ANTIOXIDANT CHANGES IN HYPERTROPHIED AND FAILING GUINEA-PIG HEARTS

Citation
Ak. Dhalla et Pk. Singal, ANTIOXIDANT CHANGES IN HYPERTROPHIED AND FAILING GUINEA-PIG HEARTS, The American journal of physiology, 266(4), 1994, pp. 80001280-80001285
Citations number
38
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
266
Issue
4
Year of publication
1994
Part
2
Pages
80001280 - 80001285
Database
ISI
SICI code
0002-9513(1994)266:4<80001280:ACIHAF>2.0.ZU;2-#
Abstract
Hypertrophy and heart failure were induced by placing a mildly constri ctive band around the ascending aorta in young guinea pigs. Based on h eart weight, left ventricular wall thickness, hemodynamic data, and ot her clinical signs, these animals were found to have physiological hyp ertrophy at 10 wk and congestive heart failure (CHF) at 20 wk. Hearts from these two groups of animals were examined for superoxide dismutas e (SOD), glutathione peroxidase (GSHPx), and catalase activities as we ll as lipid peroxidation and glutathione [reduced glutathione (GSH)/ox idized glutathione (GSSG)] levels. There was an age-dependent increase in SOD activity and GSH content in sham controls. SOD activity was 28 % higher in the 10-wk-hypertrophy group and 46% lower in the CHF group than in respective sham controls. GSHPx activity increased significan tly in the hypertrophied hearts, whereas in the failing hearts, the ac tivity was not different from the 20-wk controls but was significantly lower than in the hypertrophied hearts. Catalase activity did not cha nge at either stage. GSH content in the hypertrophied hearts was signi ficantly higher compared with sham controls. In the CHF group, GSH con tent was significantly lower and GSSG content was significantly higher than in sham controls. Lipid peroxidation, as indicated by malondiald ehyde content, was significantly decreased in the hypertrophy group bu t increased toward control levels in the failure group. It is proposed that a relative deficit in myocardial antioxidant capacity as well as in the redox state may play a role in the pathogenesis of cardiac fai lure.