Endothelium-Dependent Relaxations and Chronic Vasospasm after Subarachnoid Hemorrhage

1990 ◽  
Vol 27 (2-5) ◽  
pp. 263-268
Author(s):  
Phyo Kim ◽  
Paul M. Vanhoutte
Keyword(s):  
Subarachnoid Hemorrhage ◽  
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

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.

Alterations of mechanical properties in canine basilar arteries after subarachnoid hemorrhage

1989 ◽  
Vol 71 (3) ◽  
pp. 430-436 ◽  
Author(s):  
Phyo Kim ◽  
Thoralf M. Sundt ◽  
Paul M. Vanhoutte
Keyword(s):  
Mechanical Properties ◽  
Subarachnoid Hemorrhage ◽  
Autologous Blood ◽  
Myogenic Tone ◽  
Control Group ◽  
Resting Tension ◽  
Length Contraction ◽  
Basilar Arteries ◽  
Chronic Vasospasm

✓ The purpose of this study was to examine the hypotheses that structural stiffening of the arterial wall contributes to chronic cerebral vasospasm, and that alteration in properties of smooth muscle takes place after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage and subsequent chronic vasospasm were induced in dogs by two cisternal injections of autologous blood (on Day 0 and Day 2). Vasospasm was confirmed by angiography performed on Day 0 and Day 7. Animals in the control group underwent angiography only. On Day 8, the mechanical properties of the basilar arteries were studied in vitro. Passive compliance, measured under total inhibition of spontaneous myogenic tone with diltiazem (10−4 M) plus papaverine (10−4 M) was smaller in the SAH group. The length-contraction curve was shifted to the left and the optimum length for maximum contraction (Lmax) was significantly shorter in the spastic blood vessels. The spontaneous myogenic tone was augmented in the SAH group, resulting in an increase in resting tension at each length. By contrast, the maximum contractions in response to KCl and uridine 5′-triphosphate were markedly reduced in the SAH group, without changes in sensitivity to these agents. These differences in mechanical properties were observed in rings both with and without endothelium. The results indicate that, in chronic vasospasm, stiffening of the noncontractile component of the vasculature takes place as well as alterations in the contractile component, both of which presumably contribute to the shift in resting length-tension relationship and length-contraction relationship of the artery. The decreased distensibility, the increase in resting tension, and the shortening of the Lmax all favor a smaller diameter of the artery after SAH, possibly contributing to vasospasm.

Prevention of cerebral vasospasm by a humanized anti-CD11/CD18 monoclonal antibody administered after experimental subarachnoid hemorrhage in nonhuman primates

2003 ◽  
Vol 99 (2) ◽  
pp. 376-382 ◽  
Author(s):  
Richard E. Clatterbuck ◽  
Philippe Gailloud ◽  
Lynn Ogata ◽  
Abeyu Gebremariam ◽  
Gregory N. Dietsch ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Nonhuman Primates ◽  
Leukocyte Migration ◽  
Content Type ◽  
Areal Fraction ◽  
Chronic Vasospasm ◽  
Fine Print

Object. Leukocyte—endothelial cell interactions occurring in the first hours after subarachnoid hemorrhage (SAH) initiate changes in the endothelium and vessel wall that lead to an influx of leukocytes and the development of chronic vasospasm days later. Upregulation of intercellular adhesion molecule—1 (ICAM-1), also called CD54, appears to be a crucial step in this process. There is increasing experimental evidence that blocking the interaction between ICAM-1, which is expressed on endothelium, and integrins such as lymphocyte function—associated antigen—1 (CD11a/CD18) and macrophage antigen—1 (complement receptor 3, CD11b/CD18), which are expressed on the surface of leukocytes, prevents not only inflammation of vessel walls but also chronic vasospasm. The authors extend their previous work with monoclonal antibody (mAb) blockade of leukocyte migration to a nonhuman primate model of chronic, posthemorrhagic cerebral vasospasm. Methods. Before surgery was performed, six young adult male cynomolgus monkeys underwent baseline selective biplane common carotid and vertebrobasilar artery cerebral angiography via a transfemoral route. On Day 0, a right frontosphenotemporal craniectomy was performed with arachnoid microdissection and placement of 2 to 3 ml of clotted autologous blood in the ipsilateral basal cisterns. The animals were given daily intravenous infusions of 2 mg/kg of either a humanized anti-CD11/CD18 or a placebo mAb beginning 30 to 60 minutes postoperatively. The monkeys were killed on Day 7 after a repeated selective cerebral angiogram was obtained. The area of contrast-containing vessels observed in each hemisphere on anteroposterior angiographic views was calculated for the angiograms obtained on Day 7 and expressed as a percentage of the area on baseline angiograms (percent control areal fraction). Review of flow cytometry and enzyme immunoassay data confirmed the presence of the anti-CD11/CD18 antibody in the serum and bound to leukocytes in the peripheral blood of treated animals. Comparisons of the groups revealed 53 ± 4.8% control vascular areal fraction in the placebo group (two animals) and 95.8 ± 9.4% in the anti-CD11/CD18—treated group (three animals), a statistically significant difference (p = 0.043, t-test). Conclusions. These results show that blockade of leukocyte migration into the subarachnoid space by an anti-CD11/CD18 mAb is effective in preventing experimental cerebral vasospasm in nonhuman primates, despite the unaltered presence of hemoglobin in the subarachnoid space. These experimental data support the hypothesis that inflammation plays a role in cerebral vasospasm after SAH.

scholarly journals Haptoglobin 2-2 Genotype Determines Chronic Vasospasm After Experimental Subarachnoid Hemorrhage

