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At least 19 recordsLinked to original sources
PubMed1993

The kinetics of lymphocyte subsets and macrophages in subarachnoid space after subarachnoid hemorrhage in rats.

BACKGROUND AND PURPOSE: Although it has been suggested that humoral immunity plays a role in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage, there has been no quantitative assay for cellular immunity. We studied the kinetics of immune cells in the subarachnoid space after subarachnoid hemorrhage in the rat. METHODS: One hundred fourteen Sprague-Dawley rats were used in this study. The animals were divided into two groups and injected with either autologous blood (0.3 mL) or saline into the major cistern. They were killed at the specified time: 10 minutes or 1, 2, 3, 5, or 7 days after subarachnoid hemorrhage. For immunohistochemical analysis, the rats' whole brains were frozen, and cryostat sections were prepared. For flow cytometric analysis of immune cell presence, their whole brains underwent enzymatic digestion. RESULTS: Histopathologic study revealed pathological change of the arterial wall, and immunohistochemical study revealed the existence of macrophages and T cells in the subarachnoid space in animals with a survival time of 2 to 5 days after subarachnoid hemorrhage. A flow cytometric study revealed the peak of appearance of T cells and macrophages 2 days after subarachnoid hemorrhage. The helper-suppressor T cell ratio also reached a peak 2 days after subarachnoid hemorrhage. CONCLUSIONS: A serial response of immunoreactive cells, which resembles that of the chronic allergic reaction observed in autoimmune diseases or delayed-type hypersensitivity, exists in the subarachnoid space after subarachnoid hemorrhage. The present results suggest that the initial response in cellular immunity, which is followed by humoral immunity and eicosanoid reactions, plays a role in eliciting the development of cerebral vasospasm.

Animals↗
PubMed1988

Activation of the coagulation system in the subarachnoid space after subarachnoid haemorrhage: serial measurement of fibrinopeptide A and bradykinin of cerebrospinal fluid and plasma in patients with subarachnoid haemorrhage.

Fibrinopeptide A (FPA) levels as an indicator of thrombin activity in the cerebrospinal fluid (CSF) and plasma of 25 patients with subarachnoid haemorrhage (SAH) were measured serially by radioimmunoassay (RIA). FPA levels in CSF were extremely high on days 0-1 (1253 +/- 269 ng/ml, mean +/- standard error) but decreased rapidly (11.3 +/- 3.9 ng/ml on days 2-4, 10.7 +/- 5.9 ng/ml on days 5-7, and 6.3 +/- 1.5 ng/ml on days 8-14). In the controls the FPA concentration in CSF was 1.2 +/- 0.9 ng/ml (mean +/- standard deviation). Plasma FPA levels in patients with SAH showed no statistically significant changes with time. The bradykinin (BK) concentration in CSF and plasma in 27 patients with SAH was measured serially by RIA. The concentrations in CSF were 122.7 +/- 22.7 pg/ml (mean +/- standard error) on day 0, 38.6 +/- 6.1 pg/ml on day 1, 22.7 +/- 6.3 pg/ml on day 2, and 17.1 +/- 3.0 pg/ml or less thereafter. Plasma BK levels in patients with SAH were higher than those in the control group, but there was no statistically significant change over time. From the measurement of FPA it was apparent that the coagulation system in the subarachnoid space is strongly activated in the early stage of SAH. The formation of BK in CSF after SAH is thought to be due to the contact activation of Hageman factor (intrinsic factor) in the subarachnoid space. Trabeculae as collagen bundles in the subarachnoid space were considered to have a possible role in activating the Hageman factor of the coagulation system in SAH.

Adult↗
PubMed1977

Changes in the subarachnoid space after experimental subarachnoid haemorrhage in the dog: scanning electron microscopic observation.

