Avaliação do colágeno e das miosinas cardíacas em ratos com hipertensão arterial pulmonar submetidos a treinamento preventivo

Abstract

The purpose of this study was to investigate the effect of preventive aerobic training on collagen and cardiac myosin in the early phase (preclinical) of Pulmonary Arterial Hypertension (PAH). Thirty-two male Wistar rats were used, divided into 4 groups of 8 animals, group 1: sedentary control (S); Group 2: training control (T); Group 3: sedentary Pulmonary Arterial Hypertension (SPAH); Group 4: training Pulmonary Arterial Hypertension (TPAH). The animals trained for thirteen weeks on a treadmill, with two weeks of adaptation lasting from 15 minutes to 45 minutes and speed of the treadmill from 0.6 km / h to 0.9 km / h, while in training the time increased to 60 Minutes and the speed to 1.1km / h. PAH was induced by the application of monocrotaline, with consequent right ventricular dysfunction after the tenth week of training, and the control animals were submitted to saline solution. Two tests of the lactate threshold were performed, 24 hours and 14 days, after the application of monocrotaline. At the end of the thirteenth week, an echocardiogram was performed to confirm cardiac dysfunction. These animals were later euthanized, and the right ventricle (RV) removed for morphological and gene expression analyzes. The RV was analyzed by staining of Picrosirius red histological sections for collagen content and by quantitative PCR after reverse transcription (RT-qPCR in real time) for the gene expression of col1a1 (collagen type I alpha 1chain), Col1a2 (collagen type I alpha 2 chain), myh6 (myosin heavy chain 6) and myh7 (myosin heavy chain 7). There was confirmed cardiac dysfunction by the reduction of the maximum velocity of the pulmonary artery and the time of acceleration of the pulmonary artery. The results showed no difference in relation to the fraction of interstitial collagen. There was an increase of the col1a1 genes (p = 0.008) between the SPAH and TPAH groups. S, TPAH vs T, and myh7 (p = 0.0242) between the TPAH vs S groups. We conclude that at the beginning of the cardiac dysfunction by PAH increases myh7 and col1a1 genes without increasing the collagen fraction, but preventive training did not soften these gene alterations.