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  • 1
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    Online Resource
    Probiotic Administration Attenuates Myocardial Hypertrophy and Heart Failure After Myocardial Infarction in the Rat
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation: Heart Failure Vol. 7, No. 3 ( 2014-05), p. 491-499
    Details
    In: Circulation: Heart Failure, Ovid Technologies (Wolters Kluwer Health), Vol. 7, No. 3 ( 2014-05), p. 491-499
    Abstract: Probiotics are extensively used to promote gastrointestinal health, and emerging evidence suggests that their beneficial properties can extend beyond the local environment of the gut. Here, we determined whether oral probiotic administration can alter the progression of postinfarction heart failure. Methods and Results— Rats were subjected to 6 weeks of sustained coronary artery occlusion and administered the probiotic Lactobacillus rhamnosus GR-1 or placebo in the drinking water ad libitum. Culture and 16s rRNA sequencing showed no evidence of GR-1 colonization or a significant shift in the composition of the cecal microbiome. However, animals administered GR-1 exhibited a significant attenuation of left ventricular hypertrophy based on tissue weight assessment and gene expression of atrial natriuretic peptide. Moreover, these animals demonstrated improved hemodynamic parameters reflecting both improved systolic and diastolic left ventricular function. Serial echocardiography revealed significantly improved left ventricular parameters throughout the 6-week follow-up period including a marked preservation of left ventricular ejection fraction and fractional shortening. Beneficial effects of GR-1 were still evident in those animals in which GR-1 was withdrawn at 4 weeks, suggesting persistence of the GR-1 effects after cessation of therapy. Investigation of mechanisms showed a significant increase in the leptin:adiponectin plasma concentration ratio in rats subjected to coronary ligation, which was abrogated by GR-1. Metabonomic analysis showed differences between sham control and coronary artery ligated hearts particularly with respect to preservation of myocardial taurine levels. Conclusions— The study suggests that probiotics offer promise as a potential therapy for the attenuation of heart failure.
    Type of Medium: Online Resource
    ISSN: 1941-3289 , 1941-3297
    URL: Article
    DOI: 10.1161/CIRCHEARTFAILURE.113.000978
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2428100-1
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  • 2
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    Dehydroascorbic acid uptake by coronary artery smooth muscle: effect of intracellular acidification
    Portland Press Ltd. ; 2002
    In:  Biochemical Journal Vol. 362, No. 2 ( 2002-03-01), p. 507-512
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 362, No. 2 ( 2002-03-01), p. 507-512
    Abstract: Dehydroascorbic acid (DHAA) enters cells via Na+-independent glucose transporters (GLUT) and is converted to ascorbate. However, we found that Na+ removal inhibited [14C]DHAA uptake by smooth-muscle cells cultured from pig coronary artery. The uptake was examined for 2–12min at 10–200μM DHAA in either the presence of 134mM Na+ or in its absence (N-methyl d-glucamine, choline or sucrose replaced Na+). This inhibition of DHAA uptake by Na+ removal was paradoxical because it was inhibited by 2-deoxyglucose and cytochalasin B, as expected of transport via the GLUT pathway. We tested the hypothesis that this paradox resulted from an inefficient intracellular reduction of [14C] DHAA into [14C]ascorbate upon intracellular acidosis caused by the Na+ removal. Consistent with this hypothesis: (i) the Na+/H+-exchange inhibitors ethylisopropyl amiloride and cariporide also decreased the uptake, (ii) Na+ removal and Na+/H+-exchange inhibitors lowered cytosolic pH, with the decrease being larger in 12min than in 2min, and (iii) less of the cellular 14C was present as ascorbate (determined by HPLC) in cells in Na+-free buffer than in those in Na+-containing buffer. This inability to obtain ascorbate from extracellular DHAA may be detrimental to the coronary artery under hypoxia-induced acidosis during ischaemia/reperfusion.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj3620507
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2002
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 3
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    Na + -H + Exchange Inhibition Protects Against Mechanical, Ultrastructural, and Biochemical Impairment Induced by Low Concentrations of Lysophosphatidylcholine in Isolated Rat Hearts
    Ovid Technologies (Wolters Kluwer Health) ; 1997
    In:  Circulation Research Vol. 80, No. 1 ( 1997-01), p. 95-102
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 80, No. 1 ( 1997-01), p. 95-102
