%0 Journal Article
%~ PubMed
%A de Wit, Aletta
%A Vis, Kelly
%A Jeremy, Richmond W
%T Aortic Stiffness in Heritable Aortopathies: Relationship to Aneurysm Growth Rate.
%B Heart, Lung & Circulation
%D 2013
%C Australia
%I Elsevier Australia
%V 22
%N 1
%P 3-11
%@ 1444-2892
%X OBJECTIVE: This study compared aortic biomechanics in different heritable aortopathy syndromes and examined the clinical utility of aortic stiffness measurements. METHODS AND RESULTS: In 218 patients (55 Marfan, 47 bicuspid aortic valve (BAV), 47 isolated familial thoracic aneurysm (FTAD) and 69 matched controls) aortic biomechanics were measured by echocardiography with simultaneous blood pressure measurements. Patients were stratified by age as ?40 years or >40 years. Aortic stiffness increased with age and aortic biomechanics were abnormal in all aortopathies, particularly in BAV and FTAD. Increased stiffness and pulse wave velocity were seen in BAV and FTAD in both age cohorts (p<0.001) and both were stiffer than Marfan patients (p<0.01). Marfan patients aged ?40 years had stiffer aortas than controls, but those >40 years were similar to controls. Multivariate regression identified age as the dominant correlate with increased stiffness, and also aortic diameter and mean blood pressure (R(2)=0.64; p<0.001). Aortopathy patients with stiffness index>16 had lower rate of increase in aortic diameter (0.25±0.30mm/year) than those with normal stiffness (0.68±0.39mm/year, p<0.001). Whilst positive predictive value of increased stiffness for detection of aortopathy was high (93% in age?40 years, 87%, in age>40 years), negative predictive accuracy was low (55% and 34% respectively). CONCLUSION: Abnormal biomechanics are common to all aortopathies, with greater abnormality in BAV and FTAD than in Marfan. Increased aortic stiffness is associated with slower rate of aneurysm progression.
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Ramponi, Fabio
%A Leslie, Anthony
%A Stephen, Michael S
%A White, Geoffrey H
%A Jeremy, Richmond
%A Wilson, Michael K
%T Management of the proximal anastomosis in open, hybrid repair of thoracoabdominal aortic aneurysm.
%B The Annals of Thoracic Surgery
%D 2012
%C United States
%I Elsevier Inc.
%V 93
%N 1
%P 358-359
%@ 0003-4975
%X 
%Z FOR Codes: 110201 110323


%0 Journal Article
%~ PubMed
%A Davidson, Patricia M
%A Macisaac, Andrew
%A Cameron, James
%A Jeremy, Richmond
%A Mahar, Leo
%A Anderson, Ian
%T Problems, Solutions and Actions: Addressing Barriers in Acute Hospital Care for Indigenous Australians and New Zealanders.
%B Heart, Lung & Circulation
%D 2012
%C Australia
%I Elsevier Australia
%V 21
%N 10
%P 639-643
%@ 1444-2892
%X The burden of cardiovascular disease for Indigenous people in Australia and New Zealand is high and reflects the failings of our health care system to meet their needs. Improving the hospital care for Indigenous people is critical in improving health outcomes. This paper provides the results from a facilitated discussion on the disparities in acute hospital care and workforce issues. The workshop was held in Alice Springs, Australia at the second Cardiac Society of Australia and New Zealand (CSANZ) Indigenous Cardiovascular Health Conference. Critical issues to be addressed include: addressing systemic racism; reconfiguring models of care to address the needs of Indigenous people; cultural competence training for all health professionals; increasing participation of Indigenous people in the health workforce; improving information systems and facilitating communication across the health care sector and with Indigenous communities.
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond
%A Cameron, James
%T Towards Better Outcomes in Indigenous Cardiovascular Health: Directions from the First and Second Indigenous Cardiovascular Health Care Conferences.
%B Heart, Lung & Circulation
%D 2012
%C Australia
%I Elsevier Australia
%V 21
%N 10
%P 613-614
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T Early discharge after percutaneous intervention - we can but should we?
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Wiley-Blackwell Publishing Asia
%V 20
%N 6
%P 351-352
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Davies, Reece A
%A Black, Deborah
%A Jeremy, Richmond W
%A Bannon, Paul G
%A Bayfield, Matthew S
%A Hendel, P Nicholas
%A Hughes, Clifford F
%A Wilson, Michael K
%A Vallely, Michael P
%T Evolution in the Techniques and Outcomes of Aortic Arch Surgery: A 22 Year Single Centre Experience.
%B Heart, lung & circulation
%D 2011
%C Australia
%I Wiley-Blackwell Publishing Asia
%V 20
%N 11
%P 704-11
%@ 1444-2892
%X Aortic arch replacement is a complicated and high risk procedure. There have been many advances over recent years. We review the changes in our unit''s techniques and outcomes over the past 22 years.
%Z FOR Codes: 1103


