Vasoconstrictor activity in cerebrospinal fluid from patients subjected to early surgery for ruptured intracranial aneurysms

1981 ◽  
Vol 55 (2) ◽  
pp. 237-245 ◽  
Author(s):  
David J. Boullin ◽  
Lennart Brandt ◽  
Bengt Ljunggren ◽  
Philip Tagari
Keyword(s):  
Cerebrospinal Fluid ◽  
Content Type ◽  
Vasoactive Substances ◽  
Angiographic Vasospasm ◽  
Close Relationship ◽  
Surgical Adjunct ◽  
Serial Samples ◽  
Subarachnoid Blood ◽  
Ruptured Intracranial Aneurysms ◽  
Isolated Tissues

✓ Vasoconstrictor activity was examined in serial samples of cerebrospinal fluid (CSF) obtained from 10 patients undergoing aneurysm clipping within 48 hours after subarachnoid hemorrhage (SAH). There was no close relationship between vasoconstrictor activity in postoperative CSF samples and the patient's clinical condition or angiographic vasospasm. The identity of the vasoconstrictor substance(s) in CSF was not established, but serotonin, histamine, norepinephrine, epinephrine, acetylcholine, or angiotensinII were eliminated as prime vasoconstrictor agents inducing cerebral vasospasm. Differences in the temporal profile of the responses of isolated tissues to CSF from patients with early and late surgery suggested that differing substances were involved in the production of spasm. A correlation between CSF potassium concentrations and vasoactive substances was found, but potassium could not account for vasoconstrictor activity of CSF. A log:linear correlation between total vasoconstrictor activity and total CSF collected could not be explained. Also, because of possible differences in the identity of vasoactive substances in CSF in this study compared to earlier studies, clinical comparisons based on apparent differences in pharmacological potency of CSF were not warranted. Nevertheless, removal of subarachnoid blood by cisternal rinsing seemed to be a useful surgical adjunct.

CSF smooth-muscle constrictor activity associated with cerebral vasospasm and mortality in SAH patients

1984 ◽  
Vol 60 (5) ◽  
pp. 927-934 ◽  
Author(s):  
Andrew H. Kaye ◽  
Philip C. Tagari ◽  
Peter J. Teddy ◽  
Christopher B. T. Adams ◽  
William P. Blaso ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intracranial Aneurysms ◽  
Prostaglandin E ◽  
Rat Stomach ◽  
Content Type ◽  
Group Of Seven ◽  
Angiographic Vasospasm ◽  
Stomach Fundus ◽  
Subarachnoid Blood ◽  
Ruptured Intracranial Aneurysms

✓ Cerebrospinal fluid (CSF) was collected preoperatively (by lumbar puncture) or perioperatively (by lumbar or ventricular drain) from 32 patients with subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms. Samples were also obtained from six control patients without evidence of subarachnoid blood. Smooth-muscle constrictor activity in the CSF was measured by bioassay using the isolated rat stomach fundus preparation. Concentrations of unidentified smooth-muscle constrictor substances were considerably greater in CSF from a group of seven patients with evidence of severe angiographic vasospasm and/or delayed ischemic deficits who died (73.8 ± 39.7 nmol/liter prostaglandin E2 (PGE2) equivalents), as compared to 25 other SAH patients who survived (6.5 ± 1.4 nmol/liter PGE2 equivalents), and six control patients (1.17 ± 0.34 nmol/liter PGE2 equivalents). The data suggest that there is a relationship between smooth-muscle constrictor substances in the CSF after SAH and both the degree of angiographic vasospasm and the outcome. It is possible that this relationship might be exploited clinically.

Preoperative treatment of ruptured intracranial aneurysms with tranexamic acid and monitoring of fibrinolytic activity

1980 ◽  
Vol 52 (4) ◽  
pp. 453-455 ◽  
Author(s):  
J. A. Alvarez Garijo ◽  
J. J. Vilches ◽  
J. A. Aznar
Keyword(s):  
Cerebrospinal Fluid ◽  
Tranexamic Acid ◽  
Fibrinolytic Activity ◽  
Intracranial Aneurysms ◽  
Accurate Method ◽  
Preoperative Treatment ◽  
Careful Monitoring ◽  
Content Type ◽  
Ruptured Intracranial Aneurysms

✓ The fibrinolytic activity in cerebrospinal fluid has been monitored by determination of levels of fibrin split products (FSP) in 23 patients with ruptured intracranial aneurysms. In 20 of these 23, FSP was found in the cerebrospinal fluid (CSF), with levels ranging from 10 to 80 μg/ml. Eleven of the 23 patients were treated with 2 gm tranexamic acid daily. In these patients FSP was found in only two cases during the 2nd week, while in 12 untreated patients it was found in 10 cases. These results suggest that there exists a localized fibrinolytic activity, and monitoring the FSP levels in the CSF may be a simple and accurate method for controlling the efficiency of antifibrinolytic therapy. Thus, treatment could be begun with a lower dose, which could be increased later as deemed necessary from the results of careful monitoring.

