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J Cachexia Sarcopenia Muscle ; 7(4): 436-48, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27239406


BACKGROUND: Loss of muscle mass is a co-morbidity common to a range of chronic diseases including chronic obstructive pulmonary disease (COPD). Several systemic features of COPD including increased inflammatory signalling, oxidative stress, and hypoxia are known to increase the expression of growth differentiation factor-15 (GDF-15), a protein associated with muscle wasting in other diseases. We therefore hypothesized that GDF-15 may contribute to muscle wasting in COPD. METHODS: We determined the expression of GDF-15 in the serum and muscle of patients with COPD and analysed the association of GDF-15 expression with muscle mass and exercise performance. To determine whether GDF-15 had a direct effect on muscle, we also determined the effect of increased GDF-15 expression on the tibialis anterior of mice by electroporation. RESULTS: Growth differentiation factor-15 was increased in the circulation and muscle of COPD patients compared with controls. Circulating GDF-15 was inversely correlated with rectus femoris cross-sectional area (P < 0.001) and exercise capacity (P < 0.001) in two separate cohorts of patients but was not associated with body mass index. GDF-15 levels were associated with 8-oxo-dG in the circulation of patients consistent with a role for oxidative stress in the production of this protein. Local over-expression of GDF-15 in mice caused wasting of the tibialis anterior muscle that expressed it but not in the contralateral muscle suggesting a direct effect of GDF-15 on muscle mass (P < 0.001). CONCLUSIONS: Together, the data suggest that GDF-15 contributes to the loss of muscle mass in COPD.

Intensive Care Med Exp ; 3(1): 49, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26215813


BACKGROUND: Microcirculation and macrohemodynamics are severely compromised during septic shock. However, the relationship between these two compartments needs to be further investigated. We hypothesized that early resuscitation restores left ventricular (LV) performance and microcirculatory function but fails to prevent metabolic disorders. We studied the effects of an early resuscitation protocol (ERP) on LV pressure/volume loops-derived parameters, sublingual microcirculation, and metabolic alterations during endotoxic shock. METHODS: Twenty-five pigs were randomized into three groups: LPS group: Escherichia coli lipopolysaccharide (LPS); ERP group: LPS + ERP based on volume expansion, dobutamine, and noradrenaline infusion; Sham group. LV pressure/volume-derived parameters, systemic hemodynamics, sublingual microcirculation, and metabolic profile were assessed at baseline and after completing the resuscitation protocol. RESULTS: LPS significantly decreased LV end-diastolic volume, myocardial contractility, stroke work, and cardiac index (CI). Early resuscitation preserved preload, and myocardial contractility, increased CI and heart rate (p < .05). LPS severely diminished sublingual microvascular flow index (MFI), perfused vascular density (PVD), and the proportion of perfused vessels (PPV), while increased the heterogeneity flow index (HFI) (p < .05). Despite MFI was relatively preserved, MVD, PVD, and HFI were significantly impaired after resuscitation (p < .05). The macro- and microcirculatory changes were associated with increased lactic acidosis and mixed venous O2 saturation when compared to baseline values (p < .05). The scatter plot between mean arterial pressure (MAP) and MFI showed a biphasic relationship, suggesting that the values were within the limits of microvascular autoregulation when MAP was above 71 ± 6 mm Hg (R (2) = 0.63). CONCLUSIONS: Early hemodynamic resuscitation was effective to restore macrohemodynamia and myocardial contractility. Despite MAP and MFI were relatively preserved, the persistent microvascular dysfunction could explain metabolic disorders. The relationship between micro- and systemic hemodynamia and their impact on cellular function and metabolism needs to be further studied during endotoxic shock.

Chest ; 145(5): 1016-1024, 2014 May.
Artigo em Inglês | MEDLINE | ID: mdl-24337162


