LIVIVO - Search results -

Search results

Result 1 - 10 of total 22

Search options

Article ; Online: Subclavian venoplasty may reduce implant times and implant failures in the era of increasing device upgrades.

Ji, Sang Yong / Gundewar, Susheel / Palma, Eugen C

Pacing and clinical electrophysiology : PACE

2012 Volume 35, Issue 4, Page(s) 444–448

Abstract: Background: The incidence of subclavian venous occlusions (SCVOs) may be an increasing problem in the era of device upgrades, especially to cardiac resynchronization therapy. Venoplasty (VP) performed by the electrophysiologist as a way of managing ... ...

Abstract	Background: The incidence of subclavian venous occlusions (SCVOs) may be an increasing problem in the era of device upgrades, especially to cardiac resynchronization therapy. Venoplasty (VP) performed by the electrophysiologist as a way of managing SCVOs may be advantageous. Methods: We reviewed the implantable cardioverter defibrillator (ICD) implants of the past 5 years at Montefiore Medical Center and searched for SCVOs that required intervention and compared cases where VP was performed with cases where it was not. Results: Of 1,853 ICD implants, 41 SCVOs (2.2%) requiring intervention were identified. Its incidence increased seven-fold from 0.7% in 2005 to 5.2% in 2009. Twenty-seven of the 41 SCVOs were found during a device upgrade. Of these 41 SCVOs, 18 underwent VP and 23 did not. In the VP group, there was a trend towards a shorter total procedure time, 2:31 hours versus 3:28 hours (P=0.37), and the total fluoroscopy time was 30 minutes versus 27 minutes (P=0.55). VP was successful in all 18 patients. Among the non-VP group (n=23), five (21.5%) had a failed implantation because of the inability to gain venous access and 10 (42.7%) had to be implanted on the contralateral side. Conclusion: The incidence of SCVOs requiring intervention is increasing in the era of device upgrades. VP performed by an electrophysiologist appears to be a safe and efficient approach to manage these SCVOs. VP seems to reduce the implant time and the need to implant on the other side as well as implant failure due to the inability to gain venous access.
MeSH term(s)	Defibrillators, Implantable ; Female ; Humans ; Male ; Prosthesis Failure ; Retrospective Studies ; Subclavian Vein/surgery ; Treatment Outcome ; Vascular Patency
Language	English
Publishing date	2012-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	424437-0
ISSN	1540-8159 ; 0147-8389
ISSN (online)	1540-8159
ISSN	0147-8389
DOI	10.1111/j.1540-8159.2011.03303.x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1466: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 399: Show issues

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article: Sphingolipid therapy in myocardial ischemia-reperfusion injury.

Gundewar, Susheel / Lefer, David J

Biochimica et biophysica acta

2007 Volume 1780, Issue 3, Page(s) 571–576

Abstract: Sphingolipids are known to play a significant physiological role in cell growth, cell differentiation, and critical signal transduction pathways. Recent studies have demonstrated a significant role of sphingolipids and their metabolites in the ... ...

Abstract	Sphingolipids are known to play a significant physiological role in cell growth, cell differentiation, and critical signal transduction pathways. Recent studies have demonstrated a significant role of sphingolipids and their metabolites in the pathogenesis of myocardial ischemia-reperfusion injury. Our laboratory has investigated the cytoprotective effects of N,N,N-trimethylsphingosine chloride (TMS), a stable N-methylated synthetic sphingolipid analogue on myocardial and hepatic ischemia-reperfusion injury in clinically relevant in vivo murine models of ischemia-reperfusion injury. TMS administered intravenously at the onset of ischemia reduced myocardial infarct size in the wild-type and obese (ob/ob) mice. Following myocardial I/R, there was an improvement in cardiac function in the wild-type mice. Additionally, TMS also decreased serum liver enzymes following hepatic I/R in wild-type mice. The cytoprotective effects did not extend to the ob/ob mice following hepatic I/R or to the db/db mice following both myocardial and hepatic I/R. Our data suggest that although TMS is cytoprotective following I/R in normal animals, the cytoprotective actions of TMS are largely attenuated in obese and diabetic animals which may be due to altered signaling mechanisms in these animal models. Here we review the therapeutic role of TMS and other sphingolipids in the pathogenesis of myocardial ischemia-reperfusion injury and their possible mechanisms of cardioprotection.
MeSH term(s)	Animals ; Myocardial Reperfusion Injury/drug therapy ; Sphingolipids/classification ; Sphingolipids/therapeutic use ; Sphingosine/analogs & derivatives ; Sphingosine/therapeutic use
Chemical Substances	Sphingolipids ; N,N,N-trimethylsphingosine (138686-73-4) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2007-09-06
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2007.08.014
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.247: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Gene therapy for ischemic heart disease.

