transforming-growth-factor-beta and Subarachnoid-Hemorrhage

transforming-growth-factor-beta has been researched along with Subarachnoid-Hemorrhage* in 13 studies

Reviews

3 review(s) available for transforming-growth-factor-beta and Subarachnoid-Hemorrhage

ArticleYear
The Pathogenesis of Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage.
    International journal of molecular sciences, 2021, May-10, Volume: 22, Issue:9

    Hydrocephalus is a common complication of aneurysmal subarachnoid hemorrhage (aSAH) and reportedly contributes to poor neurological outcomes. In this review, we summarize the molecular and cellular mechanisms involved in the pathogenesis of hydrocephalus following aSAH and summarize its treatment strategies. Various mechanisms have been implicated for the development of chronic hydrocephalus following aSAH, including alterations in cerebral spinal fluid (CSF) dynamics, obstruction of the arachnoid granulations by blood products, and adhesions within the ventricular system. Regarding molecular mechanisms that cause chronic hydrocephalus following aSAH, we carried out an extensive review of animal studies and clinical trials about the transforming growth factor-β/SMAD signaling pathway, upregulation of tenascin-C, inflammation-dependent hypersecretion of CSF, systemic inflammatory response syndrome, and immune dysregulation. To identify the ideal treatment strategy, we discuss the predictive factors of shunt-dependent hydrocephalus between surgical clipping and endovascular coiling groups. The efficacy and safety of other surgical interventions including the endoscopic removal of an intraventricular hemorrhage, placement of an external ventricular drain, the use of intraventricular or cisternal fibrinolysis, and an endoscopic third ventriculostomy on shunt dependency following aSAH were also assessed. However, the optimal treatment is still controversial, and it necessitates further investigations. A better understanding of the pathogenesis of acute and chronic hydrocephalus following aSAH would facilitate the development of treatments and improve the outcome.

    Topics: Humans; Hydrocephalus; Inflammation; Retrospective Studies; Risk Factors; Signal Transduction; Smad Proteins; Subarachnoid Hemorrhage; Transforming Growth Factor beta

2021
Intracranial Aneurysms: Pathology, Genetics, and Molecular Mechanisms.
    Neuromolecular medicine, 2019, Volume: 21, Issue:4

    Intracranial aneurysms (IA) are local dilatations in cerebral arteries that predominantly affect the circle of Willis. Occurring in approximately 2-5% of adults, these weakened areas are susceptible to rupture, leading to subarachnoid hemorrhage (SAH), a type of hemorrhagic stroke. Due to its early age of onset and poor prognosis, SAH accounts for > 25% of years lost for all stroke victims under the age of 65. In this review, we describe the cerebrovascular pathology associated with intracranial aneurysms. To understand IA genetics, we summarize syndromes with elevated incidence, genome-wide association studies (GWAS), whole exome studies on IA-affected families, and recent research that established definitive roles for Thsd1 (Thrombospondin Type 1 Domain Containing Protein 1) and Sox17 (SRY-box 17) in IA using genetically engineered mouse models. Lastly, we discuss the underlying molecular mechanisms of IA, including defects in vascular endothelial and smooth muscle cells caused by dysfunction in mechanotransduction, Thsd1/FAK (Focal Adhesion Kinase) signaling, and the Transforming Growth Factor β (TGF-β) pathway. As illustrated by THSD1 research, cell adhesion may play a significant role in IA.

    Topics: Aneurysm, Ruptured; Animals; Arteritis; Case-Control Studies; Cerebral Arteries; Disease Models, Animal; Endothelial Cells; Exome Sequencing; Focal Adhesions; Genetic Predisposition to Disease; Genome-Wide Association Study; Hemorheology; Humans; Incidence; Intracranial Aneurysm; Mammals; Mechanotransduction, Cellular; Mice; Myocytes, Smooth Muscle; SOXF Transcription Factors; Subarachnoid Hemorrhage; Syndrome; Thrombospondins; Transforming Growth Factor beta; Zebrafish

2019
[Normal pressure hydrocephalus after subarachnoid hemorrhage and TGF-beta1 induced mouse hydrocephalus].
    No shinkei geka. Neurological surgery, 2005, Volume: 33, Issue:8

