The Effect of Tizanidine on Chronic Vasospasm in Rats

2000 ◽  
Vol 142 (9) ◽  
pp. 1047-1054 ◽  
Author(s):  
M. Z. Berkman ◽  
A. C. İplikçioğlu ◽  
M. K. Berkman ◽  
T. Erbengi ◽  
T. Şan ◽  
...  
Keyword(s):  
Chronic Vasospasm

Accelerated Non-Muscle Contraction after Subarachnoid Hemorrhage: Cerebrospinal Fluid Testing in a Culture Model

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 921-928 ◽  
Author(s):  
Yoshihiro Yamamoto ◽  
David H. Bernanke ◽  
Robert R. Smith
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Collagen Matrix ◽  
Aneurysm Rupture ◽  
Lattice Contraction ◽  
Symptomatic Vasospasm ◽  
Luminal Narrowing ◽  
Chronic Vasospasm ◽  
Vitro Model

Abstract The cause of chronic cerebral vasospasm after subarachnoid hemorrhage has been studied intensively, but it is still controversial whether the observable luminal narrowing should be attributed to the contraction of vascular smooth muscle cells or whether it results from some organic change in the wall. A proliferation of myointimal cells, accompanied by increased deposition of collagen, as well as myonecrosis, have been frequently observed several days after aneurysm rupture. Studies from our laboratory showed that these myointimal cells had characteristics identical to myofibroblasts. In this study, we quantitatively and morphologically examined the effect of cerebrospinal fluid on the ability of myofibroblasts to alter collagen matrices using an in vitro model. Myofibroblasts contract the collagen matrix by rearranging or compacting the framework of collagen fibers. Cerebrospinal fluid obtained from patients with recently ruptured aneurysms significantly accelerated lattice contraction, especially when the patient developed symptomatic vasospasm. This study suggests that myofibroblasts in the spastic artery can produce a contractile force that contributes to chronic vasospasm, tightening the proliferated collagen. Some unknown agent present in bloody cerebrospinal fluid accelerates the rearrangement of the collagen lattice by myofibroblasts, both of which have, until now, been considered non-contractile components.

Effect of Reserpine-Kanamycin Treatment on Chronic Vasospasm after Platelet-enriched Subarachnoid Hemorrhage in Primates

Neurosurgery ◽  
1984 ◽  
Vol 14 (2) ◽  
pp. 193-197 ◽  
Author(s):  
Thomas W. Noseworthy ◽  
Bryce Weir ◽  
Donald Boisvert ◽  
Francisco Espinosa ◽  
Thomas Overton ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Chronic Vasospasm

Protection by lloprost (stable analogue of prostacyclin) of endothelial damage due to chronic vasospasm in dogs: An electron microscope study

1995 ◽  
Vol 17 (4) ◽  
pp. 301-306 ◽  
Author(s):  
Nihat Egemen ◽  
Mustafa K. Baskaya ◽  
R. Kazim Tiirker ◽  
Agahan Unlii ◽  
siikrii caglar ◽  
...  
Keyword(s):  
Electron Microscope ◽  
Microscope Study ◽  
Electron Microscope Study ◽  
Endothelial Damage ◽  
Chronic Vasospasm

Relationship between Cytosolic Ca2+ Level and Contractile Tension in Canine Basilar Artery of Chronic Vasospasm

Neurosurgery ◽  
1994 ◽  
Vol 34 (3) ◽  
pp. 496???504 ◽  
Author(s):  
Takeshi Yamada ◽  
Yu-ichi Tanaka ◽  
Kiyoshige Fujimoto ◽  
Noboru Nakahara ◽  
Soji Shinoda ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Canine Basilar Artery ◽  
Chronic Vasospasm

Effect of the 21-aminosteroid U-74006F on cerebral vasospasm following subarachnoid hemorrhage

1989 ◽  
Vol 71 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Mario Zuccarello ◽  
Jeffery T. Marsch ◽  
Gerald Schmitt ◽  
James Woodward ◽  
Douglas K. Anderson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Autologous Blood ◽  
Contrast Material ◽  
Rabbit Model ◽  
Membrane Lipid ◽  
Basilar Arteries ◽  
Flow Through ◽  
Chronic Vasospasm

✓ The purpose of this study was to use a new 21-aminosteroid (U-74006F) with in vitro antioxidant and antilipolytic properties as a pharmacological probe to assess the role of lipid hydrolysis and peroxidation in a rabbit model of subarachnoid hemorrhage (SAH)-induced vasospasm. Cerebral angiograms were performed on 15 rabbits. Eighteen hours later, 1 cc/kg of autologous blood was infused into the cisterna magna of all 15 animals. Six rabbits received no treatment, six received U-74006F starting 30 minutes after SAH, and three rabbits received the vehicle for U-74006F starting 30 minutes after SAH. At 72 hours post-SAH, a second angiogram was obtained. Digital subtraction angiographic techniques were used to measure the diameter of and contrast material flow through the basilar artery. At 72 hours post-SAH, vasospasm was evident in all untreated and vehicle-treated rabbits. The diameter of and the flow through the basilar artery were significantly reduced 42.3% ± 6.6% and 46.8% ± 5.8%, respectively, below pre-SAH levels (means ± standard error of the means). Treatment with U-74006F eliminated the SAH-induced vasospasm; in treated animals, both the flow through and the diameter of the basilar arteries were at pre-SAH levels. These findings indicate that: 1) membrane lipid changes (that is, hydrolysis with eicosanoid production and/or peroxidation) contribute to the chronic vasospasm resulting from SAH, and 2) U-74006F prevents the SAH-induced chronic vasospasm in this model by limiting these pathological membrane events.

