Morphological Changes of Intraparenchymal Arterioles after Experimental Subarachnoid Hemorrhage in Dogs

Ohkuma, Hiroki; Itoh, Katsuhiro; Shibata, Seiko; Suzuki, Shigeharu

doi:10.1097/00006123-199707000-00036

Cited by 95 publications

(75 citation statements)

References 24 publications

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“…This hypothesis was proven experimentally in rats by showing that subarachnoid arterioles indeed constrict by B40% in the early phase, i.e., 5 minutes to 2 hours after SAH in vivo (Sun et al, 2009). Vasoconstriction also seems to affect intraparenchymal microvessels as soon as 10 minutes after SAH, as demonstrated by collagen IV and endothelial barrier antigen immunohistochemistry on fixed rat tissue (Sehba et al, 2007) and may last up to 7 days as shown using a casting technique in dogs (Ohkuma et al, 1997). That the observed changes at the level of the microcirculation are not an experimental artifact, but may indeed contribute to the post hemorrhagic pathophysiology of SAH in humans, were demonstrated by a study performed in our department which visualized the cerebral microcirculation in SAH patients during aneurysm clipping during the first 3 days after the initial bleed, i.e., at time points where macrovasospasm was not present (Uhl et al, 2003).…”

Section: Discussionmentioning

confidence: 92%

“…Another technical advantage of the current study is that it is one of the few to use intravital videomicroscopy for the direct visualization of the post hemorrhagic cerebral microcirculation in vivo (Ishikawa et al, 2009;Sun et al, 2009). In comparison with previous studies which described post hemorrhagic microvasospasm ex vivo by histology on fixed tissue or by casting techniques (Ohkuma et al, 1997;Sehba et al, 2007), the current study using in-vivo microscopy has the intrinsic advantages of studying vessels in the living brain, to be able to study the whole vascular tree of the MCA, to observe dynamic changes, e.g., thrombus formation, and to uncover dynamic interactions, e.g., vasoconstriction and microthrombosis. Finally, the current study was performed in a recently improved mouse SAH model (Feiler et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

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Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

Friedrich

Müller

Feiler

et al. 2011

J Cereb Blood Flow Metab

186

196

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Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is characterized by a severe, cerebral perfusion pressure (CPP)-independent reduction in cerebral blood flow suggesting alterations on the level of cerebral microvessels. Therefore, we aimed to use in-vivo imaging to investigate the cerebral microcirculation after experimental SAH. Subarachnoid hemorrhage was induced in C57/BL6 mice by endovascular perforation. Pial arterioles and venules (10 to 80 lm diameter) were examined using in-vivo fluorescence microscopy, 3, 6, and 72 hours after SAH. Venular diameter or flow was not affected by SAH, while > 70% of arterioles constricted by 22% to 33% up to 3 days after hemorrhage (P < 0.05 versus sham). The smaller the investigated arterioles, the more pronounced the constriction (r 2 = 0.92, P < 0.04). Approximately 30% of constricted arterioles were occluded by microthrombi and the frequency of arteriolar microthrombosis correlated with the degree of constriction (r 2 = 0.93, P < 0.03). The current study demonstrates that SAH induces microarterial constrictions and microthrombosis in vivo. These findings may explain the early CPP-independent decrease in cerebral blood flow after SAH and may therefore serve as novel targets for the treatment of early perfusion deficits after SAH.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

Friedrich

Müller

Feiler

et al. 2011

J Cereb Blood Flow Metab

186

196

View full text Add to dashboard Cite

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“…However, a recent histological study revealed that intraparenchymal small arteries or arterioles show luminal narrowing rather than dilation during cerebral vasospasm after experimental SAH. 5) Thus, although whether the peripheral arterioles are dilated or constricted at vasospasm remains unclear, disturbance of the intracerebral microcirculatory system may be involved in cerebral ischemia due to vasospasm. Microcirculatory changes manifesting as prolonged peripheral cerebral circulation time are thought to be involved in cerebral ischemia during cerebral vasospasm, 5) and the reduction in regional cerebral blood flow was significantly correlated with prolonged peripheral cerebral circulation time in our patients with angiographic vasospasm.…”