    Topics: Animals; Cognition Disorders; Disease Models, Animal; Humans; Hydrocephalus, Normal Pressure; Mice; Subarachnoid Hemorrhage; Transforming Growth Factor beta; Transforming Growth Factor beta1

2005

Other Studies

10 other study(ies) available for transforming-growth-factor-beta and Subarachnoid-Hemorrhage

ArticleYear
Statin-induced T-lymphocyte modulation and neuroprotection following experimental subarachnoid hemorrhage.
    Acta neurochirurgica. Supplement, 2013, Volume: 115

    Statins influence immune system activities through mechanisms independent of their lipid-lowering properties. T cells can be subdivided based on cytokine secretion patterns into two subsets: T-helper cells type 1 (Th1) and type 2 (Th2). Independent laboratory studies have shown statins to be potent inducers of a Th2 switch in immune cell response and be neuroprotective in several models of central nervous system (CNS) disease. This study was the first to evaluate the immune modulating effects of statins in subarachnoid hemorrhage (SAH).. Simvastatin was administered to rats intraperitoneally in two dosages (1 and 20 mg/kg) 30 min after the induction of SAH using endovascular perforation. Neurological scores were assessed 24 h later. Animals were then sacrificed, and samples of cortex and brain stem were tested for expression of the T-regulatory cell cytokine transforming growth factor (TGF) β1, as well as interleukin (IL) 1β, a proinflammatory cytokine associated with Th1 immune responses. The presence of TGF-β1 secreting T cells was evaluated with the use of brain slices.. SAH significantly impaired neurological function in all SAH groups (treated and untreated) versus sham. Animals treated with high-dose simvastatin had less neurological impairment than both untreated and low-dose groups. Cortical and brain-stem levels of TGF-β1 were significantly elevated following SAH in the high-dose group. IL-1β was significantly elevated following the induction of SAH but was inhibited by high-dose simvastatin. Double-labeled fluorescent immunohistochemical data demonstrated the presence of lymphocytes in the subarachnoid and perivascular spaces following SAH. Expression of TGF-β1 by lymphocytes was markedly increased following treatment with high-dose simvastatin.. The present study elucidated the potential role of a Th2 immune switch in statin provided neuroprotection following SAH.

    Topics: Analysis of Variance; Animals; Brain; Cytokines; Disease Models, Animal; Dose-Response Relationship, Drug; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Neurologic Examination; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Subarachnoid Hemorrhage; T-Lymphocytes, Helper-Inducer; Transforming Growth Factor beta

2013
Thrombin-induced TGF-β1 pathway: a cause of communicating hydrocephalus post subarachnoid hemorrhage.
    International journal of molecular medicine, 2013, Volume: 31, Issue:3

    The mechanism of communicating hydrocephalus after subarachnoid hemorrhage (SAH) remains unclear. Revealing a signaling cascade may provide significant insights into the molecular etiology of the accumulation of cerebrospinal fluid (CSF) in cerebral compartments during SAH. To investigate the mechanism of the communicating hydrocephalus following SAH, we infused CSF with thrombin (TH), resulting in proinflammatory and proliferative responses in rat meninges of SAH. The effect of TH could be completely blocked by a transforming growth factor β1 (TGF-β1) inhibitor, SB-431542, suggesting that TH-stimulated proliferation of meninges is through the TGF-β1 signaling pathway. The cascade of TGF β1-Smad3 was significantly upregulated by TH, which, in turn, stimulated the proliferation of subarachnoid meninges. TH-induced overexpression of TGF-β1 and activation of its downstream factors might be a mechanism of communicating hydrocephalus after SAH.

    Topics: Animals; Benzamides; Cell Proliferation; Cells, Cultured; Connective Tissue Growth Factor; Dioxoles; Female; Hydrocephalus; Inflammation; Meninges; Rats; Rats, Wistar; RNA, Messenger; Signal Transduction; Smad3 Protein; Subarachnoid Hemorrhage; Thrombin; Transforming Growth Factor beta

2013
High CSF transforming growth factor beta levels after subarachnoid haemorrhage: association with chronic communicating hydrocephalus.
    Journal of neurology, neurosurgery, and psychiatry, 2009, Volume: 80, Issue:5