The possible changes in the subarachnoid space after subarachnoid haemorrhage were studied in animals by using a scanning electron microscope (SEM). About 1 ml/kg of autogenous blood was injected intracisternally in 36 adult mongrel dogs to investigate changes in the subarachnoid space, over periods ranging from immediately after the injection to as long as 6 months. We have come to the conclusion that the injected blood disappears in about one to two weeks; the fibrosis or thickening of the arachnoid membrane appears in one to three weeks, and then returns to normal in a month in instances of rapid recovery, but there are some cases in which fibrosis persists for a long period and becomes chronic. The fact that an increase of fibrous tissue was found in the parietal region, where the injected blood had hardly reached, appears to indicate that the fibrosis is not always limited to the site of the haemorrhage but can occur in remote regions. We also discuss the usefulness of the SEM in the observation of the subarachnoid space, and the finding that vascular specimen preparations can be made by perfusing the brain with 2-10% phosphate-buffered formaldehyde solution.

Animals↗
PubMed1982

Action of lisuride on reserpine-induced muscular rigidity in rats after local application into the striatum, ventricular space or the spinal subarachnoid space.

Muscular rigidity was induced in rats by reserpine (10 mg/kg) and the tonic activity of the gastrocnemic muscle was recorded in the electromyogram. Systemic administration of lisuride, an ergoline, resulted in a dose-dependent depression of rigidity. To examine the site of action of lisuride, we injected lisuride into the striatum, the ventricular space, and the spinal subarachnoid space of intact reserpinized rats. Lisuride is effective if injected into either the striatum or the spinal subarachnoid space, the spinal effect being more pronounced. These results suggest that the spinal cord is an important site of action of lisuride.

Animals↗
PubMed1997

Recordings from brain stem neurons responding to chemical stimulation of the subarachnoid space.

The subarachnoid space at the base of the skull was perfused continuously with artificial cerebrospinal fluid in anesthetized rats. A combination of inflammatory mediators consisting of histamine, bradykinin, serotonin, and prostaglandin E2 (10(-5) M) at pH of 6.1 was introduced into the flow for defined periods to stimulate meningeal primary afferents. Secondary neurons in the caudal nucleus of the trigeminal brain stem were searched by electrical stimulation of the cornea. Of the units receiving oligosynaptic input from the cornea, 44% were excited by stimulation of the meninges with inflammatory mediators. Most of these units had small receptive fields including cornea and the periorbital region, and their responsiveness was restricted to stimuli of noxious intensity. Three types of responses to stimulation of the meninges with algogenic agents were encountered: responses that did not outlast the stimulus period, responses outlasting the stimulus period for several minutes, and oscillating response patterns containing periods of enhanced and suppressed activity. The response pattern of a unit was reproducible, however, upon repetitive stimulation at 20-min intervals; the response magnitude showed tachyphylaxis upon stimulus repetition. The preparation presented mimics pathophysiolocial states normally accompanied by headache, e.g., subarachnoidal bleeding. Responsiveness of neurons in the caudal nucleus of the trigeminal brain stem to inflammatory mediators may play a role in the generation and maintenance of headache, e.g., migraine.

Afferent Pathways↗
PubMed1976

Scanning electron microscopy of the subarachnoid space in the dog. IV. Subarachnoid macrophages.

Young dogs of both sexes were used in this study. Transmission and scanning electron microscopy were utilized for the examination of the spinal cord and choroid plexus with emphasis on the study of free cells. These procedures were modified so that, in certain cases, the same cells observed in scanning electron microscopy could be analyzed internally by transmission electron microscopy. One half of the animals were injected under anesthesia with horseradish peroxidase for observation of phagocytosis. This study confirms that the free cells observed in the subarachnoid space with the scanning and transmission electron microscopes are identical. The internal morphology of these cells corresponds to that of macrophages. This is further substantiated by the ability of these cells to localize horseradish peroxidase in discrete vacuoles within their cytoplasms. Both pial macrophages and epiplexus cells localize peroxidase in an identical manner in the same animal after one injection. In addition macrophages on the surface of the pia mater respond to extravasated red blood cells in a characteristic manner including phagocytosis. The plentiful population of macrophages on the surface of the pia mater supports the concept that these cells are of major importance in maintaining asepsis in the subarachnoid space.

