Cerebral arterial spasm

1974 ◽  
Vol 40 (4) ◽  
pp. 442-450 ◽  
Author(s):  
George S. Allen ◽  
Lavell M. Henderson ◽  
Shelley N. Chou ◽  
Lyle A. French
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Human Serum ◽  
Basilar Artery ◽  
Contractile Activity ◽  
Arterial Spasm ◽  
Content Type ◽  
Canine Basilar Artery ◽  
Fine Print

✓ In vitro experiments were performed to determine the contractile activity of human serum and cerebrospinal fluid on the canine basilar artery. The majority of contractile activity in these CSF samples, which were collected 2 to 7 days following a subarachnoid hemorrhage, was proven to be due to serotonin. Serotonin was capable of producing a prolonged contraction of the artery depending on its activity. Methylsergide reversibly blocked the artery's response to serotonin and caused a contraction of the basilar artery. Phenoxybenzamine irreversibly blocked the basilar artery's response to serotonin, serum, and CSF.

CSF leukotriene C4 following subarachnoid hemorrhage

1988 ◽  
Vol 69 (4) ◽  
pp. 488-493 ◽  
Author(s):  
Pietro Paoletti ◽  
Paolo Gaetani ◽  
Guido Grignani ◽  
Lucia Pacchiarini ◽  
Vittorio Silvani ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Subarachnoid Hemorrhage ◽  
Arterial Spasm ◽  
Lipoxygenase Pathway ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Csf Levels ◽  
Fine Print

✓ Leukotrienes derive from arachidonic acid metabolism via the lipoxygenase pathway and modulate several cellular events. In the central nervous system, leukotrienes are mainly synthesized in the gray matter and in vascular tissues. Their production is enhanced in ischemic conditions and in experimental subarachnoid hemorrhage (SAH). Previous studies have indicated the ability of the leukotrienes C4 and D4 to constrict arterial vessels in vivo and in vitro and have suggested their involvement in the pathogenesis of cerebral arterial spasm. In the present study, the authors measured lumbar and cisternal cerebrospinal fluid (CSF) levels of leukotriene C4 in 48 patients who had suffered aneurysmal SAH. In 12 of the cases, symptomatic and radiological spasm was evident. The mean lumbar CSF level of immunoreactive-like activity of leukotriene C4 (i-LTC4) was significantly higher (p < 0.005) than in control cases, while the cisternal CSF level was higher than the lumbar mean concentration (p < 0.005). Patients presenting with vasospasm had significantly higher levels of i-LTC4 compared to patients without symptomatic vasospasm. This is the first report concerning monitoring of i-LTC4 levels in the CSF after SAH. The results of this study suggest that: 1) metabolism of arachidonic acid via the lipoxygenase pathway is enhanced after SAH; 2) the higher cisternal CSF levels of i-LTC4 may be part of the biological response in the perianeurysmal subarachnoid cisterns after the hemorrhage; and 3) the higher CSF levels of i-LTC4 in patients presenting with vasospasm suggest that a relationship exists between this compound and arterial spasm and/or reflect the development of cerebral ischemic damage.

An in vitro comparative study of conducting vessels and penetrating arterioles after experimental subarachnoid hemorrhage in the rabbit

1992 ◽  
Vol 77 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Dennis G. Vollmer ◽  
Masakazu Takayasu ◽  
Ralph G. Dacey
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Isometric Tension ◽  
Channel Blockers ◽  
Cerebral Microvessels ◽  
Content Type ◽  
Large Arteries ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓ The reactivity of rabbit basilar artery and penetrating arteriolar microvessels was studied in vitro using an isometric-tension measurement technique and an isolated perfused arteriole preparation, respectively. Comparisons were made between reactivities of normal vessels and those obtained from animals subjected to experimental subarachnoid hemorrhage (SAH) 3 days prior to examination. Subarachnoid hemorrhage produced significant increases in basilar artery contraction in response to increasing concentrations of serotonin (5-hydroxytryptamine) (10−9 to 10−5 M) and prostaglandin F2α (10−9 to 10−5 M) when compared to normal arteries. In addition, SAH attenuated the relaxing effect of acetylcholine following serotonin-induced contraction and of adenosine triphosphate after KCl-induced basilar artery contractions. In contrast to the changes observed in large arteries, cerebral microvessels did not demonstrate significant differences in spontaneous tone or in reactivity to a number of vasoactive stimuli including application of calcium, serotonin, and acetylcholine. On the other hand, small but significant changes in arteriolar responsiveness to changes in extraluminal pH and to application of KCl were noted. Findings from this study suggest that intracerebral resistance vessels of the cerebral microcirculation are not greatly affected by the presence of subarachnoid clot, in contrast to the large arteries in the basal subarachnoid space. The small changes that do occur are qualitatively different from those observed for large arteries. These findings are consistent with the observation of significant therapeutic benefit with the use of calcium channel blockers without changes in angiographically visible vasospasm in large vessels. It is likely, therefore, that calcium antagonists may act to decrease total cerebrovascular resistance at the level of the relatively unaffected microcirculation after SAH without changing large vessel diameter.

