Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL048715-03
Application #
2224779
Study Section
Cardiovascular and Pulmonary Research A Study Section (CVA)
Project Start
1993-12-01
Project End
1997-11-30
Budget Start
1995-12-01
Budget End
1997-11-30
Support Year
3
Fiscal Year
1996
Total Cost
Indirect Cost
Name
Boston University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
604483045
City
Boston
State
MA
Country
United States
Zip Code
02118
Saupe, K W; Eberli, F R; Ingwall, J S et al. (2001) Metabolic support as an adjunct to inotropic support in the hypoperfused heart. J Mol Cell Cardiol 33:261-9
Cave, A C; Ingwall, J S; Friedrich, J et al. (2000) ATP synthesis during low-flow ischemia: influence of increased glycolytic substrate. Circulation 101:2090-6
Eberli, F R; Stromer, H; Ferrell, M A et al. (2000) Lack of direct role for calcium in ischemic diastolic dysfunction in isolated hearts. Circulation 102:2643-9
Jain, M; Liao, R; Ngoy, S et al. (2000) Angiotensin II receptor blockade attenuates the deleterious effects of exercise training on post-MI ventricular remodelling in rats. Cardiovasc Res 46:66-72
Saupe, K W; Eberli, F R; Ingwall, J S et al. (1999) Hypoperfusion-induced contractile failure does not require changes in cardiac energetics. Am J Physiol 276:H1715-23
Kondo, R P; Apstein, C S; Eberli, F R et al. (1998) Increased calcium loading and inotropy without greater cell death in hypoxic rat cardiomyocytes. Am J Physiol 275:H2272-82
Libonati, J R; Eberli, F R; Sesselberg, H W et al. (1997) Effects of low-flow ischemia on the positive inotropic action of angiotensin II in isolated rabbit and rat hearts. Cardiovasc Res 33:71-81
Bernstein, E A; Eberli, F R; Silverman, A M et al. (1996) Beneficial effects of felodipine on myocardial and coronary function during low-flow ischemia and reperfusion. Cardiovasc Drugs Ther 10:167-78
Cave, A C; Apstein, C S (1996) Polymyxin B, a protein kinase C inhibitor, abolishes preconditioning-induced protection against contractile dysfunction in the isolated blood perfused rat heart. J Mol Cell Cardiol 28:977-87