BACKGROUND: The Short Physical Performance Battery (SPPB) is commonly used in gerontology, but its determinants have not been previously evaluated in COPD. In particular, it is unknown whether pulmonary aspects of COPD would limit the value of SPPB as an assessment tool of lower limb function. METHODS: In 109 patients with COPD, we measured SPPB score, spirometry, 6-min walk distance, quadriceps strength, rectus femoris cross-sectional area, fat-free mass, physical activity, health status, and Medical Research Council dyspnea score. In a subset of 31 patients with COPD, a vastus lateralis biopsy was performed, and the biopsy specimen was examined to evaluate the structural muscle characteristics associated with SPPB score. The phenotypic characteristics of patients stratified according to SPPB were determined. RESULTS: Quadriceps strength and 6-min walk distance were the only independent predictors of SPPB score in a multivariate regression model. Furthermore, while age, dyspnea, and health status were also univariate predictors of SPPB score, FEV 1 was not. Stratification by reduced SPPB score identified patients with locomotor muscle atrophy and increasing impairment in strength, exercise capacity, and daily physical activity. Patients with mild or major impairment defined as an SPPB score < 10 had a higher proportion of type 2 fibers (71% [14] vs 58% [15], P = .04). CONCLUSIONS: The SPPB is a valid and simple assessment tool that may detect a phenotype with functional impairment, loss of muscle mass, and structural muscle abnormality in stable patients with COPD.

Atividades Cotidianas , Nível de Saúde , Atividade Motora/fisiologia , Força Muscular/fisiologia , Músculo Esquelético/fisiopatologia , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Idoso , Teste de Esforço , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Fenótipo , Prognóstico , Estudos Prospectivos , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Índice de Gravidade de Doença , Espirometria , Caminhada
Rev. urug. cardiol ; 23(3): 249-257, dic. 2008. ilus, graf, tab
Artigo em Espanhol | LILACS-Express | LILACS | ID: lil-694311


Introducción: los trastornos respiratorios del sueño son frecuentes en la población general y en especial entre los pacientes con insuficiencia cardíaca severa. La ocurrencia de respiración periódica de Cheyne-Stokes con apneas centrales (RPCS-AC) durante el sueño, agrava el pronóstico y aumenta significativamente la mortalidad a corto plazo. El objetivo de este estudio fue determinar la prevalencia de este trastorno y las características clínico-fisiológicas de los pacientes en nuestro medio. Material y método: se estudiaron 35 pacientes con insuficiencia cardíaca, sin respiración periódica en vigilia, a los que se les realizó polisomnografía, ecocardiograma, espirometría, gasometría arterial y evaluación de los resultados funcionales del sueño. Resultados: se diagnosticó RPCS-AC en 13 pacientes (37%). Los pacientes con RPCS-AC tuvieron un sueño significativamente más fragmentado (ID/h = 32,9 ± 19,4 versus 15,8 ± 14,3, p <0,001); más tiempo en sueño superficial (S1-2 = 77,4 ± 20,1% versus 63,0 ± 16,7%, p = 0,029); menos tiempo en sueño paradojal (REM = 9,9 ± 6,3% versus 16,6 ± 9,8%, p = 0,035) y mayor tiempo en hipoxia severa durante el sueño (TA<90% = 28,4 ± 29,0% versus 2,4 ± 4,7%, p = 0,008). No existieron diferencias en la función cardíaca, el ECG, la espirometría, los gases en sangre en vigilia, ni en las repercusiones funcionales del sueño. Conclusiones: la RPCS-AC es un trastorno frecuente en la insuficiencia cardíaca avanzada que determina repercusiones adversas sobre la estructura del sueño y la oxigenación arterial.

Introduction: sleep breathing disorders are common in general population and particularly among patients with severe heart failure. The occurrence of Cheyne Stokes periodic breathing with central apneas (RPCS-AC) during sleep, worsens the prognosis and significantly increases short term mortality. The objective of this study was to determine the prevalence of this disorder and the clinic-physiological features of patients in our hospital. Methods: thirty-five consecutive patients with heart failure, without periodic respiration during wakefulness were studied with polisomnography, echocardiogram, spirometry, arterial blood gases and functional outcomes of sleep. Results: thirteen patients were diagnosed with RPCS-AC (37%). Patients with RPCS-AC had significantly more fragmented sleep (ID)/h = 32,9 ± 19,4 versus 15,8 ± 14,3, p<0,001); more time in superficial sleep (S1-2 = 77,4 ± 20,1% versus 63,0 ± 16,7%, p = 0,029); less time in paradoxical sleep (REM = 9,9 ± 6,3% versus 16,6 ± 9,8%, p = 0,035) and more time in severe hypoxia during sleep (TA<90% = 28,4 ± 29,0% versus 2,4 ± 4,7%, p = 0,008). There were no differences in cardiac function, EGG, spirometry, arterial blood gases during wakefulness, neither in sleep functional outcomes. Conclusions: RPCS-AC is a frequent disorder in advanced heart failure patients, that causes adverse consequences on sleep structure and arterial oxygenation.