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  • 1
    Online Resource
    Online Resource
    Disruption of myoglobin in mice induces multiple compensatory mechanisms
    Proceedings of the National Academy of Sciences ; 1999
    In:  Proceedings of the National Academy of Sciences Vol. 96, No. 18 ( 1999-08-31), p. 10495-10500
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 96, No. 18 ( 1999-08-31), p. 10495-10500
    Abstract: Myoglobin may serve a variety of functions in muscular oxygen supply, such as O 2 storage, facilitated O 2 diffusion, and myoglobin-mediated oxidative phosphorylation. We studied the functional consequences of a myoglobin deficiency on cardiac function by producing myoglobin-knockout (myo −/− ) mice. To genetically inactivate the myoglobin gene, exon 2 encoding the heme binding site was deleted in embryonic stem cells via homologous recombination. Myo −/− mice are viable, fertile, and without any obvious signs of functional limitations. Hemoglobin concentrations were significantly elevated in myo −/− mice. Cardiac function and energetics were analyzed in isolated perfused hearts under resting conditions and during β-adrenergic stimulation with dobutamine. Myo −/− hearts showed no alteration in contractile parameters either under basal conditions or after maximal β-adrenergic stimulation (200 nM dobutamine). Tissue levels of ATP, phosphocreatine ( 31 P-NMR), and myocardial O 2 consumption were not altered. However, coronary flow {6.4 ± 1.3 ml⋅min −1 ⋅g −1 [wild-type (WT)] vs. 8.5 ± 2.4 ml⋅min −1 ⋅g −1 [myo −/− ]} and coronary reserve [17.1 ± 2.1 (WT) vs. 20.8 ± 1.1 (myo −/− ) ml⋅min −1 ⋅g −1 were significantly elevated in myo −/− hearts. Histological examination revealed that capillary density also was increased in myo −/− hearts [3,111 ± 400 mm −2 (WT) vs. 4,140 ± 140 mm −2 (Myo −/− )]. These data demonstrate that disruption of myoglobin results in the activation of multiple compensatory mechanisms that steepen the pO 2 gradient and reduce the diffusion path length for O 2 between capillary and the mitochondria; this suggests that myoglobin normally is important for the delivery of oxygen.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.96.18.10495
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1999
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Myoglobin facilitates oxygen diffusion
    Wiley ; 2001
    In:  The FASEB Journal Vol. 15, No. 6 ( 2001-04), p. 1077-1079
    Details
    In: The FASEB Journal, Wiley, Vol. 15, No. 6 ( 2001-04), p. 1077-1079
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v15.6
    DOI: 10.1096/fsb2fj000497fje
    Language: English
    Publisher: Wiley
    Publication Date: 2001
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Myoglobin: A scavenger of bioactive NO
    Proceedings of the National Academy of Sciences ; 2001
    In:  Proceedings of the National Academy of Sciences Vol. 98, No. 2 ( 2001-01-16), p. 735-740
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 98, No. 2 ( 2001-01-16), p. 735-740
    Abstract: The present study explored the role of myoglobin (Mb) in cardiac NO homeostasis and its functional relevance by employing isolated hearts of wild-type (WT) and myoglobin knockout mice. 1 H NMR spectroscopy was used to measure directly the conversion of oxygenated Mb (MbO 2 ) to metmyoglobin (metMb) by reaction with NO. NO was applied intracoronarily (5 nM to 25 μM), or its endogenous production was stimulated with bradykinin (Bk; 10 nM to 2 μM). We found that infusion of authentic NO solutions dose-dependently (≥ 2.5 μM NO) increased metMb formation in WT hearts that was rapidly reversible on cessation of NO infusion. Likewise, Bk-induced release of NO was associated with significant metMb formation in the WT (≥1 μM Bk). Hearts lacking Mb reacted more sensitively to infused NO in that vasodilatation and the cardiodepressant actions of NO were more pronounced. Similar results were obtained with Bk. The lower sensitivity of WT hearts to changes in NO concentration fits well with the hypothesis that in the presence of Mb, a continuous degradation of NO takes place by reaction of MbO 2 + NO to metMb + NO 3 − , thereby effectively reducing cytosolic NO concentration. This breakdown protects myocytic cytochromes against transient rises in cytosolic NO. Regeneration of metMb by metMb reductase to Mb and subsequent association with O 2 leads to reformation of MbO 2 available for another NO degradation cycle. Our data indicate that this cycle is crucial in the breakdown of NO and substantially determines the dose–response curve of the NO effects on coronary blood flow and cardiac contractility.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.98.2.735
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2001
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Myoglobin facilitates oxygen diffusion
    Wiley ; 2001
    In:  The FASEB Journal Vol. 15, No. 6 ( 2001-04), p. 1077-1079
    Details
    In: The FASEB Journal, Wiley, Vol. 15, No. 6 ( 2001-04), p. 1077-1079