%0 Journal Article
%~ PubMed
%A Edelman, James J B
%A Ramponi, Fabio
%A Bannon, Paul G
%A Jeremy, Richmond
%T Familial aortic aneurysm and dissection due to transforming growth factor-{beta} receptor-2 mutation.
%B Interactive cardiovascular and thoracic surgery
%D 2011
%C Switzerland
%I European Association for Cardio-Thoracic Surgery
%V 12
%N 5
%P 863-5
%@ 1569-9285
%X This report describes the clinical course and management of a patient with Loeys-Dietz syndrome (LDS) type 2. In 2003, a 31-year-old male was diagnosed with acute aortic dissection type B; in the following six years he underwent multiple surgical and endovascular aortic procedures at different thoracic and abdominal levels secondary to progressive enlargement of both the non-dissected thoracic aorta and the false lumen distal to the left subclavian artery. LDS is characterized by arterial tortuosity and aneurysms as a result of heterozygous mutations in genes encoding transforming growth factor-?? receptor 1 and 2. Further studies are required to establish the proper surgical management.
%Z FOR Codes: 110323


%0 Journal Article
%~ PubMed
%A Gray, B R
%A Semsarian, C
%A Sy, R W
%A Jeremy, R W
%T Left coronary artery fistula after septal myectomy in hypertrophic cardiomyopathy.
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Elsevier Australia
%V 20
%N 11
%P 738
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T Metabolic syndrome-Is the whole really greater than the sum of the parts?
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Wiley-Blackwell Publishing Asia
%V 20
%N 4
%P 211-213
%@ 1444-2892
%X 
%Z FOR Codes: 1102


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T Microvascular obstruction after infarct reperfusion What does it really mean and what should we do about it?
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Wiley-Blackwell Publishing Asia
%V 20
%N 2
%P 71-72
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T New challenges for the journal--milestones passed and those ahead.
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Elsevier Australia
%V 20
%N 10
%P 613-614
%@ 1444-2892
%X 
%Z FOR Codes: 1102


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T Secondary Prevention: Why Does it Seem to be so Hard?
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Wiley-Blackwell Publishing Asia
%V 20
%N 7
%P 423-424
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T The burden of genetic heart disease.
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Elsevier Australia
%V 20
%N 11
%P 679-680
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T To register or not?that is the question. The case for collaboration and a National Cardiac Procedures Database.
%B Heart, Lung & Circulation
%D 2011
%C Australia
%I Wiley-Blackwell Publishing Asia
%V 20
%N 1
%P 1-2
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T Cardiopulmonary bypass - Reducing the stress.
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 10
%P 577-578
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Brown, Alex
%A Brieger, David
%A Tonkin, Andrew
%A White, Harvey
%A Walsh, Warren
%A Riddell, Tania
%A Zeitz, Chris
%A Jeremy, Richmond
%A Kritharides, Leonard
%T Coronary disease in indigenous populations: summary from the CSANZ indigenous Cardiovascular Health Conference.
%B Heart, lung & circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 5-6
%P 299-305
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond
%T Do healthy hearts mean a healthy world?
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 4
%P 211-212
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond
%T Equitable access to regional cardiovascular services.
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 1
%P 1
%@ 1444-2892
%X 
%Z FOR Codes: 110299 111717


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond
%A Tonkin, Andrew
%A White, Harvey
%A Riddell, Tania
%A Brieger, David
%A Walsh, Warren
%A Zeitz, Chris
%A Brown, Alex
%A Kritharides, Leonard
%T Improving Cardiovascular Care for Indigenous Populations.
%B Heart, lung & circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 5-6
%P 344-50
%@ 1444-2892
%X The challenges and opportunities for provision of, and access to, reliable chronic cardiovascular health care for Indigenous people were addressed by expert speakers from New Zealand and Australia. It is well recognised that cardiovascular disease is a life-long concern, requiring reliable follow-up, early transition of clinical research into practice and ongoing support of patients. The clinical outcomes and long-term prognosis of individuals with cardiovascular disease are critically dependent upon the quality and availability of follow-up and chronic care facilities. This paper summarises the principal issues identified by the expert speakers for the provision of chronic cardiovascular health care to Indigenous peoples in Australia and New Zealand; identifies common challenges and describes important initiatives which the Cardiac Society of Australia and New Zealand (CSANZ), in partnership with health care professionals, communities and governments, can undertake in order to achieve the goals of uniform and equitable health care for chronic cardiovascular disease in all the Indigenous peoples, relevant to the needs of these peoples, in New Zealand and Australia. The issues addressed by the meeting include: 1) Determination of appropriate models for effective delivery of cardiovascular health care. (2) Who should deliver cardiovascular health care and what are the workforce requirements. (3) What support systems and infrastructure are required. (4) How can primary care and secondary specialist services be effectively integrated.
%Z FOR Codes: 1102


