Hindquarters vasoconstriction through central GABA(B) receptors in conscious rats.
(57/221)
The exogenous application of GABA into the cisterna magna of the freely moving rat decreases hindquarters vascular tone as well as arterial pressure. GABA could influence GABA receptor subtypes A, B or C. However, the hindquarters vascular response to the stimulation of each receptor subtype has not yet been investigated. The present study therefore characterized the response to the GABA(B) receptor agonist baclofen injected into the cisterna magna of the conscious rat. Intracisternally injected baclofen induced long-lasting increases in hindquarters vascular resistance and arterial pressure in a dose-dependent manner. Both actions induced by baclofen were completely blocked by a prior intracisternal injection with the GABA(B) receptor antagonist CGP 35348 (p-[3-aminopropyl]-p-diethoxymethylphosphinic acid), and systemically by ganglionic blockade. These actions of baclofen were also abolished centrally by sodium pentobarbital anaesthesia. The results suggest that GABA(B) receptor stimulation via the cisterna magna induced hindquarters vasoconstriction, probably due to central disinhibition of sympathetic activity. (+info)
Insular cistern hematoma. A special type of subarachnoid hemorrhage.
(58/221)
The clinical manifestations of 20 cases of insular cistern hematoma were characterized by sudden onset violent headache, vomiting, bloody CSF, and subhyaloid hemorrhage (1/3 cases). CT scan showed semilunar high density image centering on the insular cistern with serrate internal edge. The average volume of the hematoma was 20 ml. By means of cerebral angiography, operation and/or autopsy, 7 cases were identified as aneurysm of middle cerebral artery, 6 as aneurysm of posterior communicating artery, and 2 as amyloid angiopathy. In the other 5 cases, the etiology was unknown. (+info)
Perfusion of cerebral ventricles: effects of drugs on outflow from the cisterna and the aqueduct.
(59/221)
In cats under chloralose anaesthesia the cerebral ventricles were perfused with Locke solution at a rate of 0.1 ml./min. from an indwelling cannula in the lateral ventricle. The effluent was collected from a cannula either inserted into the cisterna magna or pushed into the aqueduct. When collection was from the cisterna the perfusion included relatively large areas of the subarachnoidal spaces since in cats the foramina of Luschka form the only outlet from the fourth ventricle. Tubocurarine, histamine, and adrenaline injected intravenously caused great variations in outflow from the cisterna, but these changes did not occur when the collection was from the aqueduct. The changes in outflow from the cisterna were similar whether the injection produced a fall of arterial blood pressure as after tubocurarine and histamine, or a rise, as after adrenaline. (+info)
Foramen magnum meningioma and arachnoid cyst coinciding in the lateral cerebellomedullary cistern--case report.
(60/221)
An extremely rare foramen magnum meningioma associated with an arachnoid cyst in the lateral cerebellomedullary cistern occurred in a 65-year-old female presenting with dizziness. Neuroimaging revealed a meningioma at the left lateral edge of the foramen magnum and an arachnoid cyst mainly located in the right lateral cerebellomedullary cistern, compressing the medulla oblongata bilaterally. After fenestration of the cyst wall and tumor removal, the clinical symptoms ameliorated. We recommend that where a foramen magnum tumor coexists with an arachnoid cyst of the posterior fossa, the tumor should be removed after shrinking the cyst to obviate the need for brainstem retraction. (+info)
THE TREATMENT OF COCCIDIOIDAL MENINGITIS. THE USE OF AMPHOTERICIN B IN A GROUP OF 25 PATIENTS.
(61/221)
In a study of 25 patients the usefulness of amphotericin B in the control of meningeal infection produced by Coccidioides immitis was established. Initial treatment must be intensive, consisting of intravenous and intraspinally administered amphotericin B. Serologic evaluation of coccidioidal disease provides the most important single criterion for determining the course of the meningeal infection and for estimating the response of the patient to amphotericin B therapy. Final control of coccidioidal meningitis rests upon the prevention of relapse after completion of initial intensive therapy. This requires continued suppressive fungistasis by regular intracisternal injections of amphotericin B at intervals of three to seven days after the patient returns home. Such suppressive cisternal therapy does not replace the initial intensive use of both intravenously and intraspinally administered amphotericin B. This "local" type of inhibition of C. immitis is without toxic effect upon the kidney, the red blood cells or the serum potassium values which may be associated with the intravenous administration of amphotericin B. Such intraspinal therapy, by lowering the total intravenous dosage required in the initial phase of treatment, results in a proportionate decrease in the degree of nephrotoxicity produced by amphotericin B. The total intravenous dosage given ordinarily should not exceed 5 grams. The long-term therapeutic plan as outlined permits the development of an adequate immune mechanism that appears essential to complete recovery from coccidioidal meningitis. The importance of such immunity in the recovery process has been previously indicated and confirmed by detailed study of a patient who required immunosuppression for successful homotransplantation of a kidney. (+info)
Effect on cerebral vasospasm of coil embolization followed by microcatheter intrathecal urokinase infusion into the cisterna magna: a prospective randomized study.
