Homocysteine Exposure Impairs Myocardial Resistance to Ischaemia Reperfusion and Oxidative Stress

Title
Homocysteine Exposure Impairs Myocardial Resistance to Ischaemia Reperfusion and Oxidative Stress
Publication Date
2015
Author(s)
Almashhadany, Amer
Shackebaei, Dareuosh
van der Touw, Tom
Jones, Graham L
( author )
OrcID: https://orcid.org/0000-0002-6435-1542
Email: gjones2@une.edu.au
UNE Id une-id:gjones2
Suleiman, M Saadeh
King, Nicola
Type of document
Journal Article
Language
en
Entity Type
Publication
Publisher
S Karger AG
Place of publication
Switzerland
DOI
10.1159/000438582
UNE publication id
une:18501
Abstract
Background/Aims: Hyperhomocysteinaemia is recognised as a strong independent risk factor for developing cardiovascular disease. This study investigated how an acute homocysteine dose affected cardiac performance during ischaemia reperfusion and cardiomyocyte contractility and morphology under normal conditions and during oxidative stress. Methods: Cardiac function was measured in isolated and perfused rat hearts before and after 40 minutes' global normothermic ischaemia. Where used, 0.1 mM L-homocysteine was present prior to, and throughout ischaemia, before wash out after 10 minutes' reperfusion. Calcium transients under normal conditions and changes in contractile synchronicity during oxidative stress (exposure to 0.2 mM H2O2) were measured in freshly isolated rat cardiomyocytes incubated for 60 minutes ± 0.1 mM L-homocysteine. Results: During ischaemia reperfusion 0.1 mM L-homocysteine significantly reduced the rate pressure product during reperfusion (10,038 ± 749 vs. 5955 ± 567 mmHg bpm, p < 0.001), but did not affect time to ischaemic contracture. Incubation of freshly isolated cardiomyocytes with 0.1 mM L-homocysteine significantly decreased the amplitude of the calcium transient and slowed the time to half relaxation. Conclusions: These findings suggest that homocysteine exposure affected myocardial recovery from ischaemia and contractile homeostasis although the exact mechanisms for these changes remain to be determined.
Link
Citation
Cellular Physiology and Biochemistry, 37(6), p. 2265-2274
ISSN
1421-9778
1015-8987
Start page
2265
End page
2274

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