    Chronic communicating hydrocephalus is a common sequela of subarachnoid haemorrhage and develops when the flow and drainage of CSF are impaired after fibrosis in the subarachnoid space. Released by platelets into the CSF after subarachnoid haemorrhage, transforming growth factor (TGF)beta1/beta2 are potent fibrogenic agents that may promote post-haemorrhagic fibrosis and chronic communicating hydrocephalus.. Temporal changes in total (latent plus active) TGFbeta1/beta2 CSF levels of post-haemorrhage patients developing acute hydrocephalus were measured using ELISA to discover if titres were higher in patients that subsequently developed chronic communicating hydrocephalus, compared with those that did not.. Mean (SD) CSF levels of total TGFbeta1 were 97 (42) pg/ml and total TGFbeta2 were 395 (39) pg/ml in control patients with (non-haemorrhagic) hydrocephalus. For days 1-5 post-subarachnoid haemorrhage (dph), levels of 1427 (242) pg/ml and 976 (191) pg/ml were seen for total TGFbeta1 and TGFbeta2, respectively. Beyond 5 dph, total TGFbeta1/beta2 levels declined but remained significantly elevated (p<0.01) above control patient values for at least 19 dph. Haemorrhagic patients that went on to develop chronic communicating hydrocephalus had significantly higher levels of total TGFbeta1 (p<0.01) and TGFbeta2 (p<0.05) between 1 and 9 dph, compared with those of haemorrhagic patients that did not.. Acutely measured levels of TGFbeta1/beta2 in the CSF of patients with subarachnoid haemorrhage are thus potential prognostic biomarkers for the subsequent development of chronic communicating hydrocephalus, indicating likely dependency on CSF shunting.

    Topics: Adult; Aged; Albumins; Chronic Disease; Cytokines; Enzyme-Linked Immunosorbent Assay; Female; Humans; Hydrocephalus; Male; Middle Aged; Subarachnoid Hemorrhage; Tomography, X-Ray Computed; Transforming Growth Factor beta; Transforming Growth Factor beta1; Transforming Growth Factor beta2

2009
Genes involved in the transforming growth factor beta signalling pathway and the risk of intracranial aneurysms.
    Journal of neurology, neurosurgery, and psychiatry, 2008, Volume: 79, Issue:6

    The 19q13.3 locus for intracranial aneurysms (IA) partly overlaps with the 19q13 locus for abdominal aortic aneurysms (AAA). A common genetic risk factor located in this locus for the two aneurysm types seems plausible. The transforming growth factor beta (TGF-beta) signalling pathway plays a role in aortic aneurysms but may also play a role in aneurysms in general. In the combined region of the 19q13 loci for IA and AAA we identified two candidate genes that are both involved in the TGF-beta signalling pathway: hepsin (HPN) and the latent transforming growth factor beta-binding protein 4 (LTBP4). We hypothesised that single nucleotide polymorphisms (SNP) in the HPN and LTBP4 genes are associated with IA.. We analyzed all the common variations using tag SNP in the HPN and LTBP4 genes for association with IA in 390 patients and 642 controls in the Dutch population. Six tag SNP in the HPN gene and five tag SNP in the LTBP4 gene were genotyped.. No differences in SNP frequency were observed for both the HPN and LTBP4 gene between patients and controls.. Our findings suggest that variations in or near the HPN and LTBP4 genes do not play a role in the susceptibility to IA in the Dutch population.

    Topics: Adult; Aged; Aged, 80 and over; Aneurysm, Ruptured; Aortic Aneurysm, Abdominal; Chromosome Mapping; Chromosomes, Human, Pair 19; Female; Gene Frequency; Genetic Predisposition to Disease; Genetic Testing; Humans; Intracranial Aneurysm; Latent TGF-beta Binding Proteins; Male; Middle Aged; Netherlands; Polymorphism, Single Nucleotide; Serine Endopeptidases; Signal Transduction; Subarachnoid Hemorrhage; Transforming Growth Factor beta

2008
Possible role for vascular cell proliferation in cerebral vasospasm after subarachnoid hemorrhage.
    Stroke, 2003, Volume: 34, Issue:2

