The objective of the Animal/Histomorphometry core is to provide investigators of the program project grant (PPG) scientific, technical and financial support for the design and execution of studies involving animals and histomorphometric assessment of cardiac tissue. Our state-of-the art facility houses and contains all the animals and equipment necessary to execute experiments and analyze specimens from dogs with coronary microembolization-induced heart failure (HF) as well as from dogs with rapid pacing-induced HF. Over the past 23 years, we have developed and fully characterized a canine model of chronic HF which is ideally suited for the studies outlined in the PPG. Heart failure in this model is produced by multiple sequential intracoronary embolizations with microspheres that lead to loss of viable myocardium. The model manifests many, if not all of the sequelae of HF in humans including profound systolic and diastolic LV dysfunction, LV dilation and compensatory hypertrophy, increased LV filling pressures, increased systemic vascular resistance, decreased cardiac output and, importantly, abnormalities of mitochondria and characteristic progressive worsening of LV function. The Core will the perform the following aims: 1) coordinate the acquisition, housing and preparation of dogs involved in the coronary microembolization-induced HF studies, 2) execute pharmacologic protocols involving coronary microembolization-induced HF i.e. assume responsibility for treatment regimens for project 2, 3) coordinate distribution of dogs and cardiac tissues derived from coronary microembolization-induced HF experiments and 4) perform histological analysis of tissue samples derived from coronary-microembolization induced HF and mouse studies (Projects 1, 2 and 4) as well as from dogs with rapid-pacing-induced HF that are specific to project 3 of the PPG. Services to PPG investigators will be provided by a team consisting of the Core Leader (Dr. H.N. Sabbah), the Core Co- Leader (Dr. V.G. Sharov), 1 Assistant Staff Investigator (Dr M. Wang) and 1 Licensed Veterinary Technologists (Ms. Annette Hazel). The facility veterinarian (Dr. Gregory Heisey) is an institutional resource and will provide all the necessary and required veterinary support without charge.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Research Program Projects (P01)
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Heart, Lung, and Blood Initial Review Group (HLBP)
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University of Maryland Baltimore
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Lanfear, David E; Gibbs, Joseph J; Li, Jia et al. (2017) Targeted Metabolomic Profiling of Plasma and Survival in Heart Failure Patients. JACC Heart Fail 5:823-832
Ardell, J L; Andresen, M C; Armour, J A et al. (2016) Translational neurocardiology: preclinical models and cardioneural integrative aspects. J Physiol 594:3877-909
Sabbah, Hani N; Gupta, Ramesh C; Kohli, Smita et al. (2016) Chronic Therapy With Elamipretide (MTP-131), a Novel Mitochondria-Targeting Peptide, Improves Left Ventricular and Mitochondrial Function in Dogs With Advanced Heart Failure. Circ Heart Fail 9:e002206
Kop, Willem J; Galvao, Tatiana F; Synowski, Stephen J et al. (2015) Effects of environmental stress following myocardial infarction on behavioral measures and heart failure progression: The influence of isolated and group housing conditions. Physiol Behav 152:168-74
Flori, Alessandra; Liserani, Matteo; Frijia, Francesca et al. (2015) Real-time cardiac metabolism assessed with hyperpolarized [1-(13) C]acetate in a large-animal model. Contrast Media Mol Imaging 10:194-202
Roul, David; Recchia, Fabio A (2015) Metabolic alterations induce oxidative stress in diabetic and failing hearts: different pathways, same outcome. Antioxid Redox Signal 22:1502-14
Trappanese, Danielle M; Liu, Yuchuan; McCormick, Ryan C et al. (2015) Chronic ?1-adrenergic blockade enhances myocardial ?3-adrenergic coupling with nitric oxide-cGMP signaling in a canine model of chronic volume overload: new insight into mechanisms of cardiac benefit with selective ?1-blocker therapy. Basic Res Cardiol 110:456
Recchia, Fabio A (2015) Revascularization of hibernating myocardium: uneven reflorescence after the drought. J Am Coll Cardiol 65:698-700
Meraviglia, Viviana; Azzimato, Valerio; Colussi, Claudia et al. (2015) Acetylation mediates Cx43 reduction caused by electrical stimulation. J Mol Cell Cardiol 87:54-64
Woitek, Felix; Zentilin, Lorena; Hoffman, Nicholas E et al. (2015) Intracoronary Cytoprotective Gene Therapy: A Study of VEGF-B167 in a Pre-Clinical Animal Model of Dilated Cardiomyopathy. J Am Coll Cardiol 66:139-53

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