Navegando por Palavras-chave "Chronic heart failure"

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    Changes in the pro-inflammatory cytokine production and peritoneal macrophage function in rats with chronic heart failure
    (Elsevier B.V., 2006-06-01) Batista, M. L.; Santos, Ronaldo Vagner Thomatieli dos [UNIFESP]; Cunha, L. M.; Mattos, K.; Oliveira, E. M.; Seelaender, M. C. L.; Rosa, L. F. B. P. Costa; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Chronic heart failure (CHF) is a state of immune activation, and pro-inflammatory cytokines play an important role in its development and progression. Macrophages (M phi s), when activated, are the main source of pro-inflammatory cytokines. We measured interjeukin-6 (IL-6), interleukin (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) production after lipopolysaccharide (LPS)-stimulation, as well as peritoneal M phi s migration, phagocytic capacity, chemotaxis index, and hydrogen peroxide production, in an attempt to clarify the role of this cell in an animal model of CHF. Ligature of the left coronary artery or sham operation was performed in adult Wistar rats. After 12 weeks, resident and total cell number, phagocytic capacity, chemotaxis index, and hydrogen peroxide production in M phi s were significantly higher in CHF than in control rats. the production of IL-6 and TNF-alpha was similarly significantly enhanced in CHF as compared with controls. M phi s obtained from CHF rats were more responsive to LPS, suggesting the existence, in vivo, of possible factor(s) modulating the production of pro-inflammatory cytokines. the results demonstrated that there is modification of peritoneal M phi s function along CHF development, possibly contributing to the pathophysiological process in the establishment of CHF. (c) 2006 Elsevier B.V. All rights reserved.
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    Exercise training prevents the deterioration in the arterial baroreflex control of sympathetic nerve activity in chronic heart failure patients
    (Amer Physiological Soc, 2015-05-01) Groehs, Raphaela Vilar; Toschi-Dias, Edgar; Antunes-Correa, Ligia de Moraes; Trevizan, Patricia Fernandes; Rondon, Maria Urbana Pinto Brandão; Oliveira, Patricia; Alves, Maria Janieire de Nazaré Nunes; Almeida, Dirceu Rodrigues de [UNIFESP]; Middlekauff, Holly R.; Negrao, Carlos Eduardo; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Univ Calif Los Angeles
    Arterial baroreflex control of muscle sympathetic nerve activity (ABRMSNA) is impaired in chronic systolic heart failure (CHF). the purpose of the study was to test the hypothesis that exercise training would improve the gain and reduce the time delay of ABRMSNA in CHF patients. Twenty-six CHF patients, New York Heart Association Functional Class II-III, EF <= 40%, peak (V) over dot O-2 <= 20 ml.kg(-1).min(-1) were divided into two groups: untrained (UT, n = 13, 57 +/- 3 years) and exercise trained (ET, n = 13, 49 +/- 3 years). Muscle sympathetic nerve activity (MSNA) was directly recorded by microneurography technique. Arterial pressure was measured on a beat-to-beat basis. Time series of MSNA and systolic arterial pressure were analyzed by autoregressive spectral analysis. the gain and time delay of ABRMSNA was obtained by bivariate autoregressive analysis. Exercise training was performed on a cycle ergometer at moderate intensity, three 60-min sessions per week for 16 wk. Baseline MSNA, gain and time delay of ABRMSNA, and low frequency of MSNA (LFMSNA) to high-frequency ratio (HFMSNA) (LFMSNA/HFMSNA) were similar between groups. ET significantly decreased MSNA. MSNA was unchanged in the UT patients. the gain and time delay of ABRMSNA were unchanged in the ET patients. in contrast, the gain of ABRMSNA was significantly reduced [3.5 +/- 0.7 vs. 1.8 +/- 0.2, arbitrary units (au)/mmHg, P = 0.04] and the time delay of ABRMSNA was significantly increased (4.6 +/- 0.8 vs. 7.9 +/- 1.0 s, P = 0.05) in the UT patients. LFMSNA-to-HFMSNA ratio tended to be lower in the ET patients (P < 0.08). Exercise training prevents the deterioration of ABRMSNA in CHF patients.
