In animal models of heart failure (HF), resveratrol (RESV) reduced the disease progression and increased the survival rate. Nevertheless, there are no reports in the literature about the effect of RESV on autonomic cardiocirculatory control during the establishment of HF. This study aimed to evaluate the antioxidant effect of RESV on the cardiac autonomic balance and baroreflex sensitivity of HF rats induced by myocardial infarction (MI). Wistar rats were divided into the following groups: Control; Control + RESV; HF; HF + RESV (10mg/kg/day, p.o.). The MI‐induced HF model was produced by ligation of the coronary artery. After four weeks, the animals were anaesthetized for femoral artery and vein catheterization and, 24 hours later, recordings were carried out in conscious animals. Baseline arterial pressure and heart rate (HR, bpm) were recorded during 30 minutes to assess spontaneous baroreflex sensitivity and HR variability. Phenylephrine and sodium nitroprusside (NPS), and methylatropine and propranolol were used for baroreflex evaluation and estimation of cardiac parasympathetic and sympathetic tone, respectively. At the end of the experiments, the animals were anaesthetized to evaluate the cardiac function, using the intraventricular pressure curve, and to withdraw the heart for calculation of heart weight/body weight ratio (HW/BW, mg/g) and the infarct size. The oxidative stress was assessed by measurement of thiobarbituric acid reactive substances (TBARS) in plasma samples. HF and HF+RESV showed 41±3% and 35±3% of infarct size, respectively, and HW/BW ratio increase (3.9±0.1 vs 3.7±0.2 vs 3.0±0.07). HF rats exhibited higher HR compared to control animals (374±12 vs 333±6). RESV did not alter basal parameters in the control group but prevented HR alterations in HF+RESV group (337±6). HF blunted baroreflex sensitivity to phenylephrine (1.3±0.2 vs 2.3±0.3) and NPS (−3.9±0.5 vs −6.0±0.6), increased cardiac sympathetic tone (−44±9 vs −20±4) and decreased parasympathetic tone (54±12 vs 120±7), intrinsic HR (381±8 vs. 401±5), baroreflex effectiveness index (0.06±0.01 vs 0.15±0.01) and LF/HF ratio (0.17±0.05 vs 0.43±0.06). RESV hampered alterations in baroreflex function and cardiac vagal tone (103±13), improve HR variability indexes (LF/HF: 0.3±0.07) and reduced sympathetic control of HR (−29±3) and intrinsic HR in HF+RESV group (360±9). In cardiac function, RESV improved the maximal slope of the systolic increment of left ventricular pressure in HF animals (9004±1120 vs 5956±605 vs 6914±581 mmHg/s). HF increased TBARS compared to control, whereas RESV produced an antioxidant effect in HF+RESV group (11.2±0.9 vs 21.7±3 vs 8.2±1.4 μmol/L). In conclusion, the antioxidant effect of RESV counteracts the cardiovascular autonomic dysfunction and improves systolic left ventricle function during the onset of HF.Support or Funding InformationCNPq e UnaerpThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
NASA plans to have a space station operating in 1994 and is considering a 30 month Mars flight. These plans call for exposure to microgravity for longer periods of time than space travelers have endured to date. Vascular deconditioning is known to occur during space flight and during simulated weightlessness. The degree of deconditioning for these extended flights and the amount of possible reversibility is unknown. If a sudden demanding burden should be placed on the astronaut after prolonged deconditioning, there could be serious consequences. Exercise has been tried with limited success. What is needed is a counter measure to deconditioning. Calcium channel blockers are known to protect the heart during the recovery phase after heart attacks by regulating the calcium influx, thus protecting the cell and mitochondria from calcium overload. Sudden demands also increase blood flow, mimicking the post attack reperfusion, and could be serious for a deconditioned heart. We have found nifedipine, a calcium channel blocker, to be a promising drug for prevention of structural changes during simulated weightlessness.
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