Cerebral arterial spasm

1974 ◽  
Vol 40 (4) ◽  
pp. 433-441 ◽  
Author(s):  
George S. Allen ◽  
Lavell M. Henderson ◽  
Shelly N. Chou ◽  
Lyle A. French
Keyword(s):  
Small Volume ◽  
Contractile Activity ◽  
Cerebral Arteries ◽  
Arterial Spasm ◽  
Vasoactive Agents ◽  
Response Curves ◽  
Content Type ◽  
Middle Cerebral Arteries ◽  
Fine Print

✓ In vitro experiments were performed using a small volume chamber to determine the contractile activity of various vasoactive agents on the canine basilar and middle cerebral arteries. Cumulative dose-response curves were obtained for most of the agents tested including serotonin and three different prostaglandins; many of these curves were found to be similar for segments from both arteries. It was concluded from these curves, and the known concentrations in blood, that serotonin is probably the agent in blood responsible for the cerebral arterial spasm that often follows a subarachnoid hemorrhage. This in vitro method is capable of detecting serotonin concentrations as low as 10−12 gm/ml and may prove useful as a quantitative and well-controlled method for studying the etiology of spasm and the receptor mechanisms present in the cerebral arteries.

Subarachnoid hemorrhage inhibition of endothelium-derived relaxing factor in rabbit basilar artery

1988 ◽  
Vol 69 (2) ◽  
pp. 247-253 ◽  
Author(s):  
Kazuhiro Hongo ◽  
Neal F. Kassell ◽  
Tadayoshi Nakagomi ◽  
Tomio Sasaki ◽  
Tetsuya Tsukahara ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Selective Inhibitor ◽  
Isometric Tension ◽  
The Other ◽  
Content Type ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Fine Print

✓ Vascular contractions in response to KCl and serotonin (5-hydroxytryptamine, 5-HT) in rabbit basilar artery were studied in vitro using an isometric tension-measurement technique. Hemoglobin ( 10−5 M) markedly augmented contractions induced by 5-HT (10−9 to 10−6 M) and slightly augmented those induced by KCl (20 to 80 mM) in arteries with intact endothelium. On the other hand, the augmentation induced by hemoglobin was almost abolished in arteries that were chemically denuded of endothelial cells by pretreatment with saponin. Since hemoglobin is known to be a selective inhibitor of endothelium-derived relaxing factor (EDRF), it is possible that the augmentation of contraction by hemoglobin in endothelium-intact arteries was mediated via an inhibition of spontaneously released EDRF. The effect of subarachnoid hemorrhage (SAH) on spontaneously released EDRF was investigated by injecting 5 ml of blood into the cisterna magna and sacrificing the rabbits 2 days later. Arteries after SAH showed a significant reduction in hemoglobin-induced augmentation compared to that seen in control arteries with intact endothelium. This result suggests that spontaneously released EDRF is significantly reduced after SAH. It is concluded that EDRF is released spontaneously in the rabbit basilar artery and that inhibition of its release might be involved in pathogenesis of cerebral vasospasm.

Potassium and the pathogenesis of cerebral arterial spasm in dog and man

1971 ◽  
Vol 35 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Robert H. Wilkins ◽  
Philip Levitt
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Arterial Spasm ◽  
Content Type ◽  
Blood Clots ◽  
The Individual ◽  
Fine Print

✓ This study investigates the possibility that the intracranial arterial spasm occurring in patients with subarachnoid hemorrhage might be due to potassium released from blood clots surrounding the involved cerebral arteries. Although cerebral arterial spasm could be induced in the dog by the injection of potassium into the chiasmatic cistern, it only occurred with potassium concentrations higher than those expected to result from hemolysis of subarachnoid clots. Furthermore, the potassium concentrations were not elevated in the cerebrospinal fluid of human patients with subarachnoid hemorrhage, and the individual potassium values could not be correlated with the presence or degree of spasm encountered in these patients.