Controlled-Release of Lipopolysaccharide in the Subarachnoid Space of Rabbits Induces Chronic Vasospasm

Neurosurgery ◽  
2006 ◽  
Vol 58 (2) ◽  
pp. 415
Author(s):  
Pablo F. Recinos ◽  
Gustavo Pradilla ◽  
Quoc-Anh Thai ◽  
Alia M. Hdeib ◽  
Marilyn Perez ◽  
...  
Keyword(s):  
Controlled Release ◽  
Subarachnoid Space ◽  
Chronic Vasospasm

Nimodipine and chronic vasospasm in monkeys

Neurosurgery ◽  
1985 ◽  
Vol 16 (2) ◽  
pp. 137???40 ◽  
Author(s):  
C Krueger ◽  
B Weir ◽  
M Nosko ◽  
D Cook ◽  
S Norris
Keyword(s):  
Chronic Vasospasm

Delayed CSF lavage for arteriographic and morphological vasospasm after experimental SAH

1985 ◽  
Vol 63 (6) ◽  
pp. 949-958 ◽  
Author(s):  
Eben Alexander ◽  
Peter McL. Black ◽  
Theodore M. Liszczak ◽  
Nicholas T. Zervas
Keyword(s):  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Blood Gases ◽  
Canine Model ◽  
Content Type ◽  
Clot Removal ◽  
Wilcoxon Rank Sum Test ◽  
Arterial Vasospasm ◽  
Chronic Vasospasm ◽  
Fine Print

✓ Irrigation of the subarachnoid space after aneurysmal subarachnoid hemorrhage (SAH) has been reported to alleviate subsequent arterial vasospasm. The authors have investigated the effect of lavage of the cerebrospinal fluid (CSF) space in the two-hemorrhage canine model of vasospasm. Twelve dogs had basilar cistern lavage with 120 cc of artificial CSF 24 hours after each of two SAH's, and 12 control dogs had two sequential SAH's without intervening lavage of clot. The amount of clot on the ventral brain stem was evaluated at sacrifice and was graded from 0 (no clot) to 4 (maximum clot) to assess the adequacy of clot removal. Dogs that had undergone lavage had a median grade of 1 (range Grade 0 to 2); control dogs had a median grade of 2 (range Grade 1 to 3.5, p < 0.001, Wilcoxon rank sum test), indicating significant reduction of gross clot by lavage. The neurological findings were graded from 0 to 5, based on meningismus, ataxia, paresis, and cranial nerve deficits. No significant differences in neurological grade were found on any day between the two groups. Satisfactory angiograms were obtained before and 7 days after hemorrhage and were controlled for blood pressure and blood gases; these showed significant spasm in both groups. There was a mean reduction (± standard deviation) of 21.6% ± 16.2% in basilar artery diameter in control dogs, compared to a 28.8% ± 15.1% reduction in dogs with lavage (difference not significant, t-test). There was a strong, but insignificant, trend toward reduction of endothelial desquamation in the basilar and middle cerebral arteries in dogs with lavage compared to control animals (p = 0.06). Corrugation and tearing of the elastica, thickened intima, intimal fibroplasia, vacuolization of the endothelial or smooth-muscle cells, and presence of blood cells in the adventitia occurred similarly in both groups. It appears that cisternal lavage 24 hours after hemorrhage in this model has no effect on the angiographic, neurological, or most morphological sequelae of SAH, in spite of evidence for removal of clot as seen at sacrifice. Any postulated interaction of clot and vessel resulting in chronic vasospasm must occur before this time. Evaluation of the effect of much earlier lavage (for instance, 1 hour after hemorrhage) may elucidate the point at which vasospasm is instigated after SAH, and help in determining what factors cause vasospasm.

Effect of intrathecal thrombolytic therapy on subarachnoid clot and chronic vasospasm in a primate model of SAH

1988 ◽  
Vol 69 (5) ◽  
pp. 723-735 ◽  
Author(s):  
Jay Max Findlay ◽  
Bryce K. A. Weir ◽  
David Steinke ◽  
Takamura Tanabe ◽  
Philip Gordon ◽  
...  
Keyword(s):  
Placebo Group ◽  
Controlled Trial ◽  
Cerebral Arteries ◽  
Brain Inflammation ◽  
Tissue Type ◽  
Electron Microscopic ◽  
Primate Model ◽  
Content Type ◽  
Microscopic Studies ◽  
Chronic Vasospasm

✓ The safety and efficacy of the thrombolytic agent tissue-type plasminogen activator (tPA) in the elimination of subarachnoid clot and prevention of chronic vasospasm were evaluated in a blind randomized placebo-controlled trial. Twenty-four monkeys were randomly assigned to one of two groups of 12. Each group underwent baseline cerebral angiography and coagulation analysis followed by right-sided craniectomy and experimental subarachnoid hemorrhage (SAH). An Ommaya reservoir was inserted with its catheter placed into the subarachnoid space. Twenty-four hours later one group (the tPA group) received 0.5 mg of tPA in 0.5 ml of buffer injected into the reservoir every 8 hours for three doses, while the second group (the placebo group) received the same volume of normal saline. On Day 7, angiography was repeated and the animals were sacrificed. One animal from the placebo group developed a delayed ischemic neurological deficit on Day 5 after SAH. Moderate to severe vasospasm (> 30% reduction in vessel caliber) was present on Day 7 in the internal carotid and middle cerebral arteries of the animals in the placebo group (p < 0.01), while in the tPA group only mild narrowing of the anterior cerebral artery was seen. No significant change in coagulation status occurred in either group. All animals in the placebo group had a large amount of subarachnoid clot remaining at the time of sacrifice, but 11 of the 12 animals in the tPA group were completely free of clot. The results of electron microscopic studies of the cerebral arteries correlated with angiography, and there was no histological evidence of brain inflammation associated with the intrathecal use of tPA.

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