Animals↗
PubMed1995

Subarachnoid haemorrhage induced proliferation of leptomeningeal cells and deposition of extracellular matrices in the arachnoid granulations and subarachnoid space. Immunhistochemical study.

Subarachnoid haemorrhage (SAH) often leads to subarachnoid fibrosis and resultant normal pressure hydrocephalus; however, how subarachnoid fibrosis occurs is unknown. We examined the changes within arachnoid granulations (AGs) and the subarachnoid space (SAS) chronologically at the parasagittal region obtained from patients with SAH at autopsy and made comparison with controls by immunostaining for cytokeratin, specific marker for leptomeningeal cells and by the elastica Masson-Goldner methods. Within a week some AGs were torn, and many inflammatory cells filled the AGs and SAS. Cytokeratin positive cells were scarce. During the next two weeks cytokeratin positive cells increased. After three weeks, AGs and SAS were filled by dense deposits of extracellular matrices surrounded by multiple layers of leptomeningeal cells.

Arachnoid↗
PubMed1975

Clearance of some quaternary amines from the spinal subarachnoid space.

The spinal subarachnoid space was perfused with artificial cerebrospinal fluid (CSF) from the low lumbar level to the middle thoracic level or to the cisterna magna in anesthetized rabbits. 3-H-choline, 3-H-methyl-atropine or 3-H-decamethonium with carrier in different concentrations was added to the perfusate together with 14-C-inulin, the latter serving as a marker of the dilution of the perfusate by original CSF. Choline was eliminated from the perfusate partly by a saturable mechanism probably by an uptake into the spinal cord. About 15 per cent of the radioactivity of the choline infused was recovered from the spinal cord mainly as phosphorylcholine, betaine, and phospholipids. Amphetamine decreased the elimination of choline from ventriculocisternal perfusates and partly inhibited the uptake of choline in rabbit choroid plexus in vitro. In contrast, amphetamine did not influence the saturable elimination of choline in the lumbothoracic perfusion. Neither methylatropine nor decamethonium was eliminated from the perfusate by a saturable mechanism in the lumbothoracic perfusions. However, in perfusions including the cisterna magna methylatropine was partly eliminated by such a mechanism. The concentration of radioactivity in fourth ventricular choroid plexa suggested this structure to be responsible for the saturable part of the elimination. In conclusion, there is no active removal of quaternary amines in general from spinal CSF like the choroid plexus mediated clearance from ventricular CSF.

Animals↗
PubMed1992

[Growth of the graft and astrocytic reaction following transplantation of fetal brain to adult rat's brain. Part II: Cell suspension transplantation into the subarachnoid space].

Suspensions of basal forebrain cells of fetal rats were transplanted into the subarachnoid space of adult rats through a microsyringe needle which was transcortically inserted to the subarachnoid space. Two to 3 months after the transplantation, growth of the graft, neuritic elongation, neovascularization, and astrocytic reaction were examined by Nissl staining, histochemical staining for acethylcholinesterase and Klüver-Barrera's myelin staining, vascular relief images and immunohistochemical staining for laminin, and immunocytochemical staining for glial fibrillary acidic protein (GFAP). Transplanted fetal neurons survived and grew very well over the brain surface and exhibited facilitated neuritic elongation. Several bundles of myelinated fibers linking the subarachnoid and the subpial grafted cells were noticed, but the myelinated fibers penetrating the intact pia mater were not verified. In the grafted tissue, extracellular matrix was formed and a lot of small vessels and capillaries were noticed. Many GFAP-immunoreactive cells were seen in the graft. They had a tendency to gather perivascularly and near the margin of the graft tissue facing subarachnoid space. The subarachnoid space is thought to be an adequate place for transplanted neuronal and glial cells to grow. The subarachnoid space contains the cerebrospinal fluid and also it contacts with rich pial vessels, so that it seems to be superior to the intraparenchymal area in respects of a supply of oxygen and nutrition and of low tissue pressure. Transplanted tissue may be supposed to work as the exocrine and/or endocrine organ which secretes neurotransmitters and their synthetic enzymes and neurotrophic factors. If this is true, it would imply that the subarachnoid space is considered as a promising site for implantation.