Monitoring antifibrinolytic therapy in subarachnoid hemorrhage

1973 ◽  
Vol 38 (3) ◽  
pp. 339-344 ◽  
Author(s):  
Robert R. Smith ◽  
John J. Upchurch
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Aminocaproic Acid ◽  
Antifibrinolytic Agents ◽  
Duration Of Action ◽  
Content Type ◽  
The Past ◽  
Fibrin Plate ◽  
Epsilon Aminocaproic Acid ◽  
Ruptured Intracranial Aneurysms

✓ A modification of the fibrin plate method was developed to measure fibrinolysis in patients with subarachnoid hemorrhage and those receiving antifibrinolytic agents. During the past 2 years, 21 patients with ruptured intracranial aneurysms received epsilon aminocaproic acid. Plasma and cerebrospinal fluid were monitored in 15 of these patients. Dosage factors, duration of action, and complications of therapy are presented. Fibrinolysis in normal plasma and cerebrospinal fluid is also discussed.

Effect of intrathecal fibrinolysis on cerebrospinal fluid absorption after experimental subarachnoid hemorrhage

1991 ◽  
Vol 74 (5) ◽  
pp. 789-793 ◽  
Author(s):  
Thomas Brinker ◽  
Volker Seifert ◽  
Dietmar Stolke
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Autologous Blood ◽  
Recombinant Tissue Plasminogen Activator ◽  
Outflow Resistance ◽  
Content Type ◽  
Experimental Subarachnoid Hemorrhage ◽  
Logarithmic Relationship ◽  
Subarachnoid Blood ◽  
Csf Absorption

✓ The effect of intrathecal fibrinolysis on cerebrospinal fluid (CSF) absorption was investigated after experimental subarachnoid hemorrhage (SAH). In 11 cats, SAH was induced by intracisternal application of 1 to 4 ml of fresh autologous blood. Thirty minutes after the experimental SAH, the CSF outflow resistance was found to be elevated from a median of 77 mm Hg/ml/min (range 41.3 to 109 mm Hg/ml/min) to a median of 580 mm Hg/ml/min (range 104 to 7000 mm Hg/ml/min). A logarithmic relationship could be demonstrated between the volume of subarachnoid blood and the elevation of the CSF outflow resistance. The intrathecal application of 2 mg of recombinant tissue plasminogen activator (rt-PA), which is a fibrinolytic substance suitable for lysis of subarachnoid blood clots in man, resulted in an almost total restoration of CSF absorption after experimental SAH. The CSF outflow resistance after SAH was lowered by application of rt-PA from a median of 1028.05 mm Hg/ml/min (range 394 to 7000 mm Hg/ml/min) to 79 mm Hg/ml/min (range 56.7 to 223 mm Hg/ml/min). It is concluded that the impairment of CSF absorption after SAH may play an important role in the pathogenesis of post-hemorrhagic vasospasm.

Experimental epsilon-aminocaproic acid (EACA) administration in the presence of subarachnoid blood

1971 ◽  
Vol 35 (6) ◽  
pp. 657-663 ◽  
Author(s):  
Tom Ewald ◽  
Steve Mahaley ◽  
Jack Goodrich ◽  
Robert Wilkinson ◽  
Don Silver
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Space ◽  
Aminocaproic Acid ◽  
Content Type ◽  
Epsilon Aminocaproic Acid ◽  
Subarachnoid Blood ◽  
Fine Print

✓ Epsilon-aminocaproic acid (EACA) was administered to dogs intrathecally, orally, or intravenously with blood present in the subarachnoid space. These animals were compared with appropriate controls with regard to the subsequent transport of intrathecally injected radioactive albumin from cerebrospinal fluid (CSF) to the blood and the presence of hydrocephalus or adhesive arachnoiditis at the various times of sacrifice. An adhesive arachnoiditis sufficient to produce hydrocephalus or a delay in CSF protein effluence was not observed. The administration of EACA to dogs in the presence of subarachnoid blood did not appear to be associated with any deleterious effects.

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.