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    Microvascular oxygen delivery-to-utilization mismatch at the onset of heavy-intensity exercise in optimally treated patients with CHF
    (Amer Physiological Soc, 2009-11-01) Sperandio, Priscila Abreu [UNIFESP]; Borghi-Silva, Audrey [UNIFESP]; Barroco, Adriano [UNIFESP]; Nery, Luiz Eduardo [UNIFESP]; Almeida, Dirceu Rodrigues de [UNIFESP]; Neder, Jose Alberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Federal de São Carlos (UFSCar)
    Sperandio PA, Borghi-Silva A, Barroco A, Nery LE, Almeida DR, Neder JA. Microvascular oxygen delivery-to-utilization mismatch at the onset of heavy-intensity exercise in optimally treated patients with CHF. Am J Physiol Heart Circ Physiol 297: H1720-H1728, 2009. First published September 4, 2009; doi:10.1152/ajpheart.00596.2009.-Impaired muscle blood flow at the onset of heavy-intensity exercise may transiently reduce microvascular O(2) pressure and decrease the rate of O(2) transfer from capillary to mitochondria in chronic heart failure (CHF). However, advances in the pharmacological treatment of CHF (e. g., angiotensin-converting enzyme inhibitors and third-generation beta-blockers) may have improved microvascular O(2) delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O(2) uptake ((V)over dot(O2)) kinetics. We assessed the rate of change of pulmonary (V)over dot(O2) ((V)over dot(O2p)), (estimated) fractional O(2) extraction in the vastus lateralis (similar to Delta[deoxy-Hb + Mb] by near-infrared spectroscopy), and cardiac output ((Q)over dot(T)) during high-intensity exercise performed to the limit of tolerance (Tlim) in 10 optimally treated sedentary patients (ejection fraction = 29 +/- 8%) and 11 controls. Sluggish (V)over dot(O2p) and (Q)over dot(T) kinetics in patients were significantly related to lower Tlim values (P < 0.05). the dynamics of Delta[deoxy-Hb + Mb], however, were faster in patients than controls [mean response time (MRT) = 15.9 +/- 2.0 s vs. 19.0 +/- 2.9 s; P < 0.05] with a subsequent response overshoot being found only in patients (7/10). Moreover, tau(V)over dot(O2)/MRT-[deoxy-Hb + Mb] ratio was greater in patients (4.69 +/- 1.42 s vs. 2.25 +/- 0.77 s; P < 0.05) and related to (Q)over dot(T) kinetics and Tlim (R = 0.89 and -0.78, respectively; P < 0.01). We conclude that despite the advances in the pharmacological treatment of CHF, disturbances in central and peripheral circulatory adjustments still play a prominent role in limiting (V)over dot(O2p) kinetics and tolerance to heavy-intensity exercise in nontrained patients.
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    Relação entre a oferta e a utilização muscular periférica de oxigênio na transição do exercício leve para o intenso em pacientes com insuficiência cardíaca
    (Universidade Federal de São Paulo (UNIFESP), 2010-11-24) Sperandio, Priscila Cristina de Abreu [UNIFESP]; Almeida, Dirceu Rodrigues de [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Impaired muscle blood flow at the onset of heavy-intensity exercise may transiently reduce microvascular O2 pressure and decrease the rate of O2 transfer from capillary to mitochondria in chronic heart failure (CHF). However, advances in the pharmacological treatment of CHF (e.g., angiotensin-converting enzyme inhibitors and third generation of â-blockers) may have improved microvascular O2 delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O2 uptake ( O2) kinetics. We included 10 optimally treated sedentary patients (ejection fraction = 29 ± 8%) and 11 age-matched controls. We assessed the rate of change of pulmonary O2 ( O2p), tissue O2 extraction in the vastus lateralis estimated by concentration of deoxy-hemoglobin+myoglobin (~Ä[deoxy-Hb+Mb]) measured by near-infrared spectroscopy (NIRS), and cardiac output ( T) during highintensity exercise performed to the limit of tolerance (Tlim). Sluggish O2p and T kinetics in patients were significantly related to lower Tlim values (P = 0.05). The dynamics of Ä[deoxy-Hb+Mb] were faster in patients than controls (mean response time (MRT) = 15.9 ± 2.0 s vs. 19.0 ± 2.9 s; P = 0.05) with a subsequent response “overshoot” being found only in patients (7/10). Moreover, t O2p/MRT-Ä[deoxy- Hb+Mb] ratio was greater in patients (4.69 ± 1.42 s vs. 2.25 ± 0.77 s; P = 0.05) and related to T kinetics and Tlim (R = 0.89 and 0.78, respectively; P = 0.01). We conclude that despite the advances in the pharmacological treatment of CHF, disturbances in “central” and “peripheral” circulatory adjustments still play a prominent role in limiting O2p kinetics and tolerance to heavy-intensity exercise in nontrained patients.