Animals↗
PubMed1980

The subarachnoid space: a review.

A historical review of our knowledge of the subarachnoid space dates from the ancients through the modern electron microscope era. Conflicting observation resulted from various methods of tissue preservation and species variability. A comparative submicroscopic study shows striking similarities in the ultrastructure and distribution of the subarachnoid space in mice, cats, monkeys and man. Development of the pia-arachnoid membranes in the mouse occurs in four stages: the first follows closure of the neural tube and is a period of initial vascularization of the developing telencephalon; the second is a period of delineation during which the limits of the subarachnoid space are defined; the third is a period of ensheathment of pia-arachnoidal blood vessels; and the fourth includes addition of smooth muscle to larger vessels, the appearance of macrophages in the subarachnoid space, and a general increase in extracellular collagenous and elastic fibers. The subarachnoid space over the telencephalic surface in the 10-day fetus exists prior to the secretion of cerebrospinal fluid as the typically large extracellular space of mesenchyme. By the 13th fetal day cerebrospinal fluid begins to seep into and replace the ground substance of the mesenchyme. The mesenchymal extracellular compartment is reduced peripherally, resulting in a compacted pia-arachnoidal tissue which limits the peripheral extent of the subarachnoid space. By the 21st postnatal day a subarachnoid space typical of the adult animal has been established. The developmental sequence occurring in the tissues surrounding the central nervous system is important to our understanding of the pathogenesis of hydrocephalus and congenital anomalies.

Aging↗
PubMed1993

Subarachnoid spaces in infants and young children.

In computed tomography of young children, the frontal subarachnoid spaces were sometimes noted to be prominent in scans which were otherwise normal. These apparently enlarged spaces raise the suspicion of possible subdural hygromas. The objective of this study is to show the trend and variability of the intracranial subarachnoid spaces, especially the frontal subarachnoid spaces with age in children. Computed tomographic scans of 39 children up to five years of age with normal head scans were assessed for sizes of the subarachnoid spaces which were subjectively graded from I to V. Grade I is not visible while grade V is borderline enlargement. The sizes of the subarachnoid spaces were found to be more variable in those below the age of two years, with a tendency to be larger compared to older children. Based on these observations, prominent subarachnoid spaces in those below the age of two years should be considered a normal variant. A diagnosis of subdural hygroma must, therefore, be made with caution.

Brain Neoplasms↗
PubMed2000

Lack of endotoxin tolerance with respect to TNF alpha production in the subarachnoid space.

To study endotoxin tolerance in the subarachnoid space 0.1 mg of endotoxin derived from Neisseria meningitidis was injected intracisternally into rabbits on 2 consecutive days. On day 1 the maximum peak level of TNF alpha was 7 ng/ml 2 h after injection, whereas on day 2 the highest levels were 3.6 ng/ml and 3.7 ng/ml, respectively, 1 and 2 h after injection. Pretreatment with intravenous endotoxin 5 or 21 h before consecutive intracisternal endotoxin did not affect the cerebrospinal fluid (CSF) levels of TNF alpha. In contrast, there was a marked endotoxin tolerance with respect to TNF alpha in the systemic circulation. Cells appearing in the CSF 5, 12 and 20 h after intracisternal injection of endotoxin were harvested, cultured, and then stimulated with 0.1 mg/ml of endotoxin. In 10 experiments a marked TNF alpha production in the range 10-70 ng/ml was detected in the supernatants, whereas unstimulated cells did not produce TNF alpha. We conclude that tolerance to endotoxin does not develop in the subarachnoid space as evaluated by the present experimental design. The pattern of TNF alpha production and endotoxin tolerance is distinctly different in the subarachnoid space and systemic circulation.