Lavu, Madhav / Gundewar, Susheel / Lefer, David J

Journal of molecular and cellular cardiology

2010 Volume 50, Issue 5, Page(s) 742–750

Abstract: Current pharmacologic therapy for ischemic heart disease suffers multiple limitations such as compliance issues and side effects of medications. Revascularization procedures often end with need for repeat procedures. Patients remain symptomatic despite ... ...

Abstract	Current pharmacologic therapy for ischemic heart disease suffers multiple limitations such as compliance issues and side effects of medications. Revascularization procedures often end with need for repeat procedures. Patients remain symptomatic despite maximal medical therapy. Gene therapy offers an attractive alternative to current pharmacologic therapies and may be beneficial in refractory disease. Gene therapy with isoforms of growth factors such as VEGF, FGF and HGF induces angiogenesis, decreases apoptosis and leads to protection in the ischemic heart. Stem cell therapy augmented with gene therapy used for myogenesis has proven to be beneficial in numerous animal models of myocardial ischemia. Gene therapy coding for antioxidants, eNOS, HSP, mitogen-activated protein kinase and numerous other anti apoptotic proteins have demonstrated significant cardioprotection in animal models. Clinical trials have demonstrated safety in humans apart from symptomatic and objective improvements in cardiac function. Current research efforts are aimed at refining various gene transfection techniques and regulation of gene expression in vivo in the heart and circulation to improve clinical outcomes in patients that suffer from ischemic heart disease. In this review article we will attempt to summarize the current state of both preclinical and clinical studies of gene therapy to combat myocardial ischemic disease. This article is part of a Special Section entitled "Special Section: Cardiovascular Gene Therapy".
MeSH term(s)	Clinical Trials as Topic ; Fibroblast Growth Factors/genetics ; Genetic Therapy/methods ; Hepatocyte Growth Factor/genetics ; Humans ; Myocardial Ischemia/genetics ; Myocardial Ischemia/therapy ; Nitric Oxide Synthase Type III/genetics ; Oxidative Stress/genetics ; Vascular Endothelial Growth Factor A/genetics
Chemical Substances	Vascular Endothelial Growth Factor A ; Fibroblast Growth Factors (62031-54-3) ; Hepatocyte Growth Factor (67256-21-7) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2010-06-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2010.06.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 426: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Left ventricular apical ballooning syndrome after pacemaker implantation in a male.

Mazurek, Jeremy A / Gundewar, Susheel / Ji, Sang Yong / Grushko, Michael / Krumerman, Andrew

Journal of cardiology cases

2011 Volume 3, Issue 3, Page(s) e154–e158

Abstract: Left apical ballooning syndrome, also known as Takotsubo cardiomyopathy (TTC), characterized by transient left ventricular dysfunction is increasingly recognized worldwide. Predominantly affecting females, this condition mimics myocardial infarction and ... ...

Abstract	Left apical ballooning syndrome, also known as Takotsubo cardiomyopathy (TTC), characterized by transient left ventricular dysfunction is increasingly recognized worldwide. Predominantly affecting females, this condition mimics myocardial infarction and often occurs in the setting of emotional or physical stress. We report the case of a 77-year-old male who was admitted to the hospital for complete heart block and developed TTC after pacemaker implantation. To our knowledge, this is the first report of TTC development after pacemaker implantation in a male.
Language	English
Publishing date	2011-03-27
Publishing country	Japan
Document type	Journal Article
ISSN	1878-5409
ISSN (online)	1878-5409
DOI	10.1016/j.jccase.2011.03.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Dietary nitrite restores NO homeostasis and is cardioprotective in endothelial nitric oxide synthase-deficient mice.

