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  • American Physiological Society  (13)
  • Pagel, Paul S.  (13)
Materialart
Verlag/Herausgeber
  • American Physiological Society  (13)
Person/Organisation
Sprache
Erscheinungszeitraum
Fachgebiete(RVK)
  • 1
    Online-Ressource
    Online-Ressource
    Diabetes and hyperglycemia impair activation of mitochondrial K ATP channels
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 280, No. 4 ( 2001-04-01), p. H1744-H1750
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 280, No. 4 ( 2001-04-01), p. H1744-H1750
    Kurzfassung: Hyperglycemia is an important predictor of cardiovascular mortality in patients with diabetes. We investigated the hypothesis that diabetes or acute hyperglycemia attenuates the reduction of myocardial infarct size produced by activation of mitochondrial ATP-regulated potassium (K ATP ) channels. Acutely instrumented barbiturate-anesthetized dogs were subjected to a 60-min period of coronary artery occlusion and 3 h of reperfusion. Myocardial infarct size (triphenyltetrazolium chloride staining) was 25 ± 1, 28 ± 3, and 25 ± 1% of the area at risk (AAR) for infarction in control, diabetic (3 wk after streptozotocin-alloxan), and hyperglycemic (15% intravenous dextrose) dogs, respectively. Diazoxide (2.5 mg/kg iv) significantly decreased infarct size (10 ± 1% of AAR, P 〈 0.05) but did not produce protection in the presence of diabetes (28 ± 5%) or moderate hyperglycemia (blood glucose 310 ± 10 mg/dl; 23 ± 2%). The dose of diazoxide and the degree of hyperglycemia were interactive. Profound (blood glucose 574 ± 23 mg/dl) but not moderate hyperglycemia blocked the effects of high-dose (5.0 mg/kg) diazoxide [26 ± 3, 15 ± 3 ( P 〈 0.05), and 11 ± 2% ( P 〈 0.05), respectively]. There were no differences in systemic hemodynamics, AAR, or coronary collateral blood flow (by radioactive microspheres) between groups. The results indicate that diabetes or hyperglycemia impairs activation of mitochondrial K ATP channels.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2001.280.4.H1744
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2001
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 2
    Online-Ressource
    Online-Ressource
    Reactive oxygen species modulate coronary wall shear stress and endothelial function during hyperglycemia
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 284, No. 5 ( 2003-05-01), p. H1552-H1559
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 284, No. 5 ( 2003-05-01), p. H1552-H1559
    Kurzfassung: Hyperglycemia is associated with generation of reactive oxygen species (ROS), and this action may contribute to accelerated atherogenesis. We tested the hypothesis that hyperglycemia produces alterations in left anterior descending coronary artery (LAD) wall shear stress concomitant with endothelial dysfunction and ROS production in dogs ( n = 12) instrumented for measurement of LAD blood flow, velocity, and diameter. Dogs were randomly assigned to receive vehicle (0.9% saline) or the superoxide dismutase mimetic 4- hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (tempol) and were administered intravenous infusions of d-glucose to achieve target blood glucose concentrations of 350 and 600 mg/dl (moderate and severe hyperglycemia, respectively). Endothelial function and ROS generation were assessed by coronary blood flow responses to acetylcholine (10, 30, and 100 ng/kg) and dihydroethidium fluorescence of myocardial biopsies, respectively. Indexes of wall shear stress were calculated with conventional fluid dynamics theory. Hyperglycemia produced dose-related endothelial dysfunction, increases in ROS production, and reductions in oscillatory shear stress that were normalized by tempol. The results suggest a direct association between hyperglycemia-induced ROS production, endothelial dysfunction, and decreases in oscillatory shear stress in vivo.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01013.2002
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2003
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 3
    Online-Ressource
    Online-Ressource
    K ATP channels mediate the beneficial effects of chronic ethanol ingestion
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 279, No. 5 ( 2000-11-01), p. H2574-H2579
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 279, No. 5 ( 2000-11-01), p. H2574-H2579
    Kurzfassung: Chronic ingestion of low doses of ethanol protects the myocardium from ischemic injury by activating adenosine receptors and protein kinase C. We tested the hypothesis that ATP-dependent potassium (K ATP ) channels mediate these beneficial effects. Dogs were fed with ethanol (1.5 g/kg) or water mixed with dry food twice per day for 12 wk. After they were acutely instrumented for measurement of hemodynamics, dogs received saline (vehicle) or glyburide (0.1 mg/kg iv) and were subjected to 60 min of coronary artery occlusion followed by 3 h of reperfusion. Infarct size (through triphenyltetrazolium chloride staining) was significantly ( P 〈 0.05) reduced to 14 ± 1% of the left ventricular area at risk in ethanol-pretreated dogs compared with controls (25 ± 2%). Glyburide alone did not affect infarct size (25 ± 3%) but abolished the protective effects of ethanol pretreatment (28 ± 3%). No differences in hemodynamics or coronary collateral blood flow (through radioactive microspheres) were observed among groups. The results indicate that K ATP channels mediate the protective effects of chronic consumption of ethanol.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2000.279.5.H2574
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2000
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 4
    Online-Ressource
    Online-Ressource
