The collateral circulation is the only source of blood supply to the myocardium after an acute coronary occlusion. During recovery, it constitutes nature's own repair process by developing new vascular growth. Coronary occlusion often leads to heart failure with a concomitant increase in coronary venous pressure which, in turn, can have a further deleterious effect on coronary and collateral perfusion, hence, augments heart failure. The proposed studies represent a continuation of our investigations into the mechanism(s) underlying coronary collateral growth. Our recent confirmation that intramural collaterals constitute the major component of the collateral circulation in the dog, as it does in humans, warrants studies concerned with influences affecting their ability to provide blood to the collateral dependent myocardium. The methods for this quantitation are accurate and lend themselves to repeated measurements. Recent findings from this laboratory also point to the potential importance of the coronary venous system in influencing coronary and collateral perfusion and is the subject of investigations for this application.
The specific aims of this proposal are: 1) To investigate whether a chronic increase in blood flow (velocity) provides a stimulus for coronary and/or collateral growth, 2) to identify, characterize, and quantitate the effects of myocardial forces on epicardial and intramural collateral flow in hearts with native and mature collaterals, 3) to study the effects of changes in coronary venous pressure on perfusion of the collateral dependent myocardium. The research will be performed in conscious dogs and an isolated heart system that allows the intrinsic influences of the heart on coronary flow to be studied independent of peripheral influences.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL035030-07
Application #
3348525
Study Section
Cardiovascular and Pulmonary Research A Study Section (CVA)
Project Start
1985-12-01
Project End
1995-03-31
Budget Start
1993-04-01
Budget End
1994-03-31
Support Year
7
Fiscal Year
1993
Total Cost
Indirect Cost
Name
University of North Texas
Department
Type
Schools of Osteopathy
DUNS #
110091808
City
Fort Worth
State
TX
Country
United States
Zip Code
76107
Manor, D; Williams, S; Ator, R et al. (1995) Left ventricular mechanics in arrested dog heart: effects of ventricular interaction and vascular volumes. Am J Physiol 268:H2125-32
Manor, D; Williams, S; Ator, R et al. (1995) Modulation of coronary flow by left ventricular volume in the presence and absence of vasomotor tone. Am J Physiol 269:H2010-6
Manor, D; Williams, S; Ator, R et al. (1994) Reduced collateral perfusion is a direct consequence of elevated right atrial pressure. Am J Physiol 267:H1151-6
Scheel, K W; Mass, H; Williams, S E (1993) Pressure-flow characteristics of intramural and total coronary collateral networks. Am J Physiol 264:H408-12
Scheel, K W; Williams, S E; Parker, J B (1990) Coronary sinus pressure has a direct effect on gradient for coronary perfusion. Am J Physiol 258:H1739-44
Chilian, W M; Mass, H J; Williams, S E et al. (1990) Microvascular occlusions promote coronary collateral growth. Am J Physiol 258:H1103-11
Scheel, K W; Daulat, G; Mass, H J et al. (1990) Intramural coronary collateral flow in dogs. Am J Physiol 258:H679-82
Scheel, K W; Daulat, G; Williams, S E (1990) Functional anatomical site of intramural collaterals in dogs. Am J Physiol 259:H706-11
Scheel, K W; Mass, H; Williams, S E (1989) Collateral influence on pressure-flow characteristics of coronary circulation. Am J Physiol 257:H717-25
Scheel, K W; Mass, H; Williams, S E (1989) Pressure-flow characteristics of coronary collaterals in dogs. Am J Physiol 256:H441-5

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