    During vasospasm after subarachnoid hemorrhage (SAH), cerebral blood vessels show structural changes consistent with the actions of vascular mitogens. We measured platelet-derived vascular growth factors (PDGFs) in the cerebrospinal fluid (CSF) of patients after SAH and tested the effect of these factors on cerebral arteries in vivo and in vitro.. CSF was sampled from 14 patients after SAH, 6 patients not suffering SAH, and 8 normal controls. ELISA was performed for PDGF-AB, transforming growth factor-beta1, and vascular endothelial growth factor. A mouse model was used to compare cerebral vascular cell proliferation and PDGF staining in SAH compared with sham-operated controls. Normal human pial arteries were incubated for 7 days in vitro, 2 groups with human blood clot and 1 with and 1 without PDGF antibodies.. PDGF-AB concentrations in CSF from SAH patients were significantly higher than those from non-SAH patients and normal controls, both during the first week after SAH and for all time points measured. Smooth muscle and fibroblast proliferation was observed after SAH in the mouse model, and this cellular replication was observed in conjunction with PDGF protein at the sites of thrombus. In human pial arteries, localized thrombus stimulated vessel wall proliferation, and proliferation was blocked by neutralizing antibodies directed against PDGFs.. Vascular mitogens are increased in the CSF of patients after SAH. Proliferation of cells in the vascular wall is associated with perivascular thrombus. Cellular proliferation and subsequent vessel wall thickening may contribute to the syndrome of delayed cerebral vasospasm.

    Topics: Adolescent; Adult; Aged; Aged, 80 and over; Animals; Antibodies; Cell Division; Cerebral Arteries; Disease Models, Animal; Disease Progression; Endothelial Growth Factors; Enzyme-Linked Immunosorbent Assay; Female; Fibroblasts; Humans; In Vitro Techniques; Intercellular Signaling Peptides and Proteins; Lymphokines; Male; Mice; Mice, Inbred C57BL; Middle Aged; Muscle, Smooth, Vascular; Pia Mater; Platelet-Derived Growth Factor; Subarachnoid Hemorrhage; Thrombosis; Transforming Growth Factor beta; Transforming Growth Factor beta1; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors; Vasospasm, Intracranial

2003
Quantitative analysis of gene expressions related to inflammation in canine spastic artery after subarachnoid hemorrhage.
    Stroke, 2001, Volume: 32, Issue:1

    The possible role of inflammatory reaction of the cerebral artery in the pathogenesis of cerebral vasospasm has been noted in recent studies. We quantitatively measured the levels of expression of genes related to inflammation in the spastic artery in a canine double-hemorrhage model.. Twenty dogs were assigned to 4 groups: group D0, control; group D2, dogs killed 2 days after cisternal injection of blood; group D7, dogs given double cisternal injections of blood and killed 7 days after the first injection; and group D14. Angiography was performed twice: on the first day and before the animals were killed. Total RNA was extracted from the basilar artery. The expressions of interleukin (IL)-1alpha, IL-6, IL-8, IL-10, tumor necrosis factor-alpha, E-secretin, fibronectin, intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule-1, transforming growth factor-ss, basic fibroblast growth factor, and collagen types I, III, and IV were examined with TaqMan real-time quantitative reverse transcription-polymerase chain reaction.. Prolonged arterial narrowing peaking on 7 day was observed. There was a significant difference in vessel caliber between D0, D2, D7, and D14 groups (P:<0.0001). There were significant differences in mRNA expression in the basilar artery for IL-1alpha, IL-6, IL-8, ICAM-1, and collagen type I between D0, D2, D7, and D14 groups (P:=0.0079, 0. 0196, 0.0040, 0.0017, and <0.0001, respectively). The average level of mRNA was highest in D7 for IL-1alpha, IL-6, IL-8, and ICAM-1 (17-, 16-, 131-, and 1.7-fold compared with those of D0, respectively) and in D14 for collagen type I (10.9-fold).. Increased expression of genes related to inflammation in the spastic artery suggests that inflammatory reaction of the cerebral artery is associated with sustained contraction.

