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  • 1
    Online Resource
    Online Resource
    Downregulation of Endothelial Transient Receptor Potential Vanilloid Type 4 Channel and Small-Conductance of Ca 2+ -Activated K + Channels Underpins Impaired Endothelium-Dependent Hyperpolarization in Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Hypertension Vol. 69, No. 1 ( 2017-01), p. 143-153
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 69, No. 1 ( 2017-01), p. 143-153
    Abstract: Endothelium-dependent hyperpolarization (EDH)–mediated responses are impaired in hypertension, but the underlying mechanisms have not yet been determined. The activation of small- and intermediate-conductance of Ca 2+ -activated K + channels (SK Ca and IK Ca ) underpins EDH-mediated responses. It was recently reported that Ca 2+ influx through endothelial transient receptor potential vanilloid type 4 channel (TRPV4) is a prerequisite for the activation of SK Ca /IK Ca in endothelial cells in specific beds. Here, we attempted to determine whether the impairment of EDH in hypertension is attributable to the dysfunction of TRPV4 and S/IK Ca , using isolated superior mesenteric arteries of 20-week-old stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched Wistar–Kyoto (WKY) rats. In the WKY arteries, EDH-mediated responses were reduced by a combination of SK Ca /IK Ca blockers (apamin plus TRAM-34; 1-[(2-chlorophenyl)diphenylmethl]-1 H -pyrazole) and by the blockade of TRPV4 with the selective antagonist RN-1734 or HC-067047. In the SHRSP arteries, EDH-mediated hyperpolarization and relaxation were significantly impaired when compared with WKY. GSK1016790A, a selective TRPV4 activator, evoked robust hyperpolarization and relaxation in WKY arteries. In contrast, in SHRSP arteries, the GSK1016790A-evoked hyperpolarization was small and relaxation was absent. Hyperpolarization and relaxation to cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine, a selective SK Ca activator, were marginally decreased in SHRSP arteries compared with WKY arteries. The expression of endothelial TRPV4 and SK Ca protein was significantly decreased in the SHRSP mesenteric arteries compared with those of WKY, whereas function and expression of IK Ca were preserved in SHRSP arteries. These findings suggest that EDH-mediated responses are impaired in superior mesenteric arteries of SHRSP because of a reduction in both TRPV4 and SK Ca input to EDH.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.116.07110
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2094210-2
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  • 2
    Online Resource
    Online Resource
    Abstract 232: Delayed Administration of Epinephrine is Associated with Worse Neurological Outcomes in Patients with Out-of-hospital Cardiac Arrest and Initial Pulseless Electrical Activity
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation Vol. 142, No. Suppl_4 ( 2020-11-17)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 142, No. Suppl_4 ( 2020-11-17)
    Abstract: Background: Delayed administration of epinephrine has been proven to worsen the neurological outcomes of patients with out-of-hospital cardiac arrest (OHCA) and initial shockable rhythm. We aimed to investigate whether delayed administration of epinephrine might also worsen the neurological outcomes of patients with witnessed OHCA and initial pulseless electrical activity (PEA). Methods: The Japanese Association for Acute Medicine - out-of-hospital cardiac arrest (JAAM-OHCA) Registry is a multicenter, prospective, observational registry including 34,754 OHCA patients between 2014 and 2017. The present study assessed the impact of the time to epinephrine administration on neurological outcomes in patients with witnessed non-traumatic OHCA with initial rhythm of PEA. The primary outcome was defined as Cerebral Performance Categories (CPC) Scale 1-2 at 30 days after OHCA. The association between the odds ratio for the primary outcome and the time from witnessed OHCA to epinephrine administration was assessed with a restricted cubic spline analysis. Results: Out of 34,754 patients with OHCA, 3,050 patients with OHCA and initial PEA who received epinephrine were included in the present study. Mean age was 73.7 years and 1836 (60.2%) was male. After adjusting for potential confounders, the time from witnessed OHCA to epinephrine administration was associated with lower likelihood of favorable neurological outcomes (odds ratio [OR] 0.92; 95% confidence interval [CI] 0.89-0.96; P & lt;0.001). The restricted cubic spline analysis demonstrated that delayed epinephrine administration could decrease the likelihood of a favorable neurological outcome; this was significant within the first 10 minutes. Conclusions: Delayed administration of epinephrine was associated with worse neurological outcomes in patients with witnessed OHCA patients with initial PEA.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.142.suppl_4.232