Stroke ◽  
2007 ◽  
Vol 38 (12) ◽  
pp. 3266-3271 ◽  
Author(s):  
Kaisorn L. Chaichana ◽  
Andrew P. Levy ◽  
Rachel Miller-Lotan ◽  
Sophia Shakur ◽  
Rafael J. Tamargo
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Experimental Subarachnoid Hemorrhage ◽  
Chronic Vasospasm

scholarly journals Impaired Calcium Regulation of Smooth Muscle during Chronic Vasospasm following Subarachnoid Hemorrhage

1996 ◽  
Vol 16 (2) ◽  
pp. 334-341 ◽  
Author(s):  
Phyo Kim ◽  
Yuhei Yoshimoto ◽  
Masamitsu Iino ◽  
Sasaki Tomio ◽  
Takaaki Kirino ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Intracellular Calcium ◽  
Basilar Artery ◽  
Calcium Concentration ◽  
Calcium Regulation ◽  
Control Group ◽  
Intracellular Calcium Level ◽  
Canine Basilar Artery ◽  
Chronic Vasospasm

The intracellular calcium level was determined in the canine basilar artery to investigate whether Ca2+regulation of its smooth muscle is altered during chronic vasospasm following subarachnoid hemorrhage. A double-hemorrhage model was used. The occurrence of vasospasm was confirmed angiographically 7 days after initial hemorrhage. The intracellular calcium concentration ([Ca2+]i) of smooth muscle was measured using Fura-2. Fluorescence to excitation at 340 and 356 nm was monitored and the ratio R340/356 was used as the indicator of [Ca2+]i. When the extracellular calcium concentration ([Ca2+]e) was increased from pCa 8 to 2, [Ca2+]i also increased. In the spastic arteries, the [Ca2+]e − [Ca2+]i curve was elevated as compared with the normal arteries. Treatment with ionomycin elevated the curve in the normal group, but it had little effect in the spastic arteries. Values of [Ca2+]i, calculated in multiples of Kd, were greater in the spastic arteries. Diltiazem (10;−5 mol/L) partially suppressed the augmented [Ca2+]i signal in the spastic arteries, whereas it did not affect the curve in the control group. These results indicate that calcium regulation of smooth muscle is impaired after subarachnoid hemorrhage, which may contribute to the pathogenesis of chronic vasospasm.

High-energy phosphate levels in the cerebral artery during chronic vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (6) ◽  
pp. 991-996 ◽  
Author(s):  
Phyo Kim ◽  
James D. Jones ◽  
Thoralf M. Sundt
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
High Performance ◽  
Venous Blood ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Content Type ◽  
Chronic Vasospasm

✓ High-energy phosphate levels were measured in the canine cerebral artery during chronic vasospasm. Subarachnoid hemorrhage and vasospasm were induced by percutaneous injections of autologous venous blood into the cisterna magna. Narrowing of the artery was confirmed by angiography 7 days later. Levels of adenosine phosphates (adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP)), guanosine phosphates (guanosine triphosphate (GTP) and guanosine diphosphate (GDP)), and creatine phosphate (CrP) in the basilar artery were quantified using high-performance liquid chromatography. The total creatine (Crtotal) content was measured by a spectrophotometric method after acid hydrolysis of CrP. Levels of ATP, GTP, and CrP were markedly reduced in the spastic arteries, and ratios of ATP:ADP, GTP:GDP, and CrP:Crtotal were significantly decreased. The results indicate a serious disturbance in the energy metabolism that takes place in the cerebral artery during chronic vasospasm.

Inducible nitric oxide synthase: a possible key factor in the pathogenesis of chronic vasospasm after experimental subarachnoid hemorrhage

1999 ◽  
Vol 90 (6) ◽  
pp. 1098-1104 ◽  
Author(s):  
Darius C. Widenka ◽  
Ralph J. Medele ◽  
Walter Stummer ◽  
Karl Bise ◽  
Hans J. Steiger
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Inducible Nitric Oxide Synthase ◽  
Immunohistochemical Staining ◽  
Content Type ◽  
Chronic Vasospasm ◽  
Oxide Synthase ◽  
Fine Print ◽  
Inducible Nitric Oxide

Object. The role of nitric oxide (NO) in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH) is not well understood. Nitric oxide is a well-established vasodilatory substance; however, in SAH, NO may become a major source for the production of injurious free-radical species, leading to chronic cerebral vasospasm. Reactive overproduction of NO to counteract vascular narrowing might potentiate the detrimental effects of NO. The focus of the present study is to determine the extent of reactive induction of inducible nitric oxide synthase (iNOS) after experimental SAH.Methods. Chronic vasospasm was induced in male Wistar rats by an injection of autologous blood (100 µl) into the cisterna magna followed by a second injection 24 hours later. A control group of 10 animals was treated with injections of 0.9% sodium chloride solution. Vasospasm was verified by pressure-controlled angiography after retrograde cannulation of the external carotid artery 7 days later. In 11 of 15 animals radiographic evidence of cerebral vasospasm was seen. The animals were perfusion fixed and their brains were removed for immunohistochemical assessment. With the aid of a microscope, staining for iNOS was quantified in 40-µm floating coronal sections.Immunohistochemical staining for iNOS was markedly more intense in animals with significant angiographic evidence of vasospasm. Virtually no staining was observed in control animals. Seven days after the second experimental SAH, labeling of iNOS was found in endothelial cells, in vascular smooth-muscle cells, and, above all, in adventitial cells. Some immunohistochemical staining of iNOS was observed in rod cells (activated microglia), in glial networks, and in neurons.Conclusions. The present study demonstrates induction of iNOS after experimental SAH.

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