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%A Brown, Alex
%T Measuring the gap-It may well be worse than we thought.
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 12
%P 695-696
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond
%T Neurogenic heart disease: from Voodoo to Tako-tsubo.
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 2
%P 61-62
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Kritharides, Leonard
%A Brown, Alex
%A Brieger, David
%A Ridell, Tania
%A Zeitz, Chris
%A Jeremy, Richmond
%A Tonkin, Andrew
%A Walsh, Warren
%A White, Harvey
%T Overview and determinants of cardiovascular disease in indigenous populations.
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 5-6
%P 337-343
%@ 1444-2892
%X Cardiovascular disease (CV) is an important problem among the 400 million Indigenous Populations around the world, and has been included in the World Health Organization (WHO) "2008-2013 Action Plan for Non-Communicable Diseases". Our understanding of the causes of CV disease in the Indigenous populations of Australia and New Zealand will be facilitated by better understanding the causes of CV disease in Indigenous populations around the world. The opening scientific presentations of the Inaugural CSANZ Conference on Indigenous Cardiovascular Health were from two international speakers notable for their commitment to Indigenous Health as a global problem.
%Z FOR Codes: 110201 111701


%0 Journal Article
%~ PubMed
%A Kritharides, Leonard
%A Brown, Alex
%A Brieger, David
%A Ridell, Tania
%A Zeitz, Chris
%A Jeremy, Richmond
%A Tonkin, Andrew
%A Walsh, Warren
%A White, Harvey
%T Recommendations Arising from the Inaugural CSANZ Conference on Indigenous Cardiovascular Health.
%B Heart, lung & circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 5-6
%P 269-72
%@ 1444-2892
%X 
%Z FOR Codes: 1102


%0 Journal Article
%~ PubMed
%A White, Harvey
%A Walsh, Warren
%A Brown, Alex
%A Riddell, Tania
%A Tonkin, Andrew
%A Jeremy, Richmond
%A Brieger, David
%A Zeitz, Chris
%A Kritharides, Leonard
%T Rheumatic heart disease in indigenous populations.
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 5-6
%P 273-281
%@ 1444-2892
%X Rates of acute rheumatic fever and chronic rheumatic heart disease in Aboriginal people, Torres Strait Islanders and M?ori continue to be unacceptably high. The impact of rheumatic heart disease is inequitable on these populations as compared with other Australians and New Zealanders. The associated cardiac morbidity, including the development of rheumatic valve disease, and cardiomyopathy, with possible sequelae of heart failure, development of atrial fibrillation, systemic embolism, transient ischaemic attacks, strokes, endocarditis, the need for interventions including cardiac surgery, and impaired quality of life, and shortened life expectancy, has major implications for the individual. The adverse health and social effects may significantly limit education and employment opportunities and increase dependency on welfare. Additionally there may be major adverse impacts on family and community life. The costs in financial terms and missed opportunities, including wasted young lives, are substantial. Prevention of acute rheumatic fever is dependent on the timely diagnosis and treatment of sore throats and skin infections in high-risk groups. Both Australia and New Zealand have registries for acute rheumatic fever but paradoxically neither includes all cases of chronic rheumatic heart disease many of whom would benefit from close surveillance and follow-up. In New Zealand and some Australian States there are programs to give secondary prophylaxis with penicillin, but these are not universal. Surgical outcomes for patients with rheumatic valvular disease are better for valve repair than for valve replacement. Special attention to the selection of the appropriate valve surgery and valve choice is required in pregnant women. It may be necessary to have designated surgical units managing Indigenous patients to ensure high rates of surgical repair rather than valve replacement. Surgical guidelines may be helpful. Long-term follow-up of the outcomes of surgery in Indigenous patients with rheumatic heart disease is required. Underpinning these strategies is the need to improve poverty, housing, education and employment. Cultural empathy with mutual trust and respect is essential. Involvement of Indigenous people in decision making, design, and implementation of primary and secondary prevention programs, is mandatory to reduce the unacceptably high rates of rheumatic heart disease.
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Brown, Alex
%A Tonkin, Andrew
%A White, Harvey
%A Riddell, Tania
%A Brieger, David
%A Walsh, Warren
%A Zeitz, Chris
%A Jeremy, Richmond
%A Kritharides, Leonard
%T The Cardiac Society Inaugural Cardiovascular Health Conference: conference findings and ways forward.
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 5-6
%P 264-268
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T Thoracic Aortic Dissection - Beyond the acute problem.
%B Heart, lung & circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 11
%P 641-643
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T What does a good outcome really mean and who determines it?
%B Heart, Lung & Circulation
%D 2010
%C Australia, United St
%I Wiley-Blackwell Publishing Asia
%V 19
%N 9
%P 515-516
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Jeremy, Richmond W
%T Making an impact.
%B Heart, Lung & Circulation
%D 2009
%C Australia
%I Wiley-Blackwell Publishing Asia
%V 18
%N 5
%P 317-318
%@ 1444-2892
%X 
%Z FOR Codes: 110201