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1466401-X
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  • 3
    Online Resource
    Online Resource
    Nox4 as the Major Catalytic Component of an Endothelial NAD(P)H Oxidase
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Circulation Vol. 109, No. 2 ( 2004-01-20), p. 227-233
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 109, No. 2 ( 2004-01-20), p. 227-233
    Abstract: Background— Recent evidence has suggested that reactive oxygen species are important signaling molecules in vascular cells and play a pivotal role in the development of vascular diseases. The activity of NAD(P)H oxidase has been identified as the major source of reactive oxygen species in vascular endothelial cells. However, the precise molecular structure and the mechanism of activation of the oxidase have remained poorly understood. Methods and Results— Here, we investigated the molecular identities and the superoxide-producing activity of endothelial NAD(P)H oxidase. We found that Nox4, a homologue of gp91phox/Nox2, was abundantly expressed in endothelial cells. The expression of Nox4 in endothelial cells markedly exceeded that of other Nox proteins, including gp91phox/Nox2, and was affected by cell growth. Using electron spin resonance and chemiluminescence, we measured the superoxide production and found that the endothelial membranes had an NAD(P)H-dependent superoxide-producing activity comparable to that of the neutrophil membranes, whereas the activity was not enhanced by the 2 recombinant proteins p47phox and p67phox, in contrast to that of the neutrophil membranes. Downregulation of Nox4 by an antisense oligonucleotide reduced superoxide production in endothelial cells in vivo and in vitro. Conclusions— These findings suggest that Nox4 may function as the major catalytic component of an endothelial NAD(P)H oxidase.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000105680.92873.70
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1466401-X
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  • 4
    Online Resource
    Online Resource
    Relationship Between Plasma Glutathione Levels and Cardiovascular Disease in a Defined Population : The Hisayama Study
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Stroke Vol. 35, No. 9 ( 2004-09), p. 2072-2077
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 9 ( 2004-09), p. 2072-2077
    Abstract: Background and Purpose— Glutathione (GSH) appears to have marked antioxidant activities and therefore may prevent cardiovascular disease (CVD). However, there are very few reports on this subject. In a community-based case–control study, we tested the hypothesis that low levels of plasma GSH are closely associated with CVD and its clinical types. Methods— The association between fasting plasma total GSH (tGSH) levels and CVD were assessed using conditional logistic regression analysis among 134 CVD cases and 435 age- and sex-matched healthy control subjects. Results— Mean tGSH concentrations were lower in all CVD cases than in the control subjects (3.06 versus 3.71 μmol/L; P =0.0001). Among the CVD types, both the cerebral infarction cases (2.98 versus 3.59 μmol/L; P =0.001) and cerebral hemorrhage cases (2.51 versus 3.43 μmol/L; P =0.0027) had significantly lower tGSH levels than the corresponding control groups had. The same tendency was observed for cases of subarachnoid hemorrhage (3.45 versus 3.83 μmol/L; P =0.36) and myocardial infarction (3.65 versus 3.77 μmol/L; P =0.69), but these differences were not statistically significant. After adjustment for other confounding factors, the risk of CVD was significantly lower in the third (adjusted odds ratio, 041; 95% CI, 0.21 to 0.77) and the fourth quartiles (adjusted odds ratio, 0.25; 95% CI, 0.12 to 0.51) than in the first. This association was most prominent in patients with lacunar infarction or cerebral hemorrhage. Conclusions— These findings suggest that reduced plasma tGSH levels are a risk factor for CVD, especially for cerebral small vessel disease.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/01.STR.0000138022.86509.2d
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1467823-8
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  • 5
    Online Resource
    Online Resource
