Large artery remodeling after myocardial infarction.
Rats with myocardial infarction (MI) after coronary artery ligation (n = 75) and sham operated rats (n = 40) were treated with captopril (2 g/l drinking water), hydralazine (80 mg/l drinking water), or untreated water for 3 wk. Arterial hemodynamics, carotid artery mechanical properties, and water permeability were measured. Arterial wall stress and interstitial fluid velocity were calculated. In infarcted rats, the characteristic impedance at matched pressure was increased by 135% (P < 0.02); captopril and hydralazine decreased characteristic impedance (P < 0.015). MI altered the material constants; captopril but not hydralazine normalized these constants. Water permeability was increased by 221% (P < 0.001) in infarcted rats; captopril but not hydralazine reversed water permeability (P < 0.05). MI resulted in a 59% increase (P < 0.05) in the arterial collagen area and a 22% decrease (P < 0.05) in the media thickness. Captopril but not hydralazine decreased (P < 0.03) collagen area. In conclusion, 1) arterial remodeling defined by alterations in the passive mechanical properties, water permeability, and structure occurs in rats after MI; and 2) captopril but not hydralazine reverses the arterial remodeling.
Gaballa
M A
MA
Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723, USA.
Raya
T E
TE
Goldman
S
S
D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001158:Arteries / Q000473:pathology / Q000503:physiopathology*; D001794:Blood Pressure; D001834:Body Water / Q000378:metabolism; D005110:Extracellular Space / Q000378:metabolism; D006439:Hemodynamics; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013314:Stress, Mechanical; D014655:Vascular Resistance; D014661:Vasoconstriction; D016276:Ventricular Function