%0 Journal Article
%~ PubMed
%A Prasan, Ananth M
%A McCarron, Hugh C K
%A Zhang, Yi
%A Jeremy, Richmond W
%T Myocardial Release of Nitric Oxide During Ischaemia and Reperfusion: Effects of l-Arginine and Hypercholesterolaemia.
%B Heart, lung & circulation
%D 2007
%C Australia
%I Wiley- Blackwell Publishing Asia
%V 16
%N 4
%P 274-281
%@ 1443-9506
%X AIMS: Nitric oxide (NO) may modulate myocardial ischaemia/reperfusion (I/R) injury, but effects of hypercholesterolaemia on myocardial NO release during I/R are unknown. METHODS: A NO-specific carbon fibre electrode continuously measured coronary sinus [NO] during 60min low-flow ischaemia (1ml/min) and 60min free reperfusion (I/R) in isolated rabbit hearts. Experimental groups (n=7 per group) were control, l-arginine supplement (200muM), N-nitro-l-arginine methyl ester (L-NAME) treatment (8muM) and hypercholesterolaemic. RESULTS: During early I, NO release decreased markedly in control (-1356+/-286pmol/min/g) and l-arginine (-1972+/-172) groups, but less in L-NAME (-441+/-89) and hypercholesterolaemic (-602+/-164) groups (both p<0.01 vs. controls). No increase in NO release during I was seen in any group. After R, NO release increased above baseline in control (+2333+/-591pmol/min/g) and l-arginine (+1048+/-278) groups and hypercholesterolaemic (+1100+/-478) (p<0.05 vs. pre-ischaemia each group). There was little increase in NO release in the L-NAME group (+436+/-247pmol/min/g, p<0.05 vs. controls). In each group, myocardial NO release declined towards pre-ischaemic levels during 60min R. Hearts treated with l-arginine had similar NO release but better functional recovery than controls (p<0.01). Treatment with L-NAME was also associated with better functional recovery than in controls or hypercholesterolaemic hearts. CONCLUSION: Myocardial NO release declines rapidly during ischaemia, but increases above baseline during early reperfusion. Improved function after l-arginine treatment appears to be independent of effects upon NO release. Hypercholesterolaemia is associated with reduced myocardial NO release, under both baseline conditions and during ischaemia and reperfusion.
%Z FOR Codes: 110201


%0 Book Section
%A Jeremy, Richmond
%T From sandstone to stainless steel
%B 150 years of the Faculty of Medicine
%D 2006
%C Sydney
%I Sydney University Press
%V 
%N 
%P 279-316
%@ 1920898352
%E Cossart, Yvonne
%E Sefton, Ann
%E Freckelton, Louise
%X 
%Z FOR Codes:


%0 Journal Article
%~ PubMed
%A White, Melanie Y
%A Hambly, Brett D
%A Jeremy, Richmond W
%A Cordwell, Stuart J
%T Ischemia-specific phosphorylation and myofilament translocation of heat shock protein 27 precedes alpha B-crystallin and occurs independently of reactive oxygen species in rabbit myocardium.
%B Journal of molecular and cellular cardiology
%D 2006
%C United Kingdom
%I Academic Press
%V 40
%N 6
%P 761-74
%@ 0022-2828
%X Heat shock protein 27 (Hsp27) and alpha B-crystallin (alphaBC) are small heat shock proteins that stabilize the myofilament during stress. We utilized two-dimensional gel electrophoresis (2-DE), phospho-fluorescence staining, titanium dioxide (TiO(2)) phosphopeptide purification and mass spectrometry (MS) to fully characterize isoelectric point (pI) variants of Hsp27 and alphaBC in rabbit myocardium subjected to brief ischemia/reperfusion (I/R) injury. Four variants of Hsp27 were detected, two of which were phosphorylated: HSP1 (at three sites, Ser15, Ser78 and Ser82) and HSP2 (at Ser15 and Ser82, but not Ser78). Three variants of alphaBC were detected: alphaBC1 was phosphorylated (at Ser59 alone) and alphaBC2 was deamidated (at Asn146). No modifications were found in the remaining variants. Both phospho-Hsp27 variants increased in abundance in tissue subjected to brief I/R injury (15 min I/60 min R) and ischemia without subsequent reflow (15I/0R), and these increases were not affected by addition of the potent antioxidant, N-(2-mercaptopropionyl) glycine (MPG; 15I/60R + MPG and 15I/0R + MPG). Abundance of native and phosphorylated (but not deamidated) alphaBC was elevated following 15I/60R; however, these increases were ameliorated by the presence of MPG, and did not occur in tissue subjected to 15I/0R. Both phospho-Hsp27 variants and phospho-alphaBC translocated to the myofilament following 15I/60R. Increased myofilament association of phospho-Hsp27 was not influenced by MPG, and there was a greater proportion of HSP2 than HSP1 in this fraction. MPG inhibited phospho-alphaBC translocation and increased alphaBC association with the myofilament did not occur during 15I/0R. Increased phosphorylation of Hsp27 is ischemia-specific and not influenced by reactive oxygen species (ROS), while increased expression and phosphorylation of alphaBC are ROS-dependant.
%Z FOR Codes: 110106


%0 Journal Article
%~ PubMed
%A White, Melanie Y
%A Tchen, Adrian S
%A McCarron, Hugh C K
%A Hambly, Brett D
%A Jeremy, Richmond W
%A Cordwell, Stuart J
%T Proteomics of ischemia and reperfusion injuries in rabbit myocardium with and without intervention by an oxygen-free radical scavenger.
%B Proteomics
%D 2006
%C Germany
%I Wiley - VCH Verlag GmbH & Co. KGaA
%V 6
%N 23
%P 6221-33
%@ 1615-9853
%X A brief period of ischemia followed by timely reperfusion may lead to prolonged, yet reversible, contractile dysfunction (myocardial stunning). Damage to the myocardium occurs not only during ischemia, but also during reperfusion, where a massive release of oxygen-free radicals (OFR) occurs. We have previously utilized 2-DE and MS to define 57 protein spot changes during brief ischemia/reperfusion (15 min ischemia, 60 min reperfusion; 15I/60R) injury in a rabbit model (White, M. Y., Cordwell, S. J., McCarron, H. C. K., Prasan, A. M. et al., Proteomics 2005, 5, 1395-1410) and shown that the majority of these occur because of physical and/or chemical PTMs. In this study, we subjected rabbit myocardium to 15I/60R in the presence of the OFR scavenger N-(2-mercaptopropionyl) glycine (MPG). Thirty-seven of 57 protein spots altered during 15I/60R remained at control levels in the presence of MPG (15I/60R + MPG). Changes to contractile proteins, including myosin light chain 2 (MLC-2) and troponin C (TnC), were prevented by the addition of MPG. To further investigate the individual effects of ischemia and reperfusion, we generated 2-DE gels from rabbit myocardium subjected to brief ischemia alone (15I/0R), and observed alterations of 33 protein spots, including 18/20 seen in both 15I/60R-treated and 15I/60R + MPG-treated tissue. The tissue was also subjected to ischemia in the presence of MPG (15I/0R + MPG), and 21 spot changes, representing 14 protein variants, remained altered despite the presence of the OFR scavenger. These ischemia-specific proteins comprised those involved in energy metabolism (lactate dehydrogenase and ATP synthase alpha), redox regulation (NADH ubiquinone oxidoreductase 51 kDa and GST Mu), and stress response (Hsp27 and 70, and deamidated alpha B-crystallin). We conclude that contractile dysfunction associated with myocardial stunning is predominantly caused by OFR damage at the onset of reperfusion, but that OFR-independent damage also occurs during ischemia. These ischemia-specific protein modifications may be indicative of early myocardial injury.
%Z FOR Codes: