The stresses both active and passive in cardiac ventricles are distributed by collagen, if the heart is analagous to skeletal muscle. The collagen matrix of skeletal muscle is a stress resistant structure with visco-elastic properties. Again, if the collagen matrix of the heart is analagous to skeletal muscle, alteration of the matrix will affect myocardial function. Recently we have observed that in the region of ischemia following coronary artery ligation there is near complete loss of the collagen matrix in the heart within three hours. By examining selected areas of the ischemic region using laser digital imaging to determine the strain rate, we demonstrated a very early (15 min.) increase in strain rate coincident with the loss of contraction. The strain rate remained at a plateau until 2 hrs after occlusion at which time it rose to 2.5 times control value. This rise is coincident with the loss of the collagen matrix. The goals of this proposal are to determine the material properties of the ventricle by laser digital imaging following coronary artery ligation until reasonable recovery occurs at two months. The digital image data will be correlated with histologic evaluation, both light microscopic and scanning electron microscopic, to determine the alterations in tissue constituents that contribute to abnormal material properties. This information will be compared with comparable information derived from animals with reflow after 3 hours of occlusion and reflow with streptokinase. This information may assist in understanding the mechanisms by which reflow of occluded coronary arteries on occassion is a deleterious procedure. The long term goals are to improve methods for obtaining information concerning material properties of the heart and use these in a variety of diseases associated with altered ventricular compliance to explain this phenomenon.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
7R01HL035358-01
Application #
3349176
Study Section
Cardiovascular Study Section (CVA)
Project Start
1985-03-01
Project End
1988-02-28
Budget Start
1985-03-01
Budget End
1986-02-28
Support Year
1
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Alabama Birmingham
Department
Type
School of Medicine & Dentistry
DUNS #
004514360
City
Birmingham
State
AL
Country
United States
Zip Code
35294
Holt, J C; Caulfield, J B; Norton, P et al. (1995) Human cardiac myosin light chains: sequence comparisons between myosin LC1 and LC2 from normal and idiopathic dilated cardiomyopathic hearts. Mol Cell Biochem 145:89-96
Ku, D D; Winn, M J; Grigsby, T et al. (1992) Human coronary vascular smooth muscle and endothelium-dependent responses after storage at -75 degrees C. Cryobiology 29:199-209
Caulfield, J B; Norton, P; Weaver, R D (1992) Cardiac dilatation associated with collagen alterations. Mol Cell Biochem 118:171-9
Margossian, S S; White, H D; Caulfield, J B et al. (1992) Light chain 2 profile and activity of human ventricular myosin during dilated cardiomyopathy. Identification of a causal agent for impaired myocardial function. Circulation 85:1720-33
Ku, D D; Caulfield, J B; Kirklin, J K (1991) Endothelium-dependent responses in long-term human coronary artery bypass grafts. Circulation 83:402-11
Ku, D D; Nelson, J M; Caulfield, J B et al. (1990) Release of endothelium-derived relaxing factors from canine cardiac valves. J Cardiovasc Pharmacol 16:212-8
Caulfield, J B; Wolkowicz, P E (1990) Myocardial connective tissue alterations. Toxicol Pathol 18:488-96
Ku, D D; Willis, W L; Caulfield, J B (1990) Retention of endothelium-dependent vasodilatory responses in canine coronary arteries following cryopreservation. Cryobiology 27:511-20
Caulfield, J B; Wolkowicz, P (1988) Inducible collagenolytic activity in isolated perfused rat hearts. Am J Pathol 131:199-205
Smith, S H; Kirklin, J K; Geer, J C et al. (1987) Arteritis in cardiac rejection after transplantation. Am J Cardiol 59:1171-3