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  • 1
    Online Resource
    Online Resource
    Sarcolemmal and Mitochondrial Adenosine Triphosphate– dependent Potassium Channels
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Anesthesiology Vol. 92, No. 6 ( 2000-06-01), p. 1731-1739
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 6 ( 2000-06-01), p. 1731-1739
    Abstract: Volatile anesthetic-induced preconditioning is mediated by adenosine triphosphate-dependent potassium (KATP) channels; however, the subcellular location of these channels is unknown. The authors tested the hypothesis that desflurane reduces experimental myocardial infarct size by activation of specific sarcolemmal and mitochondrial KATP channels. Methods Barbiturate-anesthetized dogs (n = 88) were acutely instrumented for measurement of aortic and left ventricular pressures. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3-h reperfusion. In four separate groups, dogs received vehicle (0.9% saline) or the nonselective KATP channel antagonist glyburide (0.1 mg/kg intravenously) in the presence or absence of 1 minimum alveolar concentration desflurane. In four additional groups, dogs received 45-min intracoronary infusions of the selective sarcolemmal (HMR 1098; 1 microg. kg-1. min-1) or mitochondrial (5-hydroxydecanoate [5-HD]; 150 microg. kg-1. min-1) KATP channel antagonists in the presence or absence of desflurane. Myocardial perfusion and infarct size were measured with radioactive microspheres and triphenyltetrazolium staining, respectively. Results Desflurane significantly (P & lt; 0.05) decreased infarct size to 10 +/- 2% (mean +/- SEM) of the area at risk as compared with control experiments (25 +/- 3% of area at risk). This beneficial effect of desflurane was abolished by glyburide (25 +/- 2% of area at risk). Glyburide (24 +/- 2%), HMR 1098 (21 +/- 4%), and 5-HD (24 +/- 2% of area at risk) alone had no effects on myocardial infarct size. HMR 1098 and 5-HD abolished the protective effects of desflurane (19 +/- 3% and 22 +/- 2% of area at risk, respectively). Conclusion Desflurane reduces myocardial infarct size in vivo, and the results further suggest that both sarcolemmal and mitochondrial KATP channels could be involved.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/00000542-200006000-00033
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 2016092-6
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  • 2
    Online Resource
    Online Resource
    Role of Heat Shock Protein 90 and Endothelial Nitric Oxide Synthase during Early Anesthetic and Ischemic Preconditioning
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Anesthesiology Vol. 110, No. 2 ( 2009-02-01), p. 317-325
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 110, No. 2 ( 2009-02-01), p. 317-325
    Abstract: Nitric oxide is known to be essential for early anesthetic preconditioning (APC) and ischemic preconditioning (IPC) of myocardium. Heat shock protein 90 (Hsp90) regulates endothelial nitric oxide synthase (eNOS) activity. In this study, the authors tested the hypothesis that Hsp90-eNOS interactions modulate APC and IPC. Methods Myocardial infarct size was measured in rabbits after coronary occlusion and reperfusion in the absence or presence of preconditioning within 30 min of isoflurane (APC) or 5 min of coronary artery occlusion (IPC), and with or without pretreatment with geldanamycin or radicicol, two chemically distinct Hsp90 inhibitors, or N-nitro-L-arginine methyl ester, a nonspecific nitric oxide synthase NOS inhibitor. Isoflurane-dependent nitric oxide production was measured (ozone chemiluminescence) in human coronary artery endothelial cells or mouse cardiomyocytes, in the absence or presence of Hsp90 inhibitors or N-nitro-L-arginine methyl ester. Interactions between Hsp90 and eNOS, and eNOS activation, were assessed with immunoprecipitation, immunoblotting, and confocal microscopy. Results APC and IPC decreased infarct size (by 50% and 59%, respectively), and this action was abolished by Hsp90 inhibitors. N-nitro-L-arginine methyl ester blocked APC but not IPC. Isoflurane increased nitric oxide production in human coronary artery endothelial cells concomitantly with an increase in Hsp90-eNOS interaction (immunoprecipitation, immunoblotting, and immunohistochemistry). Pretreatment with Hsp90 inhibitors abolished isoflurane-dependent nitric oxide production and decreased Hsp90-eNOS interactions. Isoflurane did not increase nitric oxide production in mouse cardiomyocytes, and eNOS was below the level of detection. Conclusion The results indicate that Hsp90 plays a critical role in mediating APC and IPC through protein-protein interactions, and suggest that endothelial cells are important contributors to nitric oxide-mediated signaling during APC.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/ALN.0b013e3181942cb4
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 2016092-6
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  • 3
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2001.280.4.H1744
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 4
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    Online Resource
    How Can a Large Left Atrial Myxoma Cause a Selective Mid-Diastolic Right-to-Left Atrial Shunt?
    Elsevier BV ; 2015
    In:  Journal of Cardiothoracic and Vascular Anesthesia Vol. 29, No. 3 ( 2015-06), p. 820-823
    Details
    In: Journal of Cardiothoracic and Vascular Anesthesia, Elsevier BV, Vol. 29, No. 3 ( 2015-06), p. 820-823
    Type of Medium: Online Resource
    ISSN: 1053-0770
    URL: Article
    DOI: 10.1053/j.jvca.2014.10.023
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
    detail.hit.zdb_id: 2043630-0
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  • 5
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    Online Resource
    Ethanol Enhances the Functional Recovery of Stunned Myocardium Independent of KATP Channels in Dogs
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Anesthesia & Analgesia Vol. 92, No. 2 ( 2001-02), p. 299-305
    Details
    In: Anesthesia & Analgesia, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 2 ( 2001-02), p. 299-305
    Type of Medium: Online Resource
    ISSN: 0003-2999
    URL: Article
    DOI: 10.1213/00000539-200102000-00003
    RVK:
    XA 22250
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 2018275-2
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  • 6
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01013.2002
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2000.279.5.H2574
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial‐Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy
    Wiley ; 2003
    In:  Pacing and Clinical Electrophysiology Vol. 26, No. 4p1 ( 2003-04), p. 853-861
    Details
    In: Pacing and Clinical Electrophysiology, Wiley, Vol. 26, No. 4p1 ( 2003-04), p. 853-861
    Abstract: HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs (n = 7) were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short‐axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P 〈 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing ( 2.3 ± 0.4 vs 2.1 ± 0.3 vs 2.0 ± 0.3 l/min , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO ( 65 ± 9 vs 59 ± 9 vs 54 ± 11 mmHg , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)
    Type of Medium: Online Resource
    ISSN: 0147-8389 , 1540-8159
    URL: Article
    DOI: 10.1046/j.1460-9592.2003.t01-1-00150.x
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 2037547-5
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  • 9
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2000.278.4.H1218
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 10
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    2009 ACCF/AHA Focused Update on Perioperative Beta Blockade
    Elsevier BV ; 2009
    In:  Journal of the American College of Cardiology Vol. 54, No. 22 ( 2009-11), p. 2102-2128
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 54, No. 22 ( 2009-11), p. 2102-2128
    Type of Medium: Online Resource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/j.jacc.2009.07.004
    RVK:
    XA 17760
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 1468327-1
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