    Abstract: Lysophophatidylcholine (LysoPC) accumulates rapidly in the ischemic myocardium and is an important mediator of ischemia-induced cell injury. Na + -H + exchange (NHE) inhibition has been demonstrated to protect the ischemic and reperfused myocardium. We determined whether NHE inhibition can also modulate cardiotoxicity produced by LysoPC (3 and 5 μmol/L) in isolated rat hearts. At 3 μmol/L, LysoPC produced a depression in left ventricular developed pressure (LVDP) and elevation in left ventricular end-diastolic pressure (LVEDP), which were 19±7% and 1290±205% of pre-LysoPC values, respectively, after 30 minutes of treatment. In the presence of the NHE inhibitor 4-isopropyl-3-methylsulfonylbenzoyl-guanidine methanesulfonate (HOE 642, 5 μmol/L), LVDP was reduced to only 80.8±8.6%, and LVEDP increased to 270±32% ( P 〈 .05 for both parameters). LysoPC significantly depressed tissue ATP, creatine phosphate, and glycogen contents and increased lactate levels, all of which were significantly attenuated by HOE 642. Moreover, marked LysoPC-induced ultrastructural abnormalities, including mitochondrial and myofibrillar disruption, were totally prevented by HOE 642. This protection was mimicked by another NHE inhibitor, methylisobutylamiloride (5 μmol/L). HOE 642 was also effective against injury produced by 5 μmol/L LysoPC although, generally, the protection was less marked than that observed against 3 μmol/L; LVDP depression after 30 minutes was 10.1±4.3% and 41.4±10.4% of pre-LysoPC values in control and HOE 642-treated hearts, respectively ( P 〈 .05), whereas corresponding LVEDP elevations were 1629±393% and 990±144% ( P 〉 .05). In myocytes superfused with bicarbonate-free buffer subjected to acid loading by NH 4 Cl pulsing, pH recovery (as measured by acid flux) was significantly stimulated by 3 μmol/L LysoPC, indicative of NHE activation. Our study shows that cardiac injury produced by low concentrations of LysoPC can be effectively attenuated by NHE inhibition. The results also suggest that the beneficial effects of NHE inhibitors on the ischemic myocardium may be, at least partially, mediated by inhibiting the deleterious effects of LysoPC.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.80.1.95
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1997
    detail.hit.zdb_id: 1467838-X
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  • 4
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    Orally administered NHE1 inhibitor cariporide reduces acute responses to coronary occlusion and reperfusion
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 276, No. 2 ( 1999-02-01), p. H749-H757
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 276, No. 2 ( 1999-02-01), p. H749-H757
    Abstract: Na + /H + exchange (NHE) mediates myocardial ischemic and reperfusion injury. We examined the effects of dietary administration of the potent and selective NHE1 inhibitor cariporide on acute responses to coronary artery ligation and reperfusion in the anesthetized rat. Male Sprague-Dawley rats received control rat chow or an identical diet containing 3 parts per million of cariporide for 1 wk before 225 min of occlusion of the left main coronary artery or 45 min of occlusion followed by 180 min of reperfusion. Hearts were excised and divided into left ventricle, right ventricle, and interventricular septum for analysis of NHE1 mRNA expression and apoptosis by staining with terminal deoxynucleotidyl transferase-mediated nick end labeling. Ischemia and reperfusion were associated with a threefold elevation in NHE1 mRNA expression in control animals that was significantly reduced in cariporide-fed rats. Cariporide reduced mortality from 26% of animals to 0%. The incidence of all arrhythmias was significantly reduced, including ventricular fibrillation (from 42 to 0%) and ventricular tachycardia (from 81 to 15%), as well as the number of ventricular premature beats (from 70 ± 12 to 17 ± 6). Cariporide moderately reduced apoptosis only in the reperfused left ventricle to values not significantly greater than those in sham-operated animals, and this was associated with a significantly higher ratio of Bcl-2 to Bax. This study suggests that NHE inhibition with dietary cariporide represents an effective management of acute postinfarction responses.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1999.276.2.H749
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477308-9
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  • 5
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    Redox signaling of cardiac HSF1 DNA binding
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Cell Physiology Vol. 283, No. 2 ( 2002-08-01), p. C404-C411
    Details
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 283, No. 2 ( 2002-08-01), p. C404-C411
