464-P: Linagliptin Directly Enhances Cardiac Contractile Recovery through Nitric Oxide Mediated Endothelial–Cardiomyocyte Communication

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 464-P
Author(s):  
VEERA GANESH YERRA ◽  
SRI NAGARJUN BATCHU ◽  
YOUAN LIU ◽  
THOMAS KLEIN ◽  
ANDREW ADVANI
Keyword(s):  
Nitric Oxide ◽  
Cardiac Contractile ◽  
Contractile Recovery

scholarly journals Nitric oxide and CaMKII: Critical steps in the cardiac contractile response To IGF-1 and swim training

2017 ◽  
Vol 112 ◽  
pp. 16-26 ◽  
Author(s):  
Juan I. Burgos ◽  
Alejandra M. Yeves ◽  
Jorge P. Barrena ◽  
Enrique L. Portiansky ◽  
Martín G. Vila-Petroff ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Contractile Response ◽  
Cardiac Contractile

Pentoxifylline Improves Reoxygenation-induced Contractile Recovery Through a Nitric Oxide-dependent Mechanism in Rat Papillary Muscles

2006 ◽  
Vol 47 (4) ◽  
pp. 571-577 ◽  
Author(s):  
Farzad Ebrahimi ◽  
Amir Reza Hajrasouliha ◽  
Sina Tavakoli ◽  
Hamed Sadeghipour ◽  
Mehdi Ghasemi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Papillary Muscles ◽  
Contractile Recovery ◽  
Dependent Mechanism

H-89, a Non-Specific Inhibitor of Protein Kinase A, Promotes Post-Ischemic Cardiac Contractile Recovery and Reduces Infarct Size

2005 ◽  
Vol 45 (4) ◽  
pp. 341-347 ◽  
Author(s):  
Siyanda Makaula ◽  
Amanda Lochner ◽  
Sonia Genade ◽  
Michael N Sack ◽  
Moneeb M Awan ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Infarct Size ◽  
Protein Kinase A ◽  
Specific Inhibitor ◽  
Cardiac Contractile ◽  
Contractile Recovery ◽  
Kinase A

NITRIC OXIDE SYNTHASE IS NOT INVOLVED IN CARDIAC CONTRACTILE DYSFUNCTION IN A RAT MODEL OF ENDOTOXEMIA WITHOUT SHOCK

Shock ◽  
1997 ◽  
Vol 7 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Xianzhong Meng ◽  
Lihua Ao ◽  
James M. Brown ◽  
Dave A. Fullerton ◽  
Anirban Banerjee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Model ◽  
Contractile Dysfunction ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction ◽  
Oxide Synthase

Molecular and pharmacological approaches to inhibiting nitric oxide after burn trauma

2003 ◽  
Vol 285 (4) ◽  
pp. H1616-H1625 ◽  
Author(s):  
Jean White ◽  
Deborah L. Carlson ◽  
Marita Thompson ◽  
David L. Maass ◽  
Billy Sanders ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Function ◽  
Total Body Surface Area ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Contractile Dysfunction ◽  
Wild Type ◽  
Burn Trauma ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction

Whereas controversial, several studies have suggested that nitric oxide (NO) alters cardiac contractility via cGMP, peroxynitrite, or poly(ADP ribose) synthetase (PARS) activation. This study determined whether burn-related upregulation of myocardial inducible NO synthase (iNOS) and NO generation contributes to burn-mediated cardiac contractile dysfunction. Mice homozygous null for the iNOS gene (iNOS knockouts) were obtained from Jackson Laboratory. iNOS knockouts (KO) as well as wild-type mice were given a cutaneous burn over 40% of the total body surface area by the application of brass probes (1 × 2 × 0.3 cm) heated to 100°C to the animals' sides and back for 5 s (iNOS/KO burn and wild-type burn). Additional groups of iNOS KO and wild-type mice served as appropriate sham burn groups (iNOS/KO sham and wild-type sham). Cardiac function was assessed 24 h postburn by perfusing hearts ( n = 7–10 mice/group). Burn trauma in wild-type mice impaired cardiac function as indicated by the lower left ventricular pressure (LVP, 67 ± 2 mmHg) compared with that measured in wild-type shams (94 ± 2 mmHg, P < 0.001), a lower rate of LVP rise (+dP/d tmax, 1,620 ± 94 vs. 2,240 ± 58 mmHg/s, P < 0.001), and a lower rate of LVP fall (–dP/d tmax, 1,200 ± 84 vs. 1,800 ± 42 mmHg/s, P < 0.001). Ventricular function curves confirmed significant contractile dysfunction after burn trauma in wild-type mice. Burn trauma in iNOS KO mice produced fewer cardiac derangements compared with those observed in wild-type burns (LVP: 78 ± 5 mmHg; +dP/d t: 1,889 ± 160 mmHg/s; –dP/d t: 1,480 ± 154 mmHg/s). The use of a pharmacological approach to inhibit iNOS (aminoguanidine, given ip) in additional wild-type shams and burns confirmed the iNOS KO data. Whereas the absence of iNOS attenuated burn-mediated cardiac contractile dysfunction, these experiments did not determine the contribution of cardiac-derived NO versus NO generated by immune cells. However, our data indicate a role for NO in cardiac dysfunction after major trauma.

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