Bryan, Nathan S / Calvert, John W / Gundewar, Susheel / Lefer, David J

Free radical biology & medicine

2008 Volume 45, Issue 4, Page(s) 468–474

Abstract: Endothelial production of nitric oxide (NO) is critical for vascular homeostasis. Nitrite and nitrate are formed endogenously by the stepwise oxidation of NO and have, for years, been regarded as inactive degradation products. As a result, both anions ... ...

Abstract	Endothelial production of nitric oxide (NO) is critical for vascular homeostasis. Nitrite and nitrate are formed endogenously by the stepwise oxidation of NO and have, for years, been regarded as inactive degradation products. As a result, both anions are routinely used as surrogate markers of NO production, with nitrite as a more sensitive marker. However, both nitrite and nitrate are derived from dietary sources. We sought to determine how exogenous nitrite affects steady-state concentrations of NO metabolites thought to originate from nitric oxide synthase (NOS)-derived NO as well as blood pressure and myocardial ischemia-reperfusion (I/R) injury. Mice deficient in endothelial nitric oxide synthase (eNOS-/-) demonstrated decreased blood and tissue nitrite, nitrate, and nitroso proteins, which were further reduced by low-nitrite (NOx) diet for 1 week. Nitrite supplementation (50 mg/L) in the drinking water for 1 week restored NO homeostasis in eNOS-/- mice and protected against I/R injury. Nitrite failed to alter heart rate or mean arterial blood pressure at the protective dose. These data demonstrate the significant influence of dietary nitrite intake on the maintenance of steady-state NO levels. Dietary nitrite and nitrate may serve as essential nutrients for optimal cardiovascular health and may provide a novel prevention/treatment modality for disease associated with NO insufficiency.
MeSH term(s)	Animals ; Diet ; Homeostasis ; Mice ; Mice, Knockout ; Myocardium/enzymology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/physiology ; Nitrite Reductases/metabolism ; Nitrites/administration & dosage ; Nitrites/pharmacology
Chemical Substances	Nitrites ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nitrite Reductases (EC 1.7.-)
Language	English
Publishing date	2008-05-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2008.04.040
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2109: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Cytoprotective effects of N,N,N-trimethylsphingosine during ischemia- reperfusion injury are lost in the setting of obesity and diabetes.

Gundewar, Susheel / Calvert, John W / Elrod, John W / Lefer, David J

American journal of physiology. Heart and circulatory physiology

2007 Volume 293, Issue 4, Page(s) H2462–71

Abstract: N,N,N-trimethylsphingosine chloride (TMS), a stable N-methylated synthetic sphingolipid analog, has been shown to modulate protein kinase C (PKC) activity and exert a number of important biological effects, including inhibition of tumor cell growth and ... ...

Abstract	N,N,N-trimethylsphingosine chloride (TMS), a stable N-methylated synthetic sphingolipid analog, has been shown to modulate protein kinase C (PKC) activity and exert a number of important biological effects, including inhibition of tumor cell growth and metastasis, inhibition of leukocyte migration and respiratory burst, and inhibition of platelet aggregation. We hypothesized that TMS would be cytoprotective in clinically relevant in vivo murine models of myocardial and hepatic ischemia-reperfusion (I/R) injury. Wild-type, obese (ob/ob), and diabetic (db/db) mice were subjected to 30 min of left coronary artery occlusion followed by 24 h of reperfusion in the myocardial I/R model. In additional studies, mice were subjected to 45 min of hepatic artery occlusion followed by 5 h of reperfusion. TMS was administered intravenously at the onset of ischemia. Myocardial infarct size, cardiac function, and serum liver enzymes were measured to assess the extent of tissue injury. TMS attenuated myocardial infarct size by 66% in the wild type and by 36% in the ob/ob mice. Furthermore, TMS reduced serum alanine transaminase levels by 43% in wild-type mice. These benefits did not extend to the ob/ob mice following hepatic I/R or to the db/db mice following both myocardial and hepatic I/R. A likely mechanism is the failure of TMS to inhibit PKC-delta translocation in the diseased heart. These data suggest that although TMS is cytoprotective following I/R in normal animals, the cytoprotective actions of TMS are largely attenuated in obese and diabetic animals.
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Body Weight ; Cytoprotection ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Liver/blood supply ; Liver/drug effects ; Liver/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitochondria, Heart/drug effects ; Mitochondria, Heart/enzymology ; Myocardial Infarction/etiology ; Myocardial Infarction/prevention & control ; Myocardial Reperfusion Injury/complications ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Myocardial Reperfusion Injury/physiopathology ; Myocardial Reperfusion Injury/prevention & control ; Myocardium/enzymology ; Myocardium/pathology ; Obesity/complications ; Obesity/genetics ; Obesity/metabolism ; Obesity/physiopathology ; Protective Agents/pharmacology ; Protective Agents/therapeutic use ; Protein Kinase C-delta/antagonists & inhibitors ; Protein Kinase C-delta/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Protein Transport ; Reperfusion Injury/complications ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Reperfusion Injury/physiopathology ; Reperfusion Injury/prevention & control ; Sphingosine/analogs & derivatives ; Sphingosine/pharmacology ; Sphingosine/therapeutic use ; Time Factors ; Ventricular Function, Left/drug effects
Chemical Substances	Blood Glucose ; Protective Agents ; Protein Kinase Inhibitors ; N,N,N-trimethylsphingosine (138686-73-4) ; Protein Kinase C-delta (EC 2.7.11.13) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2007-07-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00392.2007
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Developmental programming resulting from maternal obesity in mice: effects on myocardial ischaemia-reperfusion injury.

Calvert, John W / Lefer, David J / Gundewar, Susheel / Poston, Lucilla / Coetzee, William A

Experimental physiology

2009 Volume 94, Issue 7, Page(s) 805–814

Abstract: A comprehensive number of epidemiological and animal studies suggest that prenatal and early life events are important determinants for disorders later in life. Among them, prenatal stress (i.e. stress experienced by the pregnant mother with impact on ... ...

Abstract	A comprehensive number of epidemiological and animal studies suggest that prenatal and early life events are important determinants for disorders later in life. Among them, prenatal stress (i.e. stress experienced by the pregnant mother with impact on the fetal ontogeny) has clear programming effects on the cardiovascular system. A fetus developing in adverse conditions becomes an adult who is susceptible to disease, which may include hypertension, insulin resistance, altered blood lipid levels and cardiovascular disease. Recent evidence demonstrates that maternal programming can occur in the absence of other adverse environmental factors. Obesity, which is becoming a problem of large proportions in Western countries, is a possible cause of programming. With over 30% of the population of the USA currently obese, many mothers suffer from obesity during their child-bearing years (in fact, these conditions are often aggravated during pregnancy). One of the targets of programming is the cardiovascular system, and reported consequences include hypertension, endothelial dysfunction and vascular abnormalities. The overall goal of our study was to investigate the susceptibility of the heart to ischaemia-reperfusion in an animal model of maternal obesity. Our data demonstrate that normal (non-mutant) offspring from obese agouti mouse dams had an increased susceptibility to ischaemia-reperfusion injury. These data may provide insights into the long-term cardiovascular consequences of programming.
MeSH term(s)	Animals ; Disease Models, Animal ; Echocardiography ; Female ; Male ; Mice ; Myocardial Reperfusion Injury/etiology ; Myocardial Reperfusion Injury/pathology ; Obesity/physiopathology ; Pregnancy ; Pregnancy Complications/physiopathology ; Prenatal Exposure Delayed Effects ; Prenatal Nutritional Physiological Phenomena ; Sex Factors ; Ventricular Function, Left/physiology
Language	English
Publishing date	2009-04-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1016295-1
ISSN	1469-445X ; 0958-0670
ISSN (online)	1469-445X
ISSN	0958-0670
DOI	10.1113/expphysiol.2009.047183
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.102: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Nitric oxide promotes distant organ protection: evidence for an endocrine role of nitric oxide.