    Abstract: Experiments involving chemical induction of the heat shock response in simple biological systems have generated the hypothesis that protein denaturation and consequential binding of heat shock transcription factor 1 (HSF1) to proximal heat shock elements (HSEs) on heat shock protein ( hsp) genes are the result of oxidation and/or depletion of intracellular thiols. The purpose of the present investigation was to determine the role of redox signaling of HSF1 in the intact animal in response to physiological and pharmacological perturbations. Heat shock and exercise induced HSF1-HSE DNA binding in the rat myocardium ( P 〈 0.001) in the absence of changes in reduced glutathione (GSH), the major nonprotein thiol in the cell. Ischemia-reperfusion, which decreased GSH content ( P 〈 0.05), resulted in nonsignificant HSF1-HSE formation. This dissociation between physiological induction of HSF1 and changes in GSH was not gender dependent. Pharmacological ablation of GSH withl-buthionine-[ S, R]-sulfoximine (BSO) treatment increased myocardial HSF1-HSE DNA binding in estrogen-naive animals ( P = 0.007). Thus, although physiological induction of HSF1-HSE DNA binding is likely regulated by mediators of protein denaturation other than cellular redox status, the proposed signaling pathway may predominate with pharmacological oxidation and may represent a plausible and accessible strategy in the development of HSP-based therapies.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    URL: Article
    DOI: 10.1152/ajpcell.00051.2002
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477334-X
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  • 6
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    Effective protection by NHE-1 inhibition in ischemic and reperfused heart under preconditioning blockade
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 284, No. 3 ( 2003-03-01), p. H798-H803
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 284, No. 3 ( 2003-03-01), p. H798-H803
    Abstract: We compared the protective effects of ischemic preconditioning (IPC) and the Na + /H + exchanger-1 (NHE-1) inhibitor cariporide in isolated rat hearts subjected to global ischemia (45 or 90 min) and 30-min reperfusion and determined the protective effects of cariporide under IPC blockade with the mitochondrial ATP-sensitive K + channel blocker 5-hydroxydecanoate (5-HD). With 45-min ischemia, both IPC and cariporide equally increased maximum recovery of left ventricular developed pressure twofold ( P 〈 0.05), although recovery was significantly greater with cariporide for the first 15 min of reperfusion. 5-HD almost completely blocked the protective effects of IPC on recovery but had no influence on the salutary effects of cariporide. With 90-min ischemic control, recovery was only 3% of preischemia and was unaffected by IPC, although cariporide increased recovery to ∼30% ( P 〈 0.05). This was associated with a 37% preservation of viable cardiac cells, whereas no structurally intact cells were found in either IPC or control hearts. Our study shows that NHE-1 inhibition is a more effective cardioprotective strategy than IPC in this model, possibly because of enhanced myocyte salvage, and because protection by NHE-1 inhibition is completely unaffected by IPC blockade with 5-HD.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00659.2002
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477308-9
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  • 7
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    Exercise training improves myocardial tolerance to ischemia in male but not in female rats
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 293, No. 1 ( 2007-07), p. R363-R371
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 293, No. 1 ( 2007-07), p. R363-R371
    Abstract: Acute exercise increases myocardial tolerance to ischemia-reperfusion (I-R) injury in male but not in female rat hearts, possibly due to a decreased heat shock protein 70 (Hsp70) response in the female hearts. This study examined whether repetitive exercise training would increase Hsp70 and myocardial tolerance to I-R injury in female rat hearts. Adaptations in myocardial manganese superoxide dismutase (MnSOD) and endothelial nitric oxide synthase (eNOS) were also assessed. Ten-week old male (M) and female (F) Sprague-Dawley rats ( n = 40 total) exercise-trained for 14 wk; the last 8 wk consisted of running 1 h at 30 m/min (2% incline), 5 days/wk. Following training, left ventricle mechanical function (LVMF) was monitored for 30 min of reperfusion following 30 min of global ischemia (Langendorff procedure). Myocardial Hsp70 content was not different in M and F control groups, while increases were observed in both trained groups (M greater than F; P 〈 0.05). Although MnSOD content did not differ between groups, endothelial nitric oxide synthase (eNOS) levels were decreased in F, with no change in M, following training ( P 〈 0.05). Hearts from control F demonstrated a greater recuperation of all indices of LVMF following I-R compared with control M hearts ( P 〈 0.05). Hearts of trained M exhibited improved recovery of LVMF (left ventricular diastolic pressure, left ventrcular end-diastolic pressure, +dP/d t, −dP/d t) during reperfusion compared with control M hearts ( P 〈 0.05). In contrast, hearts of trained F did not show any change in recovery from I-R. Hence, exercise training is more beneficial to M than F in improving myocardial function following I-R injury.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00363.2006