Cerebral arterial spasm

1976 ◽  
Vol 44 (5) ◽  
pp. 585-593 ◽  
Author(s):  
George S. Allen ◽  
Carol J. Gross ◽  
Lavell M. Henderson ◽  
Shelley N. Chou
Keyword(s):  
Serotonin Receptor ◽  
Small Volume ◽  
Arterial Spasm ◽  
Response Curves ◽  
Content Type ◽  
Absolute Requirement ◽  
Canine Basilar Artery ◽  
High Degree ◽  
Fine Print

✓ In vitro experiments were performed using a small volume chamber to study serotonin-induced contractions of the canine basilar artery. Temperature was found to have a profound effect on the artery's response to serotonin. Raising the temperature to 40° C (104° F) increased the maximum response by 20% and lowering the temperature by 10° C caused a 40% reduction in the maximum contraction. Cumulative log-dose response curves for analogues of serotonin demonstrated a high degree of specificity for the serotonin receptor and large nonphysiological concentrations of serotonin caused relaxation of the contracted artery. Extracellular calcium was shown to be an absolute requirement for serotonin-induced contractions. Extracellular magnesium, in contrast, was shown to inhibit serotonin-induced contractions.

Evaluation of prostaglandin biosynthetic activity in canine basilar artery following subarachnoid injection of blood

1981 ◽  
Vol 55 (5) ◽  
pp. 771-778 ◽  
Author(s):  
Tomio Sasaki ◽  
Sei-itsu Murota ◽  
Susumu Wakai ◽  
Takao Asano ◽  
Keiji Sano
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Biosynthetic Activity ◽  
Content Type ◽  
Blood Injection ◽  
Canine Basilar Artery ◽  
Subarachnoid Blood ◽  
Fine Print

✓ Transformation of arachidonic acid into prostaglandins was investigated in the basilar artery by incubating sections of artery with carbon-14-labeled arachidonic acid. Thin-layer radiochromatography revealed that, in normal canine basilar arteries, 14C-arachidonic acid was transformed mainly to 6-ketoprostaglandin (PG)F1α, a spontaneous metabolite of prostacyclin (PGI2). Among other prostaglandins, only a small amount of PGF2α was detected, whereas PGD2, PGE2, and thromboxane B2 were not. Arteries removed on Days 3 and 8 after subarachnoid blood injection showed a prostaglandin synthesis profile similar to that in the normal cerebral artery. In borate-buffered saline (0.1M borate buffer, pH 9.0/0.15M NaCl = 1:9, vol/vol), canine basilar artery produced a PGI2-like substance that inhibited adenosine diphosphate (ADP)-induced platelet aggregation. Its anti-aggregatory activity was completely abolished by acidification. Aspirin likewise inhibited production of the anti-aggregatory substance. From these results, it was concluded that the anti-aggregatory activity was due solely to the production of PGI2 by the arterial specimen. Based on the above results, PGI2 biosynthetic activity in the cerebral artery exposed to subarachnoid blood injection was bioassayed by measuring the inhibitory activity of the incubation product upon ADP-induced platelet aggregation following incubation of the arteries in borate-buffered saline for 5 to 30 minutes at 20°C, using synthetic PGI2-Na as a standard. The synthetic activity of PGI2 in the artery exposed to subarachnoid blood injection had diminished remarkably by Days 3 and 8. This diminution of PGI2 synthesis in the cerebral artery may be involved in the pathogenesis of cerebral vasospasm.