    Topics: Animals; Basilar Artery; Cell Adhesion Molecules; Chemokines; Collagen; Cytokines; Disease Models, Animal; Dogs; Extracellular Matrix; Fibroblast Growth Factor 2; Gene Expression Profiling; Inflammation; Reverse Transcriptase Polymerase Chain Reaction; Subarachnoid Hemorrhage; Transforming Growth Factor beta; Vasospasm, Intracranial

2001
Transforming growth factor-beta1 in the cerebrospinal fluid of patients with subarachnoid hemorrhage: titers derived from exogenous and endogenous sources.
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2001, Volume: 21, Issue:2

    Transforming growth factor-beta1 (TGF-beta1) is a fibrogenic cytokine that is involved in postinjury repair and is implicated in the etiology of postsubarachnoid hemorrhage (SAH) chronic communicating hydrocephalus. TGF-beta1 was measured by enzyme-linked immunosorbant assay (ELISA) in sequential samples of cerebrospinal fluid (CSF) in 11 patients with hydrocephalus after SAH; levels were seen to be biphasically elevated and sources were investigated. TGF-beta1 levels were compared with albumin levels that estimated CSF blood content. Control samples from nonhemorrhagic hydrocephalics were tested similarly. Mean total TGF-beta1 levels were elevated to 4400+/-3435 (+/-SD) pg/mL greater than control levels of 97+/-42 at 1 to 2 days posthemorrhage. Thereafter, levels fell to 714+/-401 by 5 to 6 days posthemorrhage, then rose to a second peak of 1667+/-774 at 9 to 10 days posthemorrhage, remaining significantly increased until 19 days posthemorrhage (P = 0.007). The first peak probably derived from extravasated platelets and correlated with increased albumin levels in the CSF. The second TGF-beta1 peak rose greater than CSF albumin levels that had stabilized at this time, and thus was attributed to a tissue-specific response rather than a re-bleed. TGF-beta1 was detected in the choroid secretory epithelium from controls, but levels were greater in SAH patients at 10 to 12 days posthemorrhage. The authors conclude that the elevated levels of TGF-beta1 in CSF after SAH are derived initially from blood and later from endogenous sources such as the choroid plexus.

    Topics: Adult; Aged; Antibody Specificity; Choroid Plexus; Enzyme-Linked Immunosorbent Assay; Female; Humans; Hydrocephalus; Male; Middle Aged; Subarachnoid Hemorrhage; Transforming Growth Factor beta; Transforming Growth Factor beta1

2001
Inflammatory cytokine cascade released by leukocytes in cerebrospinal fluid after subarachnoid hemorrhage.
    Neurological research, 2001, Volume: 23, Issue:7

    Subarachnoid hemorrhage (SAH) elicits an inflammatory response in the subarachnoid space, which is mediated by the release of various cytokines. To assess their involvement in post-hemorrhagic complications, we determined the source and time-course of the release of inflammatory cytokines and acute-phase proteins in cerebrospinal fluid (CSF) following SAH. Concentrations of interleukin (IL)- 1beta, IL-6, transforming growth factor-beta1 (TGF-beta1) and C-reactive protein (CRP) in CSF of 36 patients with SAH were measured by enzyme-linked immunoabsorbent assay (ELISA). Floating cells collected from the CSF were centrifuged four to six days after SAH, and examined immunohistochemically. Intracellular IL-1beta and IL-6 were examined by flow cytometric analysis. The molecular weight of TGF-beta1 in CSF of 30 patients was examined by Western blot analysis. The TGF-beta1 levels of patients who had undergone ventriculoperitoneal (VP) shunt (n = 19) was significantly higher than nonshunt group (n = 16). The CRP levels of VP shunt group was significantly higher than nonshunt group. IL-6 concentration was maximal within day 0-1 and it was secreted by neutrophils and monocytes. ELISA showed consistently low levels of IL-1beta, whereas a proportion of monocytes and lymphcytes were IL- 1beta-positive by flow cytometric analysis. TGF-beta1 levels were also maximal on day 0-1 according to ELISA, although it tended to be in the inactive form derived from platelets. A 25 kDa band of TGF-1 was detectable for at least 13 days after SAH, which may have been secreted in part by neutrophils and monocytes. CRP levels in CSF peaked on day 2-3. The present results suggest that leukocytes induced by SAH play an important role in post-hemorrhagic inflammation in the subarachnoid space by releasing IL-6 and TGF-beta1. The CRP and TGF-beta1 levels in CSF are strongly concerned with communicating hydrocephalus after SAH.

