Higher antioxidative capacity during a chronic stable heart hypertrophy.
Changes in oxygen radical mechanisms during 6-48 weeks of heart hypertrophy in rats subjected to a narrowing of the subdiaphragmatic aorta were examined. During this period, hypertrophied hearts demonstrated a stable hyperfunction, as indicated by an elevated but stable left ventricular systolic pressure, dP/dt, and aortic pressure and no change in left ventricular end diastolic pressure. Experimental animals showed increased heart-to-body weight ratios; however, the conventional signs of heart failure such as increased wet-to-dry weight ratios of liver and lung, ascites, or pleural effusion were absent. Hearts were examined for superoxide dismutase, glutathione peroxidase, and lipid peroxide activities. The superoxide dismutase activity was significantly higher in hypertrophied hearts at 6 and 12 weeks as compared with sham-operated rats (sham controls), while no difference was seen at 24 and 48 weeks due to a marked increase in the superoxide dismutase activity of sham control hearts in these age groups. During the period studied, glutathione peroxidase activity remained unchanged in controls but was significantly elevated in hypertrophied hearts. Lipid peroxide activity as indicated by the malondialdehyde content was significantly lower in hypertrophied hearts. Perfusion of isolated control and hypertrophy hearts with xanthine-xanthine oxidase, an exogenous source of oxygen radicals, resulted in contractile failure and rise in resting tension. In hypertrophied hearts, however, the contractile force was better maintained and there was a lesser rise in resting tension after exposure to xanthine-xanthine oxidase. The study suggests the development of a higher antioxidative capacity during the stable phase of hypertrophy due to a chronic pressure overload.
Gupta
M
M
Cardiovascular Sciences Division, St. Boniface General Hospital Research Center, Winnipeg, Canada.
Singal
P K
PK
D000818:Animals; D006332:Cardiomegaly / Q000201:enzymology / Q000503:physiopathology*; D002908:Chronic Disease; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D008054:Lipid Peroxides / Q000096:biosynthesis; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology; D010100:Oxygen / Q000037:antagonists & inhibitors*; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000378:metabolism
D005609:Free Radicals; D008054:Lipid Peroxides; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D010100:Oxygen