64 (2) ◽  
pp. 292-297 ◽  
Author(s):  
Thomas A. Duff ◽  
Grayson Scott ◽  
John A. Feilbach
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Prolonged Exposure ◽  
Cerebral Arteries ◽  
Content Type ◽  
Ultrastructural Evidence ◽  
Experimental Subarachnoid Hemorrhage ◽  
Catecholamine Histofluorescence ◽  
Increased Sensitivity ◽  
The Media ◽  
Adult Cats

✓ Loss of catecholamine histofluorescence, increased sensitivity to norepinephrine, and changes in alpha1 receptor binding have led to the proposal that denervation hypersensitivity may play a role in cerebrovascular spasm. Because the significance of these alterations has remained unclear, the present study was undertaken to determine whether there was direct ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage. Under general anesthesia, adult cats were subjected to pre-pontine injection of blood or serum (5 to 7 ml) via a transclival approach. The animals were sacrificed 4, 7, or 10 days later and basilar artery segments were prepared for electron microscopy. Control vessels appeared normal, whereas those bathed in blood revealed unequivocal changes in neural and supporting elements, including: 1) disintegration of both clear- and dense-core vesicles; 2) fragmentation of varicosities; 3) loss of Schwann cell cytoplasm; and 4) axonal degeneration. These changes were most pronounced 7 days after instillation of blood, and correlated in time with maximal injury of the media and endothelium. Although the development of smooth-muscle hypersensitivity remains unsettled, this study indicates that prolonged exposure to blood can cause extensive denervation of cerebral arteries.

Potential role of JAK2 in cerebral vasospasm after experimental subarachnoid hemorrhage

2008 ◽  
Vol 1214 ◽  
pp. 136-144 ◽  
Author(s):  
Gang Chen ◽  
Jiang Wu ◽  
Caixia Sun ◽  
Meng Qi ◽  
Chunhua Hang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Potential Role ◽  
Experimental Subarachnoid Hemorrhage

Characterizing the role of the neuropeptide substance P in experimental subarachnoid hemorrhage

2011 ◽  
Vol 1389 ◽  
pp. 143-151 ◽  
Author(s):  
Christine M. Barry ◽  
Stephen C. Helps ◽  
Corinna van den Heuvel ◽  
Robert Vink
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Substance P ◽  
Experimental Subarachnoid Hemorrhage
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