    Altered Cerebrovascular Response to a Potassium Channel Opener in Hypertensive Rats
    Ovid Technologies (Wolters Kluwer Health) ; 1996
    In:  Hypertension Vol. 28, No. 1 ( 1996-07), p. 143-146
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 28, No. 1 ( 1996-07), p. 143-146
    Abstract: We examined whether the effect of Y-26763, an ATP-sensitive potassium channel opener, on cerebral blood flow is altered in stroke-prone spontaneously hypertensive rats (SHRSP) and, if altered, whether long-term antihypertensive treatment with cilazapril, an angiotensin-converting enzyme inhibitor, is capable of preventing the change. Cerebral blood flow during intracarotid infusion of Y-26763 was measured in anesthetized SHRSP and normotensive Wistar-Kyoto rats (WKY) as control. Y-26763 increased cerebral blood flow in a dose-dependent manner in WKY, and glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, inhibited the Y-26763–induced increase in cerebral blood flow. In contrast, the response to Y-26763 in SHRSP was significantly impaired compared with that in WKY. Antihypertensive treatment with cilazapril lowered blood pressure toward normal and prevented the impaired response in cerebral blood flow to Y-26763 in SHRSP. These findings suggest that (1) ATP-sensitive potassium channels contribute to the regulation of cerebral blood flow in rats, (2) the response to an ATP-sensitive potassium channel opener is markedly diminished in hypertensive rats, and (3) the altered response to an ATP-sensitive potassium channel opener during chronic hypertension can be prevented by long-term antihypertensive treatment.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.28.1.143
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1996
    detail.hit.zdb_id: 2094210-2
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  • 6
    Online Resource
    Online Resource
    The gene–treatment interaction of paraoxonase-1 gene polymorphism and statin therapy on insulin secretion in Japanese patients with type 2 diabetes: Fukuoka diabetes registry
    Springer Science and Business Media LLC ; 2017
    In:  BMC Medical Genetics Vol. 18, No. 1 ( 2017-12)
    Details
    In: BMC Medical Genetics, Springer Science and Business Media LLC, Vol. 18, No. 1 ( 2017-12)
    Type of Medium: Online Resource
    ISSN: 1471-2350
    URL: Article
    DOI: 10.1186/s12881-017-0509-1
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2041359-2
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  • 7
    Online Resource
    Online Resource
    Association of aortic valve calcification with carotid artery lesions and peripheral artery disease in patients with chronic kidney disease: a cross-sectional study
    Springer Science and Business Media LLC ; 2020
    In:  BMC Nephrology Vol. 21, No. 1 ( 2020-12)
    Details
    In: BMC Nephrology, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2020-12)
    Abstract: Patients with chronic kidney disease (CKD) reportedly have a high prevalence of aortic valve calcification (AVC). In population-based studies, AVC is considered a manifestation of systemic atherosclerosis. The association of AVC with atherosclerotic lesions has not been fully investigated in predialysis patients. The present study was performed to determine whether carotid artery lesions and peripheral artery disease (PAD) are associated with AVC in patients with CKD not on dialysis. Methods In total, 749 patients were included in this cross-sectional study. AVC was evaluated using echocardiography. Carotid artery lesions including carotid artery plaque (CAP) and PAD were simultaneously examined in each patient. A logistic regression analysis was applied to determine the factors associated with AVC. Results AVC, CAP, and PAD were found in 201, 583, and 123 patients, respectively. In the multivariable analyses adjusted for covariates including the estimated glomerular filtration rate and makers of mineral metabolism (serum calcium, serum phosphorus, parathyroid hormone, 1,25-dihydroxyvitamin D, and fibroblast growth factor 23), AVC was significantly associated with the presence of CAP [odds ratio (OR), 3.37; 95% confidence interval (CI), 1.43–7.95], the presence of PAD (OR, 1.76; 95% CI, 1.10–2.81), the CAP score (per 1.0-point increase) (OR, 1.06; 95% CI, 1.02–1.11), and the ankle-brachial blood pressure index (per 0.1-point increase) (OR, 0.83; 95% CI, 0.72–0.95). Conclusions AVC was associated with atherosclerotic lesions independent of kidney function and mineral metabolism. We consider that this association between AVC and atherosclerosis might reflect the burden of shared atherosclerotic risk factors.
