Efeitos negativos da insuficiência renal crônica sobre a função pulmonar e a capacidade funcional / Negative effects of chronic kidney failure on lung function and functional capacity

OBJETIVO: Avaliar a função pulmonar e a capacidade funcional em pacientes com insuficiência renal crônica (IRC) em hemodiálise e em pacientes após transplante renal. MÉTODOS: Foram avaliados 72 indivíduos, sendo 32 pacientes com IRC em hemodiálise (GD) há mais de 6 meses, 10 pacientes transplantados renais (GT) há, pelo menos, 6 meses e 30 sujeitos saudáveis para grupo controle (GC). Todos os grupos foram avaliados utilizando espirometria, pressões inspiratória (PImax) e expiratória (PEmax) máximas e teste da caminhada em seis minutos (TC6min). Para análise estatística, foi utilizado o programa SPSS 12.0, com nível mínimo de significância α<0,05. RESULTADOS: Foram encontrados resultados estatisticamente significativos (p<0,01) para: diminuição da função pulmonar no GD para Capacidade vital forçada (CVF), Volume expirado forçado (VEF1), Ventilação voluntária máxima (VVM), Capacidade vital (CV), PImax, PEmax e, para o GT, diminuição do VEF1 e VVM, quando comparados ao GC (ANOVA uma via/post hoc Fischer); associação (qui-quadrado) entre diminuição da PImax e pertencer ao GD (α=0,5, p<0,001); menor desempenho no TC6min no GD e GT (p<0,01) quando comparados ao GC (ANOVA uma via/post hoc Fischer). Encontrou-se correlação significativa (coeficiente de Pearson) entre PImax e PEmax (r=0,752, P<0,01). CONCLUSÕES: Pode-se concluir que existem alterações na capacidade funcional e na função pulmonar do paciente com IRC em hemodiálise, as quais são indicativas de prejuízos funcionais que não se apresentam completamente revertidos no paciente transplantado renal.

OBJECTIVE: To evaluate lung function and functional capacity in patients with chronic kidney failure (CKF) undergoing dialysis and in patients after kidney transplant. METHODS: Seventy-two participants were evaluated: 32 patients with CKF on dialysis (DG) for at least six months, ten patients who had kidney transplants (TG) at least six months earlier, and 30 healthy subjects as a control group (CG). All groups were evaluated using spirometry, with maximum inspiratory pressure (MIP) and maximum expiratory pressure (MEP), and using the six-minute walking test (6MWT). The SPSS 12.0 software was used for statistical analysis, with a minimum significance level of α<0.05. RESULTS: There was a decreased lung function in the DG for FVC, FEV1, MVV, VC, MIP and MEP, and decreased FEV1 and MVV in the TG compared to the CG (one-way ANOVA/Fisher's post-hoc; p<0.01). There was also an association (chi-square) between decreased MIP and belonging to the DG (α=0.5, p<0.001), between lower performance in the 6MWT for the DG and TG (p<0.01) compared to the CG (one-way ANOVA/Fisher's post-hoc), and between MIP and MEP (Pearson's coefficient; r=0.752; p<0.01). CONCLUSIONS: Patients with CKF undergoing dialysis showed impaired functional capacity and lung function that were not completely reverted in the kidney transplant patients.

Hydrogen peroxide as a tool for studying oxidative stress in the heart

Hydrogen peroxide (H2O2) was observed to depolarize the frog sartorius muscle and promote rhythmic contraction of frog cardiac ventricular rings or their contracture. This last effect was sodium-dependent. H2O2 perfused or injected into the aorta of the isolated rat heart induces a positive inotropic effect (with cardiac arrhythmias such as extrasystolic potentiations) followed by deoression of contractility or cardiac contractures, according to the dose employed. The last effects is similar to the "stone heart"observed in the reperfusion injury and may be ascribed to lipoperoxidation (LPO) of the membrane lipids, to protein damage, to reduction in the ATP level and/or to cardioactive compounds liberated by LPO. Besides its direct effect on the ATP level, H2O2 would react with iron ions to produce hydroxyl radicals that attack the cellular membranes. Deferoxamine, an iron chelator and scavenger of hydroxyl radicals, reduced the contractures induced by H2O2. Perfusion with H2O2 increased the LPO of cardiac homogenates measured by chemiluminescence, oxygen uptake and malonaldehyde formation. The fall in ATP levels and the LPO would result in calcium overload of the cardiac fibers and contracture ("stone heart"). The 45Ca uptake was increased by incubation of cardiac strips with H2O2. Previous perfusion of the isolated rat heart with nifedipine or indomethacin reduced the H2O2 cardiac contracture. Vitamin A, a quencher of singlet oxygen liberated during LPO, reduces the H2O2 cardiac contractures and also LPO. Gradual physical exercises, besides increasing the oxygen consumption, protected the heart from oxidative stress. The experimental production of hypothyroidism protected the heart against the H2O2 oxidative stress. The hearts of rats submitted to hypertension with high renin levels showed increased LPO, measured by chemiluminescence and oxygen uptake, indicating that this condition may be produced by oxygen species or causes their production. All these findings give support to the idea that the ischemia-reperfusion injury is an active oxygen species associated disorder that induces cardiac stiffness or contractures that would be produced by calcium overload. Thus, H2O2 may be useful for inducing experimental oxidative stress in the heart and for studying its oxidative status in physiological and pathological situations.