Elrod, John W / Calvert, John W / Gundewar, Susheel / Bryan, Nathan S / Lefer, David J

Proceedings of the National Academy of Sciences of the United States of America

2008 Volume 105, Issue 32, Page(s) 11430–11435

Abstract: Endothelial NOS (eNOS)-derived NO has long been considered a paracrine signaling molecule only capable of affecting nearby cells because of its short half-life in blood and relatively limited diffusion distance in tissues. To date, no studies have ... ...

Abstract	Endothelial NOS (eNOS)-derived NO has long been considered a paracrine signaling molecule only capable of affecting nearby cells because of its short half-life in blood and relatively limited diffusion distance in tissues. To date, no studies have demonstrated that endogenously generated NO possesses a clearly defined endocrine function. Therefore, we evaluated whether enzymatic generation of NO in the heart is capable of modulating remote physiological actions and cell signaling. Mice with cardiac-specific overexpression of the human eNOS gene (CS-eNOS-Tg) were used to address this hypothesis. Cardiac-specific eNOS overexpression resulted in significant increases in nitrite, nitrate, and nitrosothiols in the heart, plasma, and liver. To examine whether the increase in hepatic NO metabolites could modulate cytoprotection, we subjected CS-eNOS-Tg mice to hepatic ischemia-reperfusion (I/R) injury. CS-eNOS-Tg mice displayed a significant reduction in hepatic I/R injury (4.2-fold reduction in the aminotransferase and a 3.5-fold reduction in aspartate aminotransferase) compared with WT littermates. These findings demonstrate that endogenously derived NO is transported in the blood, metabolized in remote organs, and mediates cytoprotection in the setting of I/R injury. This study presents clear evidence for an endocrine role of NO generated endogenously from eNOS and provides additional evidence for the profound cytoprotective actions of NO in the setting of I/R injury.
MeSH term(s)	Animals ; Biological Transport/genetics ; Cytoprotection/genetics ; Liver/metabolism ; Mice ; Mice, Transgenic ; Myocardium/enzymology ; Nitrates/blood ; Nitric Oxide/genetics ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Nitric Oxide Synthase Type III ; Nitrites/blood ; Organ Specificity/genetics ; Paracrine Communication/genetics ; Reperfusion Injury/metabolism
Chemical Substances	Nitrates ; Nitrites ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2008-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0800700105
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Genetic and pharmacologic hydrogen sulfide therapy attenuates ischemia-induced heart failure in mice.

Calvert, John W / Elston, Marah / Nicholson, Chad K / Gundewar, Susheel / Jha, Saurabh / Elrod, John W / Ramachandran, Arun / Lefer, David J

Circulation

2010 Volume 122, Issue 1, Page(s) 11–19

Abstract: Background: Hydrogen sulfide (H(2)S) is an endogenous signaling molecule with potent cytoprotective effects. The present study evaluated the therapeutic potential of H(2)S in murine models of heart failure.: Methods and results: Heart failure was ... ...