    Diabetes abolishes ischemic preconditioning: role of glucose, insulin, and osmolality
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 278, No. 4 ( 2000-04-01), p. H1218-H1224
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 278, No. 4 ( 2000-04-01), p. H1218-H1224
    Kurzfassung: Recent evidence indicates that hyperglycemia is an important risk factor for the development of cardiovascular disease. We tested the hypothesis that myocardial infarct size is related to blood glucose concentration in the presence or absence of ischemic preconditioning (PC) stimuli in canine models of diabetes mellitus and acute hyperglycemia. Barbiturate-anesthetized dogs were subjected to a 60-min period of coronary artery occlusion and 3-h reperfusion. Infarct size was 24 ± 2% of the area at risk (AAR) for infarction in control dogs. PC significantly ( P 〈 0.05) decreased the extent of infarction in normal (8 ± 2% of AAR), but not diabetic (22 ± 4% of AAR), dogs. Infarct size was linearly related to blood glucose concentration during acute hyperglycemia ( r = 0.96; P 〈 0.001) and during diabetes ( r= 0.74; P 〈 0.002) in the presence or absence of PC stimuli. Increases in serum osmolality caused by administration of raffinose (300 g) did not increase infarct size (11 ± 3% of AAR) or interfere with the ability of PC to protect against infarction (2 ± 1% of AAR). The results indicate that hyperglycemia is a major determinant of the extent of myocardial infarction in the dog.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2000.278.4.H1218
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2000
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 5
    Online-Ressource
    Online-Ressource
    Stent implantation alters coronary artery hemodynamics and wall shear stress during maximal vasodilation
    American Physiological Society ; 2002
    In:  Journal of Applied Physiology Vol. 93, No. 6 ( 2002-12-01), p. 1939-1946
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 93, No. 6 ( 2002-12-01), p. 1939-1946
    Kurzfassung: Coronary stents improve resting blood flow and flow reserve in the presence of stenoses, but the impact of these devices on fluid dynamics during profound vasodilation is largely unknown. We tested the hypothesis that stent implantation affects adenosine-induced alterations in coronary hemodynamics and wall shear stress in anesthetized dogs ( n = 6) instrumented for measurement of left anterior descending coronary artery (LAD) blood flow, velocity, diameter, and radius of curvature. Indexes of fluid dynamics and shear stress were determined before and after placement of a slotted-tube stent in the absence and presence of an adenosine infusion (1.0 mg/min). Adenosine increased blood flow, Reynolds (Re) and Dean numbers (De), and regional and oscillatory shear stress concomitant with reductions in LAD vascular resistance and segmental compliance before stent implantation. Increases in LAD blood flow, Re, De, and indexes of shear stress were observed after stent deployment ( P 〈 0.05). Stent implantation reduced LAD segmental compliance to zero and potentiated increases in segmental and coronary vascular resistance during adenosine. Adenosine-induced increases in coronary blood flow and reserve, Re, De, and regional and oscillatory shear stress were attenuated after the stent was implanted. The results indicate that stent implantation blunts alterations in fluid dynamics during coronary vasodilation in vivo.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00544.2002
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2002
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 6
    Online-Ressource
    Online-Ressource
    Reactive oxygen species are critical mediators of coronary collateral development in a canine model
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 285, No. 4 ( 2003-10), p. H1582-H1589
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 285, No. 4 ( 2003-10), p. H1582-H1589
    Kurzfassung: Recent evidence suggests that reactive oxygen species (ROS) promote proliferation and migration of vascular smooth muscle (VSMC) and endothelial cells (EC). We tested the hypothesis that ROS serve as crucial messengers during coronary collateral development. Dogs were subjected to brief (2 min), repetitive coronary artery occlusions (1/h, 8/day, 21 day duration) in the absence (occlusion, n = 8) or presence of N-acetylcysteine (NAC) (occlusion + NAC, n = 8). A sham group ( n = 8) was instrumented identically but received no occlusions. In separate experiments, ROS generation after a single 2-min coronary artery occlusion was assessed with dihydroethidium fluorescence. Coronary collateral blood flow (expressed as a percentage of normal zone flow) was significantly increased (71 ± 7%) in occlusion dogs after 21 days but remained unchanged (13 ± 3%) in sham dogs. Treatment with NAC attenuated increases in collateral blood flow (28 ± 8%). Brief coronary artery occlusion and reperfusion caused ROS production (256 ± 33% of baseline values), which was abolished with NAC (104 ± 12%). Myocardial interstitial fluid produced tube formation and proliferation of VSMC and EC in occlusion but not in NAC-treated or sham dogs. The results indicate that ROS are critical for the development of the coronary collateral circulation.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00318.2003
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2003
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 7
    Online-Ressource
    Online-Ressource
    Isoflurane-induced preconditioning is attenuated by diabetes
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 282, No. 6 ( 2002-06-01), p. H2018-H2023
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 282, No. 6 ( 2002-06-01), p. H2018-H2023
