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Gomis, Philippe; Kacem, Kamel; Sercombe, Christine; Seylaz, Jacques; Sercombe, Richard

doi:10.1023/a:1004115432660

Cited by 10 publications

(3 citation statements)

References 29 publications

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“…This type of denervation could be expected to result in loss of neurogenic control of cerebral arteries [55] and impairment of autoregulation. In the media, myonecrosis occurs with loss of contractile protein in the smooth muscle [58, 59]; additionally, the amount of interstitial collagen increases [58]. Together these processes contribute to arterial narrowing which is not vasospasm-mediated [60].…”

Section: Introductionmentioning

confidence: 99%

Intracranial Hemorrhage: Mechanisms of Secondary Brain Injury

Lok

Leung

Murphy

et al. 2011

Acta Neurochirurgica Supplementum

108

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SUMMARY ICH is a disease with high rates of mortality and morbidity, with a substantial public health impact. Spontaneous ICH (sICH) has been extensively studied and a large body of data has been accumulated on its pathophysiology. However, the literature on traumatic ICH (tICH) is more limited, and there is a need for further investigations of this important topic. This review will highlight some of the cellular pathways in ICH with an emphasis on the mechanisms of secondary injury due to heme toxicity and to events in the coagulation process, which are common to both sICH and tICH.

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Section: Introductionmentioning

confidence: 99%

Intracranial Hemorrhage: Mechanisms of Secondary Brain Injury

Lok

Leung

Murphy

et al. 2011

Acta Neurochirurgica Supplementum

108

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“…As early as 1997, however, evidence began to accumulate indicating that the blood-brain barrier, and possibly small arteries, were also injured by ICH (4). Further evidence demonstrated that intracerebral blood could alter cytoskeletal organization within cerebral arteries (17) and even induce contractile dedifferentiation (36). Current evidence strongly implies that phenotypic transformation of cerebrovascular smooth muscle and altered contractile function are prominent consequences of ICH (42,52), although the mechanisms mediating this vascular injury remain unclear.…”

mentioning

confidence: 99%

Imatinib attenuates cerebrovascular injury and phenotypic transformation after intracerebral hemorrhage in rats

Pearce

Doan

Carreon

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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This study explored the hypothesis that intracerebral hemorrhage (ICH) promotes release of diffusible factors that can significantly influence the structure and function of cerebral arteries remote from the site of injury, through action on platelet-derived growth factor (PDGF) receptors. Four groups of adult male Sprague-Dawley rats were studied (n = 8 each): 1) sham; 2) sham + 60 mg/kg ip imatinib; 3) ICH (collagenase method); and 4) ICH + 60 mg/kg ip imatinib given 60 min after injury. At 24 h after injury, sham artery passive diameters (+3 mM EGTA) averaged 244 ± 7 µm (at 60 mmHg). ICH significantly increased passive diameters up to 6.4% and decreased compliance up to 42.5%. For both pressure- and potassium-induced contractions, ICH decreased calcium mobilization up to 26.2% and increased myofilament calcium sensitivity up to 48.4%. ICH reduced confocal colocalization of smooth muscle α-actin (αActin) with nonmuscle myosin heavy chain (MHC) and increased its colocalization with smooth muscle MHC, suggesting that ICH promoted contractile differentiation. ICH also enhanced colocalization of myosin light chain kinase (MLCK) with both αActin and regulatory 20-kDa myosin light chain. All effects of ICH on passive diameter, compliance, contractility, and contractile protein colocalization were significantly reduced or absent in arteries from animals treated with imatinib. These findings support the hypothesis that ICH promotes release into the cerebrospinal fluid of vasoactive factors that can diffuse to and promote activation of cerebrovascular PDGF receptors, thereby altering the structure, contractile protein organization, contractility, and smooth muscle phenotype of cerebral arteries remote from the site of hemorrhage.

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“…Vascular remodeling after SAH, as well as cellular growth, could be mainly attributed to increased beta-actin mRNA expression [ 543 ]. The decreased alpha-actin intensity in VSMC probably contributes to the VSMC shift towards a more synthetic (less differentiated) phenotype [ 544 ].…”

Section: Reaction To Sah Of Neurovascular Unit Cellsmentioning

confidence: 99%

The blood–brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments

Solar

Zamani

Lakatosová

et al. 2022

Fluids Barriers CNS

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The response of the blood–brain barrier (BBB) following a stroke, including subarachnoid hemorrhage (SAH), has been studied extensively. The main components of this reaction are endothelial cells, pericytes, and astrocytes that affect microglia, neurons, and vascular smooth muscle cells. SAH induces alterations in individual BBB cells, leading to brain homeostasis disruption. Recent experiments have uncovered many pathophysiological cascades affecting the BBB following SAH. Targeting some of these pathways is important for restoring brain function following SAH. BBB injury occurs immediately after SAH and has long-lasting consequences, but most changes in the pathophysiological cascades occur in the first few days following SAH. These changes determine the development of early brain injury as well as delayed cerebral ischemia. SAH-induced neuroprotection also plays an important role and weakens the negative impact of SAH. Supporting some of these beneficial cascades while attenuating the major pathophysiological pathways might be decisive in inhibiting the negative impact of bleeding in the subarachnoid space. In this review, we attempt a comprehensive overview of the current knowledge on the molecular and cellular changes in the BBB following SAH and their possible modulation by various drugs and substances.

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Untitled

Cited by 10 publications

References 29 publications

Intracranial Hemorrhage: Mechanisms of Secondary Brain Injury

Intracranial Hemorrhage: Mechanisms of Secondary Brain Injury

Imatinib attenuates cerebrovascular injury and phenotypic transformation after intracerebral hemorrhage in rats

The blood–brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments

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