Investigation of Postmortem Functional Changes in Human Cerebral Arteries

Onoue, Hisashi; Kaito, Nobuyoshi; Tokudome, Shogo; Abe, Toshiaki; Tashibu, Koichi; Nagashima, Hiroyasu; Nakamura, Norio

doi:10.1038/jcbfm.1993.44

Cited by 18 publications

(7 citation statements)

References 17 publications

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“…(b) A second limitation is the change in vascular muscle tone postmortem. It is known that postmortem the arterial smooth muscle relaxation and contractility change (Patel and Janicki, ; Onoue et al, ). This change could have an impact on cast production and radius measurements performed on dissection material.…”

Section: Discussionmentioning

confidence: 99%

Branching Pattern of the Cerebral Arterial Tree

Helthuis

Doormaal

Hillen

et al. 2018

The Anatomical Record

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Quantitative data on branching patterns of the human cerebral arterial tree are lacking in the 1.0–0.1 mm radius range. We aimed to collect quantitative data in this range, and to study if the cerebral artery tree complies with the principle of minimal work (Law of Murray). To enable easy quantification of branching patterns a semi‐automatic method was employed to measure 1,294 bifurcations and 2,031 segments on 7 T‐MRI scans of two corrosion casts embedded in a gel. Additionally, to measure segments with a radius smaller than 0.1 mm, 9.4 T‐MRI was used on a small cast section to characterize 1,147 bifurcations and 1,150 segments. Besides MRI, traditional methods were employed. Seven hundred thirty‐three bifurcations were manually measured on a corrosion cast and 1,808 bifurcations and 1,799 segment lengths were manually measured on a fresh dissected cerebral arterial tree. Data showed a large variation in branching pattern parameters (asymmetry‐ratio, area‐ratio, length‐radius‐ratio, tapering). Part of the variation may be explained by the variation in measurement techniques, number of measurements and location of measurement in the vascular tree. This study confirms that the cerebral arterial tree complies with the principle of minimum work. These data are essential in the future development of more accurate mathematical blood flow models. Anat Rec, 302:1434–1446, 2019. © 2018 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.

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Section: Discussionmentioning

confidence: 99%

Branching Pattern of the Cerebral Arterial Tree

Helthuis

Doormaal

Hillen

et al. 2018

The Anatomical Record

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“…Most studies report on brain homogenates rather than isolated cell types. Further, the cerebral endothelial cell layer is fragile, and they rapidly deteriorate post mortem or during the preparation for experimental procedures rendering it difficult to identify the function of this specific cell type (Onoue et al 1993). PDE activities were initially measured in cerebral microvessels isolated from bovine cortex (Stefanovich 1979), where both cGMP and cAMP hydrolytic activity was detected.…”

Section: Overview Of the Distribution Of Pdes In The Cerebral Vasculaturementioning

confidence: 99%

Cyclic nucleotide phosphodiesterases (PDEs) and endothelial function in ischaemic stroke. A review

Yasmeen

Akram

Hainsworth

et al. 2019

Cellular Signalling

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Background: Endothelial dysfunction is a hallmark of cerebrovascular disease, including ischemic stroke. Modulating endothelial signalling by cyclic nucleotides, cAMP and cGMP, is a potential therapeutic target in stroke. Inhibitors of the cyclic nucleotide degrading phosphodiesterase (PDE) enzymes may restore cerebral endothelial function. Current knowledge on PDE distribution and function in cerebral endothelial cells is sparse. This review explores data on PDE distribution and effects of PDEi in cerebral endothelial cells and identifies which PDEs are potential treatment targets in stroke. Method: We performed a systematic search of electronic databases (Medline and Embase). Our search terms were cerebral ischaemia, cerebral endothelial cells, cyclic nucleotide, phosphodiesterase and phosphodiesterase inhibitors. Results: We found 23 publications which described effects of selective inhibitors of only three PDE families on endothelial function in ischemic stroke. PDE3 inhibitors (PDE3i) (11 publications) and PDE4 inhibitors (PDE4i) (3 publications) showed anti-inflammatory, anti-apoptotic or proangiogenic effects. PDE3i also reduced leucocyte infiltration and MMP-9 expression. Both PDE3i and PDE4i increased expression of tight junction proteins and protected the blood-brain barrier. PDE5 inhibitors (PDE5i) (6 publications) reduced inflammation and apoptosis. In preclinical models, PDE5i enhanced cGMP/NO signalling associated with microvascular angiogenesis, increased cerebral blood flow and improved functional recovery. Non-specific PDEi (3 publications) had mainly anti-inflammatory effects. Conclusion:This review demonstrates that non-selective and selective PDEi of PDE3, PDE4 and PDE5 modulated endothelial function in cerebral ischemic stroke by regulating processes involved in vascular repair and neuroprotection and thus reduced cell death and inflammation. Of note, they promoted angiogenesis, microcirculation and improved functional recovery; all are important in stroke prevention and recovery, and effects should be further evaluated in humans.

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“…The majority of evidence for NO-dependent relaxation of cerebral vessels comes from experiments performed on large cerebral arteries in vitro and in vivo. NO-dependent relaxation in these vessels has been observed in response to shear stress, acetylocholine and a number of other receptor mediated agonists in both animals and humans using NOS inhibitors [7,24,25,27,29]. These inhibitors have been demonstrated to decrease cerebral blood flow and increase cerebral vascular resistance under basal conditions in several species [9,16,19,23].…”

Section: Introductionmentioning

confidence: 95%