scholarly journals Changes of Subarachnoid Space after the Experimental Subarachnoid Hemorrhage in the Dog

1976 ◽  
Vol 16pt2 (4) ◽  
pp. 323-330
Author(s):  
SHIGEHARU SUZUKI ◽  
KUNIHIKO EBINA ◽  
MASAMI ISHII ◽  
TAKASHI IWABUCHI
2007 ◽  
Vol 107 (1) ◽  
pp. 128-135 ◽  
Author(s):  
Keiichi Iseda ◽  
Shigeki Ono ◽  
Keisuke Onoda ◽  
Motoyoshi Satoh ◽  
Hiroaki Manabe ◽  
...  

Object Inflammation in the subarachnoid space and apoptosis of arterial endothelial cells have been implicated in the development of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). The authors investigated mechanisms of possible antivasospastic effects of N-benzyl-oxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK), a caspase inhibitor that can inhibit both inflammatory and apoptotic systems, in animal models of SAH. Methods Rabbits were assigned to three groups of eight animals each and were subjected to SAH by injection of blood into the cisterna magna. The experiments were performed in the following groups: SAH only, SAH + vehicle, and SAH + Z-VAD-FMK. The Z-VAD-FMK (1 mg) or vehicle (5% dimethyl sulfoxide) was intrathecally administered before SAH induction. Diameters of the basilar artery (BA) were measured on angiograms obtained before and 2 days after SAH. The BA diameter on Day 2 was expressed as a percentage of that before SAH. Interleukin (IL)–1β in the cerebrospinal fluid (CSF) was examined using Western blotting, and brains were immunohistochemically examined for caspase-1 and IL-1β. In a separate experiment, 20 rats were subjected to SAH and their brains were immunohisto-chemically assessed for caspase-1, IL-1β, and macrophages. Results In rabbits, Z-VAD-FMK significantly attenuated cerebral vasospasm (the BA diameter on Day 2 in SAH-only, SAH + vehicle, and SAH + Z-VAD-FMK groups was 66.6 ± 3.2%, 66.3 ± 3.7%, and 82.6 ± 4.9% of baseline, respectively), and suppressed IL-1β release into the CSF and also suppressed immunoreactivities of caspase-1 and IL-1β in macrophages infiltrating into the subarachnoid space. Immunoreactivities for caspase-1 and IL-1β were observed in immunohistochemically proven infiltrating macrophages in rats. Conclusions These results indicate that caspase activation may be involved in the development of SAH-induced vasospasm through inflammatory reaction.


1987 ◽  
Vol 7 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Robert A. Solomon ◽  
Robert L. Lovitz ◽  
Margaret T. Hegemann ◽  
George B. Schuessler ◽  
William L. Young ◽  
...  

A new experimental model was employed to investigate alterations of cerebral metabolic activity in rats subjected to extensive subarachnoid hemorrhage (SAH). The hemorrhages were produced in anesthetized animals by inserting 0.37 ml fresh autologous arterial blood into the subarachnoid space. Rats that underwent sham operations received subarachnoid injections of mock CSF to study the effects of sudden raised intracranial pressure (ICP). Forty-eight hours after subarachnoid injection, the unanesthetized rats were given intravenous injections of [14C]2-deoxyglucose. Experiments were terminated 45 min later by decapitation, and the brains were removed and frozen. Regional brain metabolic activity was studied employing quantitative autoradiography. In comparison with control animals, cerebral metabolic activity was diffusely decreased following SAH. Statistically significant decreases in metabolic activity of <34% were observed in 17 of 30 brain regions studied. The largest percentage reductions were in regions displaying the highest basal metabolic rates. Subarachnoid injections of mock CSF also produced depression of cerebral metabolic activity, but quantitatively these changes were not as pronounced as in the hemorrhage group. These studies demonstrate regional changes in brain function following SAH. The data relate these changes to both the presence of blood in the subarachnoid space and sudden raised ICP.


2021 ◽  
pp. 0271678X2098029
Author(s):  
Hoyee Wan ◽  
Shakira Brathwaite ◽  
Jinglu Ai ◽  
Kullervo Hynynen ◽  
R Loch Macdonald

The distribution and clearance of erythrocytes after subarachnoid hemorrhage (SAH) is poorly understood. We aimed to characterize the distribution of erythrocytes after SAH and the cells involved in their clearance. To visualize erythrocyte distribution, we injected fluorescently-labelled erythrocytes into the prechiasmatic cistern of mice. 10 minutes after injection, we found labelled erythrocytes in the subarachnoid space and ventricular system, and also in the perivascular spaces surrounding large penetrating arterioles. 2 and 5 days after SAH, fluorescence was confined within leptomeningeal and perivascular cells. We identified the perivascular cells as perivascular macrophages based on their morphology, location, Iba-1 immunoreactivity and preferential uptake of FITC-dextran. We subsequently depleted meningeal and perivascular macrophages 2 days before or 3 hours after SAH with clodronate liposomes. At day 5 after SAH, we found increased blood deposition in mice treated prior to SAH, but not those treated after. Treatment post-SAH improved neurological scoring, reduced neuronal cell death and perivascular inflammation, whereas pre-treatment only reduced perivascular inflammation. Our data indicate that after SAH, erythrocytes are distributed throughout the subarachnoid space extending into the perivascular spaces of parenchymal arterioles. Furthermore, meningeal and perivascular macrophages are involved in erythrocyte uptake and play an important role in outcome after SAH.


2015 ◽  
Vol 12 (1) ◽  
pp. 967-973 ◽  
Author(s):  
BINGJIE ZHENG ◽  
HUAILEI LIU ◽  
RUKE WANG ◽  
SHANCAI XU ◽  
YAOHUA LIU ◽  
...  

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