Collagen deposition and the reversal of coronary reserve in cardiac hypertrophy.
The aim of this study was to clarify how collagen deposition or medial hypertrophy of the vascular wall affects the coronary dilator reserve in pressure-overloaded hearts and whether inhibition of collagen deposition reverses the abnormalities after relief of pressure overload. We used ascending aortic banding and debanding methods and superimposed beta-aminopropionitrile in some of the banded rats (50 mg/kg i.p., twice a day). Ten weeks of banding increased in vivo peak systolic left ventricular pressure and produced medial hypertrophy, an increase in collagen deposition in the myocardial and perivascular tissues, and myocardial hypertrophy in the banded group without beta-aminopropionitrile treatment. Superimposition of beta-aminopropionitrile treatment on banding inhibited the increase in collagen deposition. In the groups debanded after the 10-week banding period, both with and without beta-amino-propionitrile treatment, medial and myocardial hypertrophy regressed 4 weeks after debanding. We estimated coronary dilator reserve in Langendorff preparations perfused with modified Tyrode's solution containing oxygenated bovine red blood cells and serum albumin. The ratio of reactive peak flow after brief ischemia-to-resting flow decreased in both of the banded groups. After debanding, the ratio remained lower in the banded group without beta-aminopropionitrile treatment than in the control group. However, debanding in the group with beta-aminopropionitrile treatment increased the ratio to a level similar to that of the control group. Thus, in pressure-overloaded cardiac hypertrophy with coronary hypertension, coronary reserve seems to be determined by medial hypertrophy independently of collagen deposition, but collagen deposition plays an important role in the reversal of vasodilator reserve after relief of the overload.
Isoyama
S
S
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Ito
N
N
Satoh
K
K
Takishima
T
T
D000629:Aminopropionitrile / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000473:pathology; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight; D002245:Carbon Dioxide / Q000097:blood; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D003094:Collagen / Q000096:biosynthesis*; D003326:Coronary Circulation / Q000187:drug effects; D006321:Heart / Q000033:anatomy & histology; D006339:Heart Rate / Q000187:drug effects; D006400:Hematocrit; D006863:Hydrogen-Ion Concentration; D006909:Hydroxyproline / Q000494:pharmacology; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D009929:Organ Size; D010100:Oxygen / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
D002245:Carbon Dioxide; D000629:Aminopropionitrile; D003094:Collagen; D006909:Hydroxyproline; D010100:Oxygen