    Kurzfassung: Volatile anesthetics stimulate, but hyperglycemia attenuates, the activity of mitochondrial ATP-regulated K + channels. We tested the hypothesis that diabetes mellitus interferes with isoflurane-induced preconditioning. Acutely instrumented, barbiturate-anesthetized dogs were randomly assigned to receive 0, 0.32, or 0.64% end-tidal concentrations of isoflurane in the absence or presence of diabetes (3 wk after administration of alloxan and streptozotocin) in six experimental groups. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Myocardial infarct size (triphenyltetrazolium staining) was 29 ± 3% ( n = 8) of the left ventricular area at risk in control experiments. Isoflurane reduced infarct size (15 ± 2 and 13 ± 1% during 0.32 and 0.64% concentrations; n = 8 and 7 dogs, respectively). Diabetes alone did not alter infarct size (30 ± 3%; n = 8) but blocked the protective effects of 0.32% (27 ± 2%; n = 7) and not 0.64% isoflurane (18 ± 3%; n = 7). Infarct size was directly related to blood glucose concentrations in diabetic dogs, but this relationship was abolished by higher concentrations of isoflurane. The results indicate that blood glucose and end-tidal isoflurane concentrations are important determinants of infarct size during anesthetic-induced preconditioning.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01130.2001
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2002
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 8
    Online-Ressource
    Online-Ressource
    Acute hyperglycemia abolishes ischemic preconditioning in vivo
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 275, No. 2 ( 1998-08-01), p. H721-H725
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 275, No. 2 ( 1998-08-01), p. H721-H725
    Kurzfassung: Ischemic preconditioning provides a powerful means to reduce myocardial infarct size in vivo and has been proposed to limit the extent of myocardial infarction in patients. In contrast, hyperglycemia correlates with increases in mortality after acute myocardial infarction. Thus we hypothesized that acute hyperglycemia alters the protection afforded by ischemic preconditioning, and this hypothesis was tested in acutely instrumented dogs subjected to a prolonged (60 min) coronary artery occlusion and 3 h of reperfusion. Ischemic preconditioning was elicited by four 5-min occlusion-reperfusion periods in the presence or absence of an intravenous infusion of 15% dextrose in water to produce acute hyperglycemia (plasma glucose concentration of 300 mg/dl). The dose-dependent effects of hyperglycemia on myocardial infarct size independent of preconditioning stimuli were further evaluated in dogs subjected to increases in plasma glucose concentrations to either 300 or 600 mg/dl. Infarct size (triphenyltetrazolium staining) was 24 ± 2% of the area at risk in control dogs and was significantly ( P 〈 0.05) decreased by ischemic preconditioning (8 ± 1%). Modest degrees of hyperglycemia (300 mg/dl) had no effect on infarct size (34 ± 4%) but abolished the protective effect of ischemic preconditioning (30 ± 5%). In contrast, profound hyperglycemia (600 mg/dl) increased infarct size (44 ± 6%). Hemodynamics and coronary collateral blood flow (radioactive microspheres) were similar between groups. Thus acute hyperglycemia adversely modulates myocardial injury in response to ischemia in vivo.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1998.275.2.H721
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1998
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 9
    Online-Ressource
    Online-Ressource
    Cardioprotection by glucose-insulin-potassium: dependence on K ATP channel opening and blood glucose concentration before ischemia
    American Physiological Society ; 2004
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 287, No. 2 ( 2004-08), p. H601-H607
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 287, No. 2 ( 2004-08), p. H601-H607
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00122.2004
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2004
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 10
    Online-Ressource
    Online-Ressource
    Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 281, No. 5 ( 2001-11-01), p. H2097-H2104
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 281, No. 5 ( 2001-11-01), p. H2097-H2104
    Kurzfassung: We tested the hypothesis that hyperglycemia alters retrograde coronary collateral blood flow by a nitric oxide-mediated mechanism in a canine Ameriod constrictor model of enhanced collateral development. Administration of 15% dextrose to increase blood glucose concentration to 400 or 600 mg/dl decreased retrograde blood flow through the left anterior descending coronary artery to 78 ± 9 and 82 ± 8% of baseline values, respectively. In contrast, saline or l-arginine (400 mg · kg −1 · h −1 ) had no effect on retrograde flow. Coronary hypoperfusion and 1 h of reperfusion decreased retrograde blood flow similarly in saline- orl-arginine-treated dogs (76 ± 11 and 89 ± 4% of baseline, respectively), but these decreases were more pronounced in hyperglycemic dogs (47 ± 10%). l-Arginine prevented decreases in retrograde coronary collateral blood flow during hyperglycemia (100 ± 5 and 95 ± 6% of baseline at blood glucose concentrations of 400 and 600 mg/dl, respectively) and after coronary hypoperfusion and reperfusion (84 ± 14%). The results suggest that hyperglycemia decreases retrograde coronary collateral blood flow by adversely affecting nitric oxide availability.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2001.281.5.H2097
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2001
    ZDB Id: 1477308-9
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
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