Combined effect of L-arginine and superoxide dismutase on the spastic basilar artery after subarachnoid hemorrhage in dogs

1994 ◽  
Vol 80 (3) ◽  
pp. 476-483 ◽  
Author(s):  
Yasukazu Kajita ◽  
Yoshio Suzuki ◽  
Hirofumi Oyama ◽  
Toshihiko Tanazawa ◽  
Masakazu Takayasu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Superoxide Anion ◽  
Content Type ◽  
Vasodilator Effect ◽  
Intracisternal Injection ◽  
Dose Dependent ◽  
Fine Print

✓ To investigate the function of nitric oxide (a major endothelium-derived relaxing factor) in cerebral arteries after subarachnoid hemorrhage (SAH) in vivo, several nitric oxide-related substances were administered to dogs that had undergone double SAH. These included L-arginine (a substrate for the formation of nitric oxide), NG-monomethyl-L-arginine (L-NMMA, an analog of L-arginine that inhibits the formation of nitric oxide from L-arginine), and superoxide dismutase (SOD, which protects nitric oxide from oxidation by superoxide anion), which were given via intracisternal injection. The diameter of the basilar artery was assessed angiographically. In intact dogs, intracisternal bolus injections of L-arginine (1, 10, or 100 µmol) produced a dose-dependent increase in the internal diameter of the basilar artery; conversely, L-NMMA reduced the diameter of the basilar artery from baseline in a dose-dependent manner. On Days 4 and 7, after two intracisternal injections of autologous blood, L-arginine produced transient vasodilation of the spastic basilar artery, whereas L-NMMA produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on Day 4 than on Day 7, but less than in intact dogs. Intracisternal injection of SOD, which caused no effect per se, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on Day 4 and both the magnitude and duration of that effect on Day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. The finding that the simultaneous injection of SOD enhanced and prolonged the vasodilation induced by sufficient exogenous L-arginine suggests that the inactivation of nitric oxide by superoxide anion contributes to the development of vasospasm.

Calpain-calpastatin system of canine basilar artery in vasospasm

1993 ◽  
Vol 79 (4) ◽  
pp. 537-543 ◽  
Author(s):  
Ikuya Yamaura ◽  
Eiichi Tani ◽  
Takaomi C. Saido ◽  
Koichi Suzuki ◽  
Nobutaka Minami ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Early Stage ◽  
Local Application ◽  
Neutral Protease ◽  
Control Group ◽  
Calpain Activity ◽  
Fresh Blood ◽  
Content Type ◽  
Canine Basilar Artery ◽  
Fine Print

✓ Vasospasm was produced in the canine basilar artery by a two-hemorrhage method, while contraction was induced in the normal canine basilar artery by a local application of KCl or serotonin after transclival exposure. The control animals were injected with saline instead of fresh blood. The activation of μ-calpain, a Ca++-dependent neutral protease, in the basilar artery was studied by evaluating the conversion from its inactivated into its activated form on immunoblots. In addition, the activity of calpastatin, an intrinsic inhibitor of calpain, in the basilar artery was determined by assay. The majority of the μ-calpain was inactivated in the control group. In the spastic group, μ-calpain was generally activated markedly in the early stage of vasospasm and moderately thereafter. The contraction induced by KCl or serotonin application was classified into the early phasic and the later tonic stages; μ-calpain was usually activated in the phasic stage and inactivated in the tonic stage. Calpastatin activity was significantly decreased during vasospasm, whereas it was not significantly changed in KCl- or serotonin-induced contraction. The final activity of μ-calpain results from the balance of μ-calpain and calpastatin. This suggests that μ-calpain activity was enhanced continuously in the spastic group and transiently in the KCl or serotonin group, and that the continuous activation of μ-calpain during vasospasm probably induced more proteolytic changes compared to those in the KCl or serotonin group.

Significance of a small bulge on the basilar artery in patients with perimesencephalic nonaneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (2) ◽  
pp. 426-429 ◽  
Author(s):  
Yuji Matsumaru ◽  
Kiyoyuki Yanaka ◽  
Ai Muroi ◽  
Hiroaki Sato ◽  
Takao Kamezaki ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Three Dimensional ◽  
Distinct Type ◽  
Rotational Angiography ◽  
Bleeding Pattern ◽  
Content Type ◽  
Nonaneurysmal Subarachnoid Hemorrhage ◽  
Excellent Clinical Outcome ◽  
Fine Print

✓ Perimesencephalic nonaneurysmal subarachnoid hemorrhage (SAH) is a distinct type of hemorrhage with a characteristic bleeding pattern and an excellent clinical outcome. The cause of this benign form of SAH remains unknown. The authors report on two cases of perimesencephalic nonaneurysmal SAH in which a small bulge on the basilar artery (BA) was demonstrated on three-dimensional rotational angiography studies. Based on data from these cases, one may infer that the lesion on the BA is responsible for the SAH. The possible pathogenesis is discussed.

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