Abstract	Background: Hydrogen sulfide (H(2)S) is an endogenous signaling molecule with potent cytoprotective effects. The present study evaluated the therapeutic potential of H(2)S in murine models of heart failure. Methods and results: Heart failure was induced by subjecting mice either to permanent ligation of the left coronary artery for 4 weeks or to 60 minutes of left coronary artery occlusion followed by reperfusion for 4 weeks. Transgenic mice with cardiac-restricted overexpression of the H(2)S-generating enzyme cystathione gamma-lyase (alphaMHC-CGL-Tg(+)) displayed a clear protection against left ventricular structural and functional impairment as assessed by echocardiography in response to ischemia-induced heart failure, as well as improved survival in response to permanent myocardial ischemia. Exogenous H(2)S therapy (Na(2)S; 100 microg/kg) administered at the time of reperfusion (intracardiac) and then daily (intravenous) for the first 7 days after myocardial ischemia also protected against the structural and functional deterioration of the left ventricle by attenuating oxidative stress and mitochondrial dysfunction. Additional experiments aimed at elucidating some of the protective mechanisms of H(2)S therapy found that 7 days of H(2)S therapy increased the phosphorylation of Akt and increased the nuclear localization of 2 transcription factors, nuclear respiratory factor 1 and nuclear factor-E2-related factor (Nrf2), that are involved in increasing the levels of endogenous antioxidants, attenuating apoptosis, and increasing mitochondrial biogenesis. Conclusions: The results of the present study suggest that either the administration of exogenous H(2)S or the modulation of endogenous H(2)S production may be of therapeutic benefit in the treatment of ischemia-induced heart failure.
MeSH term(s)	Animals ; Body Weight ; Cardiomegaly/enzymology ; Cardiomegaly/prevention & control ; Cystathionine gamma-Lyase/genetics ; Gene Expression Regulation, Enzymologic ; Heart Failure/drug therapy ; Heart Failure/etiology ; Heart Failure/genetics ; Hydrogen Sulfide/therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myocardial Ischemia/complications ; Myocardial Ischemia/genetics ; NF-E2-Related Factor 2/drug effects ; NF-E2-Related Factor 2/metabolism ; Nuclear Respiratory Factor 1/drug effects ; Nuclear Respiratory Factor 1/metabolism ; Organ Size ; Sulfates/pharmacology ; Survival Rate ; Vasodilation/drug effects ; Vasodilation/genetics ; Ventricular Dysfunction, Left/genetics ; Ventricular Function, Left/genetics
Chemical Substances	NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; Nrf1 protein, mouse ; Nuclear Respiratory Factor 1 ; Sulfates ; sodium sulfate (0YPR65R21J) ; Cystathionine gamma-Lyase (EC 4.4.1.1) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2010-06-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.109.920991
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.60: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Nitric oxide promotes distant organ protection: Evidence for an endocrine role of nitric oxide

Elrod, John W / Calvert, John W / Gundewar, Susheel / Bryan, Nathan S / Lefer, David J

Proceedings of the National Academy of Sciences of the United States of America. 2008 Aug. 12, v. 105, no. 32

2008

Abstract	Endothelial NOS (eNOS)-derived NO has long been considered a paracrine signaling molecule only capable of affecting nearby cells because of its short half-life in blood and relatively limited diffusion distance in tissues. To date, no studies have demonstrated that endogenously generated NO possesses a clearly defined endocrine function. Therefore, we evaluated whether enzymatic generation of NO in the heart is capable of modulating remote physiological actions and cell signaling. Mice with cardiac-specific overexpression of the human eNOS gene (CS-eNOS-Tg) were used to address this hypothesis. Cardiac-specific eNOS overexpression resulted in significant increases in nitrite, nitrate, and nitrosothiols in the heart, plasma, and liver. To examine whether the increase in hepatic NO metabolites could modulate cytoprotection, we subjected CS-eNOS-Tg mice to hepatic ischemia-reperfusion (I/R) injury. CS-eNOS-Tg mice displayed a significant reduction in hepatic I/R injury (4.2-fold reduction in the aminotransferase and a 3.5-fold reduction in aspartate aminotransferase) compared with WT littermates. These findings demonstrate that endogenously derived NO is transported in the blood, metabolized in remote organs, and mediates cytoprotection in the setting of I/R injury. This study presents clear evidence for an endocrine role of NO generated endogenously from eNOS and provides additional evidence for the profound cytoprotective actions of NO in the setting of I/R injury.
Language	English
Dates of publication	2008-0812
Size	p. 11430-11435.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Bonn / Germany

Z 4' 63/44: Show issues
87/25270: Show issues
Qa 4' 169/3: Show issues
Z 8.7: Show issues

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Bonn / Germany

Order via subito

Inter-library loan at ZB MED