    Type of Medium: Online Resource
    ISSN: 1471-2369
    URL: Article
    DOI: 10.1186/s12882-020-01864-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2041348-8
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  • 8
    Online Resource
    Online Resource
    Diagnosis and follow-up of posterior inferior cerebellar artery dissection complicated with ischemic stroke assisted by T1-VISTA: a report of two cases
    Springer Science and Business Media LLC ; 2016
    In:  BMC Neurology Vol. 16, No. 1 ( 2016-12)
    Details
    In: BMC Neurology, Springer Science and Business Media LLC, Vol. 16, No. 1 ( 2016-12)
    Type of Medium: Online Resource
    ISSN: 1471-2377
    URL: Article
    DOI: 10.1186/s12883-016-0637-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2041347-6
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  • 9
    Online Resource
    Online Resource
    Photothrombotic Middle Cerebral Artery Occlusion and Reperfusion Laser System in Spontaneously Hypertensive Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Stroke Vol. 34, No. 11 ( 2003-11), p. 2716-2721
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. 11 ( 2003-11), p. 2716-2721
    Abstract: Background and Purpose— To establish a less invasive and reproducible focal ischemia model in the rat, we adopted a 2-laser system (ie, photothrombosis and YAG laser–induced reperfusion). Methods— The distal middle cerebral artery (MCA) of spontaneously hypertensive rats was occluded by 568-nm krypton laser and intravenous infusion of the photosensitizing dye rose bengal and was recanalized by 355-nm ultraviolet laser irradiation. Cerebral blood flow was determined by laser-Doppler flowmetry at the penumbral cortex. Infarct volume was determined at 3 days after distal MCA occlusion. Results— Brain temperature determined with infrared thermography was maintained within an acceptable range of approximately 1°C upper shift of the center of brain temperature distribution during krypton or YAG laser irradiation. The average of the values (23 experiments; n=163) of coefficient of variation of infarct volume was 21±6%, indicating high reproducibility of this model. After distal MCA occlusion, cerebral blood flow was decreased to 32±16% of the control values and was increased to 98±21% after YAG laser–induced reperfusion. Infarct volume in these rats was 61±18 mm 3 (coefficient of variation=30%; n=6). Conclusions— We have characterized a highly reproducible focal ischemia model utilizing a 2-laser system, one to induce thrombotic MCA occlusion and the other to facilitate reperfusion.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/01.STR.0000094730.38343.73
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1467823-8
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  • 10
    Online Resource
    Online Resource
    Role of Phosphatidylinositol 3-Kinase in Acetylcholine-Induced Dilatation of Rat Basilar Artery
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Stroke Vol. 31, No. 10 ( 2000-10), p. 2487-2493
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 10 ( 2000-10), p. 2487-2493
    Abstract: Background and Purpose —We tested the hypothesis that activation of phosphatidylinositol (PI) 3-kinase is involved in dilator responses of the basilar artery to acetylcholine in vivo. Methods —Responses of the basilar artery were measured by the cranial window technique in anesthetized rats. To examine the role of PI 3-kinase in acetylcholine-induced calcium signaling, we measured intracellular free calcium concentration ([Ca 2+ ] i ) of cultured rat basilar arterial endothelial cells using a fluorescent calcium indicator, indo 1. Results —Topical application of acetylcholine (10 − 6 , 10 − 5.5 , and 10 − 5 mol/L) increased the diameter of the basilar artery by 8±1%, 14±2%, and 24±3%, respectively. An inhibitor of PI 3-kinase, wortmannin (10 − 8 mol/L), did not change the baseline diameter of the artery. In the presence of wortmannin, acetylcholine (10 − 6 , 10 − 5.5 , and 10 − 5 mol/L) dilated the artery only by 3±2%, 6±2%, and 12±2%, respectively. Thus, wortmannin attenuated acetylcholine-induced dilatation of the basilar artery ( P 〈 0.05 versus control). Wortmannin had no effect on dilatation of the artery in response to a nitric oxide donor, sodium nitroprusside. LY294002, another inhibitor of PI 3-kinase, also inhibited dilator response of the basilar artery to acetylcholine. Acetylcholine produced an increase in [Ca 2+ ] i of the endothelial cells. Genistein, an inhibitor of tyrosine kinase, markedly attenuated acetylcholine-induced calcium influx to the cells; however, wortmannin had no effect on acetylcholine-induced calcium changes. Conclusions —These results suggest that acetylcholine-induced dilatation of the basilar artery is mediated, at least in part, by activation of PI 3-kinase in vivo. Acetylcholine-induced [Ca 2+ ] i changes of the endothelial cells may not be mediated by activation of the kinase. PI 3-kinase as well as [Ca 2+ ] i may play an important role in the acetylcholine-induced nitric oxide production of the basilar arterial endothelial cells.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/01.STR.31.10.2487
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 1467823-8
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