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Article
    DOI: 10.1096/fj.00-0497fje
    Language: English
    Publisher: Wiley
    Publication Date: 2001
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Endothelial NO formation does not control myocardial O 2 consumption in mouse heart
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 285, No. 1 ( 2003-07), p. H392-H397
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 285, No. 1 ( 2003-07), p. H392-H397
    Abstract: To test whether endothelium-derived nitric oxide (NO) regulates mitochondrial respiration, NO was pharmacologically modulated in isolated mouse hearts, which were perfused at constant flow to sensitively detect small changes in myocardial O 2 consumption (MV̇O 2 ). Stimulation of NO formation by 10 μM bradykinin (BK) increased coronary venous nitrite release fivefold to 58 ± 33 nM ( n = 17). Vasodilatation by BK, adenosine (1 μM), or papaverine (10 μM) decreased perfusion pressure, left ventricular developed pressure (LVDP), and MV̇O 2 . In the presence of adenosine-induced vasodilatation, stimulation of endothelial NO synthesis by BK had no effect on LVDP and MV̇O 2 . Also, inhibition of NO formation by N G -monomethyl-l-arginine (l-NMMA, 100 μM) did not significantly alter LVDP and MV̇O 2 . Similarly, intracoronary infusion of authentic NO ≤2 μM did not influence LVDP or MV̇O 2 (-1 ± 1%). Only when NO was 〉 2 μM were contractile dysfunction and MV̇O 2 reduction observed. Because BK-induced stimulation of endothelial NO formation and basal NO are not sufficient to impair MV̇O 2 in the saline-perfused mouse heart, a tonic control of the respiratory chain by endothelial NO is difficult to conceive.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00836.2002
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    High-resolution imaging reveals a limit in spatial resolution of blood flow measurements by microspheres
    American Physiological Society ; 2004
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 287, No. 3 ( 2004-09), p. H1132-H1140
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 287, No. 3 ( 2004-09), p. H1132-H1140
    Abstract: Density of 15-μm microspheres after left atrial application is the standard measure of regional perfusion. In the heart, substantial differences in microsphere density are seen at spatial resolutions 〈 5 ml, implying perfusion heterogeneity. Microsphere deposition imaging permits a superior evaluation of the distribution pattern. Therefore, fluorescent microspheres (FMS) were applied, FMS deposition in the canine heart was imaged by epifluorescence microscopy in vitro, and the patterns were observed compared with MR images of iron oxide microspheres (IMS) obtained in vivo and in vitro. FMS deposition in myocardial slices revealed the following: 1) a nonrandom distribution, with sequentially applied FMS of different color stacked within the same vessel, 2) general FMS clustering, and 3) rather large areas devoid of FMS ( n = 3). This pattern was also seen in reconstructed three-dimensional images ( 〈 1 nl resolution) of FMS distribution ( n = 4). Surprisingly, the deposition pattern of sequentially applied FMS remained virtually identical over 3 days. Augmenting flow by intracoronary adenosine ( 〉 2 μM) enhanced local microsphere density, but did not alter the deposition pattern ( n = 3). The nonrandom, temporally stable pattern was quantitatively confirmed by a three-dimensional intermicrosphere distance analysis of sequentially applied FMS. T 2 -weighted short-axis MR images (2-μl resolution) of IMS revealed similar patterns in vivo and in vitro ( n = 6), as seen with FMS. The observed temporally stable microsphere patterns are not consistent with the notion that microsphere deposition is solely governed by blood flow. We propose that at high spatial resolution ( 〈 2 μl) structural aspects of the vascular network dominate microsphere distribution, resulting in the organized patterns observed.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00119.2004
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Adenosine produced via the CD73/ecto-5′-nucleotidase pathway has no impact on erythropoietin production but is associated with reduced kidney weight
    Springer Science and Business Media LLC ; 2006
    In:  Pflügers Archiv - European Journal of Physiology Vol. 452, No. 3 ( 2006-6), p. 324-331
    Details
    In: Pflügers Archiv - European Journal of Physiology, Springer Science and Business Media LLC, Vol. 452, No. 3 ( 2006-6), p. 324-331
    Type of Medium: Online Resource
    ISSN: 0031-6768 , 1432-2013
    URL: Article
    DOI: 10.1007/s00424-006-0045-x
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2006
    detail.hit.zdb_id: 1463014-X
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Coronary Hemodynamics in Endothelial NO Synthase Knockout Mice
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Circulation Research Vol. 82, No. 2 ( 1998-02-09), p. 186-194
