title: Association of the time course of pulmonary arterial hypertension with changes in oxidative stress in the left ventricle.
abstract: 1. This study investigates the time course of pulmonary arterial hypertension (PAH) due to monocrotaline (MCT) and its association with cardiac function and oxidative stress markers in the left ventricle (LV). 2. Male Wistar rats were divided into six groups: 7 days, 21 days, and 31 days for both control and MCT groups. Following echocardiographic analysis, the heart was removed. The LV was separated and homogenized to analyze oxidized-to-total glutathione ratio and thioredoxin reductase (TrxR) activity as well as hydrogen peroxide (H(2) O(2) ) and ascorbic acid levels. 3. There was significant (P < 0.01) cardiac and right ventricle (RV) hypertrophy and pulmonary congestion in the MCT 21 day and 31 day groups. Echocardiography showed a change in the flow wave of the pulmonary artery at 21 days after MCT treatment. There was an increase in the LV ejection time (P < 0.05) at 31 days after MCT. The LV H(2)O(2) concentration was increased (P < 0.05) in the MCT 21 day and MCT 31 day groups compared with controls. There was a reduction (P < 0.05) in the LV ascorbic acid concentration and an increase (P < 0.05) in TrxR activity in the MCT 31 day rats. 4. Our findings showed RV changes due to pulmonary hypertension at 21 days after MCT injection. There was a correlation between the degree of dysfunction and the morphometry of the heart chambers, along with impairment of the antioxidant/pro-oxidant balance in the LV 31 days after the beginning of the protocol. This study suggests that LV changes follow RV dysfunction subsequent to pulmonary hypertension.
authors.affiliation: Physiology Department, Federal University of Rio Grande do Sul, Brazil.
authors.forename: Fabiano
authors.initials: F
authors.lastname: Leichsenring-Silva
authors.forename: Angela Maria Vicente
authors.initials: AM
authors.lastname: Tavares
authors.forename: Francisca
authors.initials: F
authors.lastname: Mosele
authors.forename: Bruno
authors.initials: B
authors.lastname: Berger
authors.forename: Susana
authors.initials: S
authors.lastname: Llesuy
authors.forename: Adriane
authors.initials: A
authors.lastname: Belló-Klein
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000032:analysis; D006332:Cardiomegaly / Q000000981:diagnostic imaging / Q000503:physiopathology; D065627:Familial Primary Pulmonary Hypertension; D005978:Glutathione / Q000032:analysis; D006352:Heart Ventricles / Q000737:chemistry* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006861:Hydrogen Peroxide / Q000032:analysis; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology*; D008297:Male; D016686:Monocrotaline / Q000633:toxicity; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013880:Thioredoxin-Disulfide Reductase / Q000032:analysis; D014463:Ultrasonography
chemical_list: D016686:Monocrotaline; D006861:Hydrogen Peroxide; D013880:Thioredoxin-Disulfide Reductase; D005978:Glutathione; D001205:Ascorbic Acid