    Topics: Adult; Aged; Aged, 80 and over; Blotting, Western; C-Reactive Protein; Cerebrospinal Fluid; Chemotaxis, Leukocyte; Cytokines; Encephalitis; Enzyme-Linked Immunosorbent Assay; Female; Flow Cytometry; Humans; Immunohistochemistry; Interleukin-1; Interleukin-6; Leukocytes; Male; Middle Aged; Monocytes; Neutrophils; Subarachnoid Hemorrhage; Transforming Growth Factor beta

2001
Elevation of transforming growth factor-beta 1 level in cerebrospinal fluid of patients with communicating hydrocephalus after subarachnoid hemorrhage.
    Stroke, 1994, Volume: 25, Issue:7

    Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional polypeptide that controls the production of extracellular matrix protein. Platelets store a large quantity of TGF-beta 1, which is released at hemorrhage. We recently reported that human recombinant TGF-beta 1 induced communicating hydrocephalus in mice. The aim of this study was to determine whether TGF-beta 1 is related to the development of communicating hydrocephalus after subarachnoid hemorrhage (SAH).. TGF-beta 1 in the cerebrospinal fluid of 24 patients with SAH was measured with enzyme-linked immunosorbent assay. The levels were compared between hydrocephalic and nonhydrocephalic groups. Western blot analysis was performed to determine active TGF-beta 1 in the cerebrospinal fluid.. TGF-beta 1 rapidly decreased from the onset of SAH. The level of TGF-beta 1 of 13 patients showing ventricular dilatation with periventricular low density on computed tomographic scan was 1.07 +/- 0.37 ng/mL on days 12 through 14, which was significantly higher than 0.52 +/- 0.21 ng/mL in patients without ventricular dilatation (P < .02). Furthermore, the TGF-beta 1 level of patients who had undergone ventriculoperitoneal shunt (n = 11) was 1.11 +/- 0.09 ng/mL on days 12 through 14, which was also higher than the level of the nonshunt group (n = 13) (0.56 +/- 0.22 ng/mL; P < .01). A 25-kD band was demonstrated by Western blot analysis in the cerebrospinal fluid of a patient with SAH.. Our results strongly suggest that TGF-beta 1 plays an important role in generating communicating hydrocephalus after SAH.

    Topics: Adult; Aged; Cerebral Ventricles; Dilatation, Pathologic; Female; Humans; Hydrocephalus; Male; Middle Aged; Subarachnoid Hemorrhage; Transforming Growth Factor beta

1994
Procollagen types I and III and transforming growth factor-beta gene expression in the arterial wall after exposure to periarterial blood.
    Neurosurgery, 1993, Volume: 33, Issue:4

    The stiffening and thickening of the arterial wall after subarachnoid hemorrhage may reflect increased connective tissue. The purpose of this study was to examine the nature of collagen synthesis in response to periarterial blood. Rat femoral arteries were exposed to periarterial blood for varying lengths of time (control, 1, 3, 7, and 14 d). Dot-blot analysis of total ribonucleic acid extracted from the arteries (n = 10 to 15 animals each) demonstrated that the expression of procollagen Types I and III messenger ribonucleic acid increased at 7 (threefold) and 14 days. The expression of transforming growth factor-beta (TGF-beta), an important regulator of collagen synthesis, was markedly increased by 3 days (threefold), followed by a gradual decline. There were marked differences in procollagen Types I and III and TGF-beta gene expression between arteries exposed to blood and sham-operated arteries for a period of 7 days (n = 25 animals). Northern blot analysis of total ribonucleic acid extracted from cultured vascular smooth muscle cells showed that the treatment with a higher concentration of serum for 48 hours increased the expression of procollagen Types I and III and TGF-beta, whereas exposure to oxyhemoglobin did not. After exposure to periarterial blood, arterial walls show increased synthesis of procollagen Types I and III, perhaps a response to the increased secretion of TGF-beta, which in turn could be the result of exposure to serum factors.

    Topics: Animals; Culture Techniques; Gene Expression Regulation; Ischemic Attack, Transient; Male; Muscle, Smooth, Vascular; Peptide Fragments; Procollagen; Rats; Rats, Sprague-Dawley; Subarachnoid Hemorrhage; Transforming Growth Factor beta; Vascular Resistance

1993
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