Section: Discussionmentioning

confidence: 99%

Intro-arterial Administration of Fasudil Hydrochloride for Vasospasm Following Subarachnoid Hemorrhage-Analysis of Time-Density Curve With Digital Subtraction Angiography-

Iwabuchi

Yokouchi

Hayashi

et al. 2006

Neurol. Med. Chir.(Tokyo)

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The cerebral circulatory dynamics were evaluated before and after intra-arterial administration of fasudil hydrochloride in 20 patients with angiographic vasospasm after subarachnoid hemorrhage (SAH). The region of interest time-density curves obtained before and after intra-arterial administration of fasudil hydrochloride were compared in the proximal portion of the middle cerebral artery in the early arterial phase, the distal portion of the middle cerebral artery in the late arterial phase, and the transverse sinus in the venous phase. In the early arterial phase, the time to peak and the time to halfpeak were significantly reduced. In the late arterial phase and venous phase, the time to peak was significantly reduced. These results suggest that intra-arterial administration of fasudil hydrochloride induced dilation of the proximal arteries, and improved cerebral microcirculation. The present study suggests that intra-arterial administration of fasudil hydrochloride is effective as a treatment for vasospasm following SAH.

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“…Even deterioration due to ischemia has been attributed to causes other than angiographic vasospasm; these include microvascular vasospasm, thromboembolism, and delayed neuronal apoptosis triggered by global ischemia occurring at the time of SAH. 38,39,49,52 Here we use the term delayed cerebral ischemia to mean ischemia from angiographic vasospasm.…”

Section: Definitions Of Terminologymentioning

confidence: 99%

Can angiographic vasospasm be used as a surrogate marker in evaluating therapeutic interventions for cerebral vasospasm?

Nolan

Macdonald²

2006

FOC

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✓ The authors tested the null hypothesis that published literature with a high level of evidence does not support the assertion that subarachnoid hemorrhage (SAH) causes cerebral vasospasm, which in turn causes cerebral infarction and poor outcome after aneurysmal SAH. The medical literature on SAH was searched in MEDLINE. The author's personal files of all published literature on SAH were reviewed. References cited in Cochrane reviews as well as the published papers that were reviewed were also retrieved. There is no question that SAH causes what the authors have chosen to call “angiographic vasospasm.” However, the incidence and severity of vasospasm in recent series of patients is not well defined. There is reasonable evidence that vasospasm causes infarction, but again, accurate data on how severe and how diffuse vasospasm has to be to cause infarction and how often vasospasm is the primary cause of infarction are not available. There are good data on the incidence of cerebral infarction after SAH, and these data indicate that it is highly associated with poor outcome. The link between angiographic vasospasm and poor outcome is particularly poorly described in terms of what would be considered data of a high level of evidence. The question as to whether there is a clear pathway from SAH to vasospasm to cerebral infarction to poor outcome seems so obvious to neurosurgeons as to make it one not worth asking. Nevertheless, the obvious is not always true or accurate, so it is important to note that published literature only weakly supports the causative association of vasospasm with infarction and poor outcome after SAH. It behooves neurosurgeons to document this seemingly straightforward pathway with high-quality evidence acceptable to the proponents of evidence-based medicine.

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Morphological Changes of Intraparenchymal Arterioles after Experimental Subarachnoid Hemorrhage in Dogs

Abstract: These results suggest that constriction of intraparenchymal arterioles occurs after SAH and may contribute to delayed cerebral ischemia.

Cited by 95 publications

References 24 publications

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

Intro-arterial Administration of Fasudil Hydrochloride for Vasospasm Following Subarachnoid Hemorrhage-Analysis of Time-Density Curve With Digital Subtraction Angiography-

Can angiographic vasospasm be used as a surrogate marker in evaluating therapeutic interventions for cerebral vasospasm?

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