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 82, No. 2 ( 1998-02-09), p. 186-194
    Abstract: Abstract —For the specific analysis of endothelial NO synthase (eNOS) function in the coronary vasculature, we generated a mouse homozygous for a defective eNOS gene (eNOS−/−). Western blot as well as immunohistochemical staining revealed the absence of eNOS protein in eNOS−/− mice. Aortic endothelial cells derived from eNOS−/− mice displayed only background levels of NO x formation compared with wild-type (WT) cells (88 versus 1990 pmol NO x · h −1 /mg protein −1 ). eNOS−/− mice were hypertensive (mean arterial pressure, 135±15 versus 107±8 mm Hg in WT) without the development of cardiac hypertrophy. Coronary hemodynamics, analyzed in Langendorff-perfused hearts, showed no differences either in basal coronary flow or in maximal and repayment flow of reactive hyperemia. Acute NOS inhibition with N ω -nitro- l -arginine methyl ester (L-NAME) in WT hearts substantially reduced basal flow and reactive hyperemia. The coronary response to acetylcholine (ACh) (500 nmol/L) was biphasic: An initial vasoconstriction (flow, −35%) in WT hearts was followed by sustained vasodilation (+190%). L-NAME significantly reduced vasodilation in WT hearts (+125%) but did not alter the initial vasoconstriction. In eNOS−/− hearts, the initial vasoconstriction was augmented (−70%), whereas the ACh-induced vasodilation was not affected. Inhibition of cyclooxygenase with diclofenac converted the ACh-induced vasodilation into vasoconstriction (−49% decrease of basal flow). This effect was even more pronounced in eNOS−/− hearts (−71%). Our results demonstrate that (1) acute inhibition of eNOS reveals a role for NO in setting the basal coronary vascular tone as well as participation in reactive hyperemia and the response to ACh; (2) chronic inhibition of NO formation in eNOS−/− mutant mice induces no changes in basal coronary flow and reactive hyperemia, suggesting the activation of important compensatory mechanisms; and (3) prostaglandins are the main mediators of the ACh-induced vasodilation in both WT and eNOS−/− mice.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.82.2.186
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1998
    detail.hit.zdb_id: 1467838-X
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  • 9
    Online Resource
    Online Resource
    Purinogen is not an endogenous substrate used in endothelial cells during substrate deprivation
    Portland Press Ltd. ; 1999
    In:  Biochemical Journal Vol. 338, No. 2 ( 1999-03-01), p. 523-527
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 338, No. 2 ( 1999-03-01), p. 523-527
    Abstract: Porcine aortic endothelial cells (PAEC) are known to be metabolically robust. They are capable of surviving extended periods of complete lack of exogenous substrate, and purine release has been shown to be significantly up-regulated. The endogenous substrates used during substrate deprivation, as well as the sources responsible for the increased purine release, have not been completely identified. We tested the possibility that a phosphoglyceroyl-ATP-containing polymer, purinogen, might support PAEC hibernation induced by lack of exogenous substrate. This involved isolation of the acid-insoluble fraction of PAEC, which was presumed to contain purinogen, and analysis by HPLC and 31P NMR. No evidence supporting the presence of triphosphate-containing compounds (purinogen) was found. Similar results were obtained in the rat heart. The majority of the products in the acid-insoluble, alkaline-treated fraction were identified as RNA degradation products (2´- and 3´-nucleoside monophosphates). A [14C]adenosine labelling experiment showed that incorporation of adenosine into the acid-insoluble fraction was almost completely prevented after inhibition of RNA synthesis with actinomycin D. Furthermore, RNA isolated from PAEC and subsequently treated with alkali showed a profile that was almost identical with the HPLC profile of the acid-insoluble fraction. Finally, substrate-free incubation of the cells did not quantitatively or qualitatively influence the distribution of acid-insoluble derivatives. We conclude that PAEC survival during the absence of exogenous substrate is not supported by purinogen but rather by some other, yet-to-be-identified, endogenous substrate.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj3380523
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1999
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Myocardial proteome analysis reveals reduced NOS inhibition and enhanced glycolytic capacity in areas of low local blood flow
    Wiley ; 2002
    In:  The FASEB Journal Vol. 16, No. 6 ( 2002-04), p. 628-630
    Details
    In: The FASEB Journal, Wiley, Vol. 16, No. 6 ( 2002-04), p. 628-630
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v16.6
    DOI: 10.1096/fj.01-0574fje
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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