(62/221)
BACKGROUND AND PURPOSE: Vasospasm remains the leading cause of death and permanent neurological disability in patients with aneurysmal subarachnoid hemorrhage (SAH). The objective of our prospective randomized trial of coil embolization followed by intrathecal urokinase infusion into the cisterna magna (ITUKI therapy) was to test its effectiveness in preventing or alleviating the severity of ischemic neurological deficits caused by vasospasm. METHODS: We enrolled 110 patients with ruptured intracranial aneurysms eligible for coil embolization and randomly assigned them to embolization with (n=57) or without (n=53) ITUKI therapy performed within 24 hours of aneurysmal SAH. The incidence of symptomatic vasospasms and the clinical outcomes, based on the Glasgow Outcome Scale, 6 months after SAH onset were assessed. RESULTS: There were no side effects or adverse reactions attributable to ITUKI therapy. Symptomatic vasospasm occurred in 5 patients (8.8%) with and 16 (30.2%) without ITUKI therapy; the difference was significant (P=0.012). Although the mortality rate did not differ between the groups, patients with ITUKI therapy had significantly better outcomes than those without (P=0.036). CONCLUSIONS: Our results demonstrate that ITUKI therapy significantly reduced the occurrence of symptomatic vasospasm. Although it did not completely prevent vasospasms, ITUKI therapy resulted in a lower rate of permanent neurological deficits. (+info)
Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin-releasing factor-induced inhibition of gastric acid secretion in rats.
(63/221)
1. The central interactions between the sigma ligand, JO 1784, [(+)-N-cyclopropylmethyl-N-methyl-1,4-diphenyl-1-ethylbut-3- en-1-ylamine hydrochloride], or neuropeptide Y (NPY) and corticotropin-releasing factor (CRF)-induced inhibition of gastric acid secretion were investigated in rats anaesthetized with urethane. Drugs were injected intracisternally (i.c.) or into specific hypothalamic nuclei. Gastric acid secretion was measured by the flushed technique under basal and pentagastrin (10 micrograms kg-1 h-1, i.v.) stimulated conditions. 2. Intracisternal injection of CRF (10 micrograms), bombesin (0.1 microgram) and human recombinant interleukin-1 beta (hIL-1 beta, 0.1 microgram) inhibited gastric acid response to pentagastrin by 72%, 56% and 62%, respectively. NPY (0.5 microgram) or JO 1784 (0.5 microgram) injected i.c. did not alter acid secretion but completely prevented the inhibitory effect of CRF. The antagonistic effect of NPY and JO 1784 against CRF was dose-related (0.01-0.5 microgram) and peptide-specific since NPY and JO 1784 did not alter the antisecretory action of bombesin or hIL-1 beta. 3. The putative sigma receptor antagonist, BMY 14802, (1 mg kg-1, s.c.) did not influence pentagastrin-stimulated acid secretion nor CRF-induced inhibition of gastric acid secretion; however, BMY 14802 administered s.c. 20 min before JO 1784 or NPY, abolished the antagonistic effect of both JO 1784 and NPY. 4. CRF (3 micrograms) microinjected into the hypothalamic paraventricular nucleus (PVN) and the lateral hypothalamus (LH) inhibited pentagastrin-stimulated gastric acid secretion by 61% and 51%; NPY (0.03 micrograms) or JO 1784 (0.03 micrograms) microinjected into the PVN had no effect by themselves but blocked CRF antisecretory action.There were more VPBs (220 +/- 75), a higher incidence of VT (60%) and more episodes of VT (11.5 +/- 6.0 compared to 0.7 +/- 0.3 episodes in the preconditioned dogs not given L-NAME); none of the animals survived reperfusion (incidence of VF 100%). The improvement in the severity of the degree of inhomogeneity which resulted from preconditioning was abolished by L-NAME administration.5. L-NAME itself elevated blood pressure (from 96 +/- 5 mmHg diastolic to 119 +/- 7 mmHg), reduced heart rate (from 155 +/- 7 to 144 +/- 4 beats min-') but did not change LVEDP, LVdP/dt,,,,, coronary blood flow, ST-segment elevation or the degree of inhomogeneity of conduction. When given 10 min before the prolonged coronary artery occlusion in dogs not subjected to preconditioning, L-NAME had no significant effect on the severity of arrhythmias except for more periods of VT (a mean of 11.7 +/- 4.7 episodes per dog).6. It is concluded from these studies that the generation of nitric oxide contributes to the marked antiarrhythmic effects of preconditioning in the canine myocardium, probably through elevation of cyclic GMP. (+info)
Tissue plasminogen activator levels after single intracisternal injection in patients with subarachnoid hemorrhage.
(64/221)
Tissue plasminogen activator (tPA) levels were investigated in the cisternal fluid of patients with subarachnoid hemorrhage treated with single intracisternal injection of recombinant tPA during radical surgery for ruptured aneurysms. Seven patients received different doses of tPA: two of 400 microg/ml, three of 500 microg/ml, one of 700 microg/ml, and one of 800 microg/ml in a total amount of 20 ml distilled water at pH 7. Cerebrospinal fluid samples were taken directly from the cisternal fluid at 15-minute incubation after injection, immediately after irrigation during surgery, and by lumbar tap 2 days after surgery. Cisternal tPA levels decreased to about 60% of the mean injected doses after 15-minute incubation. Simple linear regression analysis showed these tPA levels after incubation correlated with the initial doses. After copious irrigation with Ringer solution at pH 8, tPA levels decreased rapidly without correlation with the initial doses. After spinal drainage for 2 days, tPA levels further decreased by an order of 10(-4) to 10(-6) from the initial dose. These values were still greater than normal controls. The final values of tPA levels were not related to the initial dose. None of the patients suffered from systemic or wound complications. Cisternal tPA injection with increased doses and irrigation may be beneficial for the selective rapid removal of blood clots with controllable safety. (+info)