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 8
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    Ginseng Inhibits Cardiomyocyte Hypertrophy and Heart Failure via NHE-1 Inhibition and Attenuation of Calcineurin Activation
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Circulation: Heart Failure Vol. 4, No. 1 ( 2011-01), p. 79-88
    Details
    In: Circulation: Heart Failure, Ovid Technologies (Wolters Kluwer Health), Vol. 4, No. 1 ( 2011-01), p. 79-88
    Abstract: Ginseng is a medicinal plant used widely in Asia that has gained popularity in the West during the past decade. Increasing evidence suggests a therapeutic role for ginseng in the cardiovascular system. The pharmacological properties of ginseng are mainly attributed to ginsenosides, the principal bioactive constituents in ginseng. The present study was carried out to determine whether ginseng exerts a direct antihypertrophic effect in cultured cardiomyocytes and whether it modifies the heart failure process in vivo. Moreover, we determined the potential underlying mechanisms for these actions. Methods and Results— Experiments were performed on cultured neonatal rat ventricular myocytes as well as adult rats subjected to coronary artery ligation (CAL). Treatment of cardiomyocytes with the α 1 adrenoceptor agonist phenylephrine (PE) for 24 hours produced a marked hypertrophic effect as evidenced by significantly increased cell surface area and ANP gene expression. These effects were attenuated by ginseng in a concentration-dependent manner with a complete inhibition of hypertrophy at a concentration of 10 μg/mL. Phenylephrine-induced hypertrophy was associated with increased gene and protein expression of the Na + -H + exchanger 1 (NHE-1), increased NHE-1 activity, increased intracellular concentrations of Na + and Ca 2+ , enhanced calcineurin activity, increased translocation of NFAT3 into nuclei, and GATA-4 activation, all of which were significantly inhibited by ginseng. Upregulation of these systems was also evident in rats subjected to 4 weeks of CAL. However, animals treated with ginseng demonstrated markedly reduced hemodynamic and hypertrophic responses, which were accompanied by attenuation of upregulation of NHE-1 and calcineurin activity. Conclusions— Taken together, our results demonstrate a robust antihypertrophic and antiremodeling effect of ginseng, which is mediated by inhibition of NHE-1–dependent calcineurin activation.
    Type of Medium: Online Resource
    ISSN: 1941-3289 , 1941-3297
    URL: Article
    DOI: 10.1161/CIRCHEARTFAILURE.110.957969
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 2428100-1
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  • 9
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    The Obesity-Related Peptide Leptin Sensitizes Cardiac Mitochondria to Calcium-Induced Permeability Transition Pore Opening and Apoptosis
    Public Library of Science (PLoS) ; 2012
    In:  PLoS ONE Vol. 7, No. 7 ( 2012-7-25), p. e41612-
    Details
    In: PLoS ONE, Public Library of Science (PLoS), Vol. 7, No. 7 ( 2012-7-25), p. e41612-
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1371/journal.pone.0041612
    DOI: 10.1371/journal.pone.0041612.g001
    DOI: 10.1371/journal.pone.0041612.g002
    DOI: 10.1371/journal.pone.0041612.g003
    DOI: 10.1371/journal.pone.0041612.g004
    DOI: 10.1371/journal.pone.0041612.g005
    DOI: 10.1371/journal.pone.0041612.g006
    DOI: 10.1371/journal.pone.0041612.g007
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2012
    detail.hit.zdb_id: 2267670-3
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  • 10
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    Sodium–hydrogen exchange inhibition attenuates glycoside-induced hypertrophy in rat ventricular myocytes
    Oxford University Press (OUP) ; 2010
    In:  Cardiovascular Research Vol. 85, No. 1 ( 2010-1-1), p. 79-89
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 85, No. 1 ( 2010-1-1), p. 79-89
    Type of Medium: Online Resource
    ISSN: 1755-3245 , 0008-6363
    URL: Article
    DOI: 10.1093/cvr/cvp283
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2010
    detail.hit.zdb_id: 1499917-1
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