Examinando por Autor "Karla G. Schwarz"

Mostrando 1 - 4 de 4
  • Miniatura
    Ítem
    Dietary supplementation of a sulforaphane-enriched broccoli extract protects the heart from acute cardiac stress
    (2020) Katherin V. Pereyra; David C. Andrade; Camilo Toledo; Karla G. Schwarz; Atenea Uribe-Ojeda; Angélica P. Ríos-Gallardo; Rodrigo A. Quintanilla; Samuel Contreras; Andrea Mahn; Rodrigo Del Rio
    Cardiac arrythmias play a critical role in several pathological conditions. Importantly, increased arrhythmic risk is associated with systemic oxidative stress and activation of the autonomic nervous system. Thus, we hypothesized that dietary antioxidant supplementation may help in reducing cardiac stress-induced arrhythmias. Sulforaphane (SFN), an isothiocyanate present in Brassicaceaes, is recognized as a powerful health-promoting compound with known antioxidant properties. Then, we aimed to generate a broccoli extract (BE) enriched in SFN and determine whether oral BE supplementation induced cardio-protection during acute cardiac stress in rats. BE decreases cardiac sympathetic drive and increases parasympathetic cardiac modulation as evidenced by heart rate variability (HRV) shifts. In addition, isoproterenol-induced cardiac stress (a sympathomimetic agent) induced a ~ 4-fold increase in arrhythmia incidence and this effect was almost completely abolished by BE treatment. In conclusion, dietary supplementation with a BE regulates cardiac autonomic drive and protects the heart from acute cardiac stress.
  • Miniatura
    Ítem
    Effects of enriched‑potassium diet on cardiorespiratory outcomes in experimental non‑ischemic chronic heart failure
    (2021) Karla G. Schwarz; Katherin V. Pereyra; Camilo Toledo; David C. Andrade; Hugo S. Díaz; Esteban Díaz‑Jara; Domiziana Ortolani; Angélica Rios‑Gallardo; Paulina Arias; Alexandra Las Heras; Ignacio Vera; Fernando C. Ortiz; Nibaldo C. Inestrosa; Carlos P. Vio; Rodrigo Del Rio
    Background: Chronic heart failure (CHF) is a global health problem. Increased sympathetic outflow, cardiac arrhythmogenesis and irregular breathing patterns have all been associated with poor outcomes in CHF. Several studies showed that activation of the renin-angiotensin system (RAS) play a key role in CHF pathophysiology. Interestingly, potassium (K+) supplemented diets showed promising results in normalizing RAS axis and autonomic dysfunction in vascular diseases, lowering cardiovascular risk. Whether subtle increases in dietary K+ consumption may exert similar effects in CHF has not been previously tested. Accordingly, we aimed to evaluate the effects of dietary K+ supplementation on cardiorespiratory alterations in rats with CHF. Methods: Adult male Sprague–Dawley rats underwent volume overload to induce non-ischemic CHF. Animals were randomly allocated to normal chow diet (CHF group) or supplemented K+ diet (CHF+K+ group) for 6 weeks. Cardiac arrhythmogenesis, sympathetic outflow, baroreflex sensitivity, breathing disorders, chemoreflex function, respiratory–cardiovascular coupling and cardiac function were evaluated. Results: Compared to normal chow diet, K+supplemented diet in CHF significantly reduced arrhythmia incidence (67.8 ± 15.1 vs. 31.0 ± 3.7 events/hour, CHF vs. CHF+K+), decreased cardiac sympathetic tone (ΔHR to propranolol:− 97.4 ± 9.4 vs. − 60.8 ± 8.3 bpm, CHF vs. CHF+K+), restored baroreflex function and attenuated irregular breathing patterns. Additionally, supplementation of the diet with K+ restores normal central respiratory chemoreflex drive and brogates pathological cardio-respiratory coupling in CHF rats being the outcome an improved cardiac function. Conclusion: Our findings support that dietary K+ supplementation in non-ischemic CHF alleviate cardiorespiratory dysfunction.
  • Miniatura
    Ítem
    Exercise intolerance in volume overload heart failure is associated with low carotid body mediated chemoreflex drive
    (2021) David C. Andrade; Esteban Díaz‑Jara; Camilo Toledo; Karla G. Schwarz; Katherin V. Pereyra; Hugo S. Díaz; Noah J. Marcus; Fernando C. Ortiz; Angélica P. Ríos‑Gallardo; Domiziana Ortolani; Rodrigo Del Rio
    Mounting an appropriate ventilatory response to exercise is crucial to meeting metabolic demands, and abnormal ventilatory responses may contribute to exercise‑intolerance (EX‑inT) in heart failure (HF) patients. We sought to determine if abnormal ventilatory chemoreflex control contributes to EX‑inT in volume‑overload HF rats. Cardiac function, hypercapnic (HCVR) and hypoxic (HVR) ventilatory responses, and exercise tolerance were assessed at the end of a 6 week exercise training program. At the conclusion of the training program, exercise tolerant HF rats (HF + EX‑T) exhibited improvements in cardiac systolic function and reductions in HCVR, sympathetic tone, and arrhythmias. In contrast, HF rats that were exercise intolerant (HF + EX‑inT) exhibited worse diastolic dysfunction, and showed no improvements in cardiac systolic function, HCVR, sympathetic tone, or arrhythmias at the conclusion of the training program. In addition, HF + EX‑inT rats had impaired HVR which was associated with increased arrhythmia susceptibility and mortality during hypoxic challenges (~ 60% survival). Finally, we observed that exercise tolerance in HF rats was related to carotid body (CB) function as CB ablation resulted in impaired exercise capacity in HF + EX‑T rats. Our results indicate that: (i) exercise may have detrimental effects on cardiac function in HF‑EX‑inT, and (ii) loss of CB chemoreflex sensitivity contributes to EX‑inT in HF.
  • Miniatura
    Ítem
    Exercise intolerance in volume overload heart failure is associated with low carotid body mediated chemoreflex drive
    (2021) David C. Andrade; Esteban Díaz‑Jara; Camilo Toledo; Karla G. Schwarz; Katherin V. Pereyra; Hugo S. Díaz; Noah J. Marcus; Fernando C. Ortiz; Angélica P. Ríos‑Gallardo; Domiziana Ortolani; Rodrigo Del Rio
    Mounting an appropriate ventilatory response to exercise is crucial to meeting metabolic demands, and abnormal ventilatory responses may contribute to exercise-intolerance (EX-inT) in heart failure (HF) patients. We sought to determine if abnormal ventilatory chemoreflex control contributes to EX-inT in volume-overload HF rats. Cardiac function, hypercapnic (HCVR) and hypoxic (HVR) ventilatory responses, and exercise tolerance were assessed at the end of a 6 week exercise training program. At the conclusion of the training program, exercise tolerant HF rats (HF + EX-T) exhibited improvements in cardiac systolic function and reductions in HCVR, sympathetic tone, and arrhythmias. In contrast, HF rats that were exercise intolerant (HF + EX-inT) exhibited worse diastolic dysfunction, and showed no improvements in cardiac systolic function, HCVR, sympathetic tone, or arrhythmias at the conclusion of the training program. In addition, HF + EX-inT rats had impaired HVR which was associated with increased arrhythmia susceptibility and mortality during hypoxic challenges (~ 60% survival). Finally, we observed that exercise tolerance in HF rats was related to carotid body (CB) function as CB ablation resulted in impaired exercise capacity in HF + EX-T rats. Our results indicate that: (i) exercise may have detrimental effects on cardiac function in HF-EX-inT, and (ii) loss of CB chemoreflex sensitivity contributes to EX-inT in HF.