Animals↗
PubMed2000

Changes in echogenicity of spinal subarachnoid space associated with intracranial hemorrhage: new observations.

PURPOSE: The role of subarachnoid blood and secondary, sterile inflammation in the pathogenesis of posthemorrhagic hydrocephalus (PHH) is not well understood. The aims of this study were to study the frequency and rate of spread of blood into the spinal subarachnoid space (SSS) and to evaluate the relationship of this finding and PHH. MATERIALS AND METHODS: Nine premature babies with major intracerebral hemorrhage (ICH, grade 3 or higher), and ten premature infants with minor ICH (grade 1) or no evidence of ICH (control group) were identified and underwent serial cranial and spinal sonography at the time of initial diagnosis, 12-24 h after the ICH and weekly thereafter for at least 9 weeks. Sagittal and axial scans of the thoracolumbar spine were obtained and evaluated for the presence of echogenic debris in the dorsal SSS. Six additional patients who had cranial and spinal sonography died within the 1st week of life and underwent post-mortem examinations. RESULTS: The SSS was echo-free (normal) in all cases at the time of initial sonographic diagnosis of ICH. Within 24 h, all babies with major ICH had developed increased echogenicity of the cervical and thoracic SSS. Echogenicity of the SSS decreased gradually over several weeks. Although transient ventricular dilatation was present in every patient, only one patient had rapidly progressive PHH requiring shunt placement. Transient cysts of the cervicothoracic subarachnoid space were identified in two patients 6-7 weeks after ICH. The subarachnoid space remained echo-free in all control infants At autopsy, all four infants with echogenic spinal debris had blood or blood products in the spinal subarachnoid space, whereas two infants with echo-free spinal images did not. CONCLUSIONS: Spread of blood from the ventricular system into the spinal subarachnoid space after ICH is common and can be seen within 24 h of initial ICH. Subarachnoid blood is associated with post-hemorrhagic ventricular dilatation and transient spinal subarachnoid cyst formation.

Case-Control Studies↗
PubMed2000

The subarachnoid space: normal fetal development as demonstrated by transvaginal ultrasound.

Enlargement of the subarachnoid spaces can be seen in the following conditions: communicating hydrocephalus, brain atrophy and benign enlargement of the subarachnoid spaces. These disorders may begin in utero. There are no established normograms for the fetal subarachnoid spaces. This study was conducted in order to determine its normal development. Transvaginal sonography was used to examine the subarachnoid space in 80 fetuses between 16 and 40 weeks' gestation. The sinocortical width (SCW) and craniocortical width (CCW) were measured in a coronal plane at the level of the foramen of Monro. The SCW remained relatively constant during the gestational period. The CCW increased in size from the 20th to the 28th week of pregnancy, with a subsequent gradual decrease until term. Determination of fetal subarachnoid space normograms may potentially help in the diagnosis of pathological conditions affecting this space and allow prenatal counselling.

Adult↗
PubMed1992

US measurement of the subarachnoid space in infants: normal values.

The subarachnoid space was examined with real-time ultrasonography (US) in 89 healthy infants. US of the brain in all infants revealed no abnormalities. Three variables were measured in the coronal plane at the level of the foramen of Monro: the sinocortical width (SCW) ranged from 0.4 to 3.3 mm, the craniocortical width (CCW) from 0.3 to 6.3 mm, and the interhemispheric width (IHW) from 0.5 to 8.2 mm. All variables can be used routinely, as the SCW could be demonstrated in all infants, and the CCW and IHW were demonstrated in 96% (85 of 89). Correlation of sonographic measurements with the independent variables age, head circumference, body weight, and body length was poor. To differentiate normal from pathologically dilated subarachnoid spaces, the following upper limits are proposed on the basis of the 95th percentile: 3 mm for SCW, 4 mm for CCW, and 6 mm for IHW.

Female↗