Recurrent intracranial solitary fibrous tumor with cerebrospinal fluid dissemination

2004 ◽  
Vol 101 (6) ◽  
pp. 1045-1048 ◽  
Author(s):  
Katsuyoshi Miyashita ◽  
Yutaka Hayashi ◽  
Hironori Fujisawa ◽  
Mitsuhiro Hasegawa ◽  
Junkoh Yamashita
Keyword(s):  
Cerebrospinal Fluid ◽  
Malignant Transformation ◽  
Solitary Fibrous Tumor ◽  
S100 Protein ◽  
Spinal Tumors ◽  
Content Type ◽  
Csf Dissemination ◽  
Fibrous Tumor ◽  
Fine Print ◽  
Mib 1

✓ Solitary fibrous tumor (SFT) is a benign and rare neoplasm. To date, only 37 patients with intracranial SFTs have been reported. Although a number of the tumors were recurrent and some later underwent malignant transformation, none of these lesions progressed to cerebrospinal fluid (CSF) dissemination. In this paper the authors report a case of SFT in which the lesion recurred several times and ultimately was disseminated by the CSF. The patient was a 63-year-old woman with multiple intracranial and spinal tumors. Fifteen years before this presentation, at the age of 48 she had been hospitalized for resection of a falcotentorial tumor. During the ensuing 15 years she underwent multiple surgeries and sessions of radiation therapy for recurrent lesions. The exclusive location of her tumors in the subarachnoid space at the end of this 15-year period indicate CSF dissemination of the tumor. The tumor that was resected when the patient was 48 years old and the latest resected lesion were analyzed by performing immunohistological CD34, epithelial membrane antigen, vimentin, S100 protein, and reticulin staining, and determining the MIB-1 labeling index (LI). Most of the results were identical, and both tumors were diagnosed as SFT according to a staining pattern that showed a strong and diffuse positive reaction for CD34. Nevertheless, the authors noted that the MIB-1 LI increased from less than 1% in the original tumor to 13% in the latest tumor. The increased proliferation of MIB-1 indicates that the malignant transformation could have occurred during tumor recurrence with CSF dissemination.

Evaluation of endorphin content in the CSF of patients with trigeminal neuralgia before and after Gasserian ganglion thermocoagulation

1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza
Keyword(s):  
Cerebrospinal Fluid ◽  
Trigeminal Neuralgia ◽  
Control Group ◽  
Gasserian Ganglion ◽  
Content Type ◽  
Group Of Seven ◽  
Idiopathic Trigeminal Neuralgia ◽  
Significant Difference ◽  
Before And After ◽  
Fine Print

✓ The β-endorphin content in cerebrospinal fluid (CSF) was evaluated in 10 patients with idiopathic trigeminal neuralgia during medical treatment (with or without carbamazepine) and after selective thermocoagulation of the Gasserian ganglion. These values were compared with those obtained in a control group of seven patients without pain problems. No statistically significant difference was found between patients suffering from trigeminal neuralgia and those without pain. Furthermore, neither pharmacological treatment nor surgery changed CSF endorphin values. It is concluded that there is no pathogenetic relationship between trigeminal neuralgia and endorphins.

Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor, OKY-1581

1982 ◽  
Vol 57 (1) ◽  
pp. 74-82 ◽  
Author(s):  
Tomio Sasaki ◽  
Susumu Wakai ◽  
Takao Asano ◽  
Kintomo Takakura ◽  
Keiji Sano
Keyword(s):  
Cerebral Vasospasm ◽  
Morphological Changes ◽  
Content Type ◽  
Synthetase Inhibitor ◽  
Thromboxane Synthetase Inhibitor ◽  
Thromboxane Synthetase ◽  
Basilar Arteries ◽  
Blood Injection ◽  
Subarachnoid Blood ◽  
Fine Print

✓ The efficacy of thromboxane synthetase inhibitor in the prevention of cerebral vasospasm after subarachnoid hemorrhage (SAH) was evaluated in a prolonged experiment using dogs. Changes in the diameter of the basilar artery were followed by angiography, and morphological changes were studied by photomicroscopy and electron microscopy. As a thromboxane synthetase inhibitor, OKY-1581 (sodium-(E)-3-(4(-3-pyridylmethyl)phenyl)-2-methylacrylate)was used. Dogs received intravenous injections of 160 mg of OKY-1581 dissolved in 2 ml of physiological saline immediately after subarachnoid blood injection. Subsequently, the animals received continuous intravenous infusion of the drug at the rate of 4 gm/50 ml/24 hours until sacrifice 4 days after induction of SAH. Control dogs received subarachnoid blood injection without treatment with OKY-1581. Angiographic examination revealed that the late spasm was almost completely abolished by the treatment with OKY-1581. Early spasm was also prevented, but the drug's effect was less prominent than it was on the late spasm. Morphological study revealed degenerative changes in the endothelium and myonecrotic changes in the tunica media following SAH in the basilar arteries of the treated as well as the untreated dogs. However, corrugation of the internal elastic lamina was almost completely absent in the treated dogs. The above results indicate that a disproportionate synthesis of thromboxane A2 plays an important role in the evolution of chronic cerebral vasospasm following SAH, and that drugs such as OKY-1581 that selectively inhibit thromboxane synthetase might be useful in the prevention of vasospasm.

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