NDLI: Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide

Content Provider	Springer Nature Link
Author	Maury, Philippe Sarre, Alexandre Terrand, Jérôme Rosa, Antonio Kucera, Pavel Kappenberger, Lukas Raddatz, Eric
Copyright Year	2004
Abstract	Background/Aim. Excitation–contraction coupling is modulated by nitric oxide (NO) which otherwise has either beneficial or detrimental effects on myocardial function during hypoxia-reoxygenation. This work aimed at characterizing the variations of electromechanical delay (EMD) induced by anoxia-reoxygenation within the developing heart and determining whether atrial and ventricular EMD are modulated by NO to the same extent. Methods. Hearts of 4 or 4.5-day-old chick embryos were excised and submitted in vitro to normoxia (45 min), anoxia (30 min) and reoxygenation (60 min). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout experiment. Anoxia-reoxygenation-induced chrono-, dromo- and inotropic disturbances and changes in EMD in atrium (EMDa) and ventricle (EMDv) were investigated in control hearts and in hearts exposed to 0.1, 1, 10, 50 and 100 μM of DETA-NONOate (a NO donating agent) or to 50 μM of L-NAME (a NOS inhibitor). Results. Under normoxia, heart rate, PR interval, ventricular shortening velocity, EMDa and EMDv were similar in control, L-NAME-treated and DETA-NONOate-treated hearts. Under anoxia, cardiac activity became markedly erratic within less than 10 min in all groups. At the onset of reoxygenation, EMDv was increased by about 300% with respect to the preanoxic value while EMDa did not vary significatively. Compared to control conditions, L-NAME or DETA-NONOate had no influence on the negative chrono-, dromo- and inotropic effects induced by anoxia-reoxygenation. However, L-NAME prolonged EMDv during anoxia and delayed EMDv recovery during reoxygenation while 100 μM DETA-NONOate had the opposite effects. EMDa was neither affected by NOS inhibitor nor NO donor. At the end of reoxygenation, all the investigated parameters returned to their basal values. Conclusion. This work provides evidence that a NO-dependent pathway is involved in regulation of the ventricular excitation-contraction coupling in the anoxic-reoxygenated developing heart. (Mol Cell Biochem 265: 141–149, 2004)
Starting Page	141
Ending Page	149
Page Count	9
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	265
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2004-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cardiology Medical Biochemistry Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

Postanoxic functional recovery of the developing heart is slightly altered by endogenous or exogenous nitric oxide

Ets-1 is involved in transcriptional regulation of the chick inducible nitric oxide synthase gene in embryonic ventricular myoctyes

Modulation of the c-Jun N-terminal kinase activity in the embryonic heart in response to anoxia-reoxygenation: involvement of the Ca$^{2+}$ and mitoK$_{ATP}$ channels

Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart

Nitric oxide inhibition decreases bleomycin-detectable iron in spleen, bone marrow cells and heart but not in liver in exercise rats

Does proteasome regulate the level of microRNA-1 in cardiomyocytes? Application to anoxia-reoxygenation

Sex-specific differences in natriuretic peptide and nitric oxide synthase expression in ANP gene-disrupted mice

Diastolic function during hemorrhagic shock in rabbits

Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide

Similar Documents

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

Postanoxic functional recovery of the developing heart is slightly altered by endogenous or exogenous nitric oxide

Ets-1 is involved in transcriptional regulation of the chick inducible nitric oxide synthase gene in embryonic ventricular myoctyes

Modulation of the c-Jun N-terminal kinase activity in the embryonic heart in response to anoxia-reoxygenation: involvement of the Ca$^{2+}$ and mitoK$_{ATP}$ channels

Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart

Nitric oxide inhibition decreases bleomycin-detectable iron in spleen, bone marrow cells and heart but not in liver in exercise rats

Does proteasome regulate the level of microRNA-1 in cardiomyocytes? Application to anoxia-reoxygenation

Sex-specific differences in natriuretic peptide and nitric oxide synthase expression in ANP gene-disrupted mice

Diastolic function during hemorrhagic shock in rabbits

Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide