Hemodialysis improves endothelial venous function in end-stage renal disease

The objective of the present study was to determine the acute effect of hemodialysis on endothelial venous function and oxidative stress. We studied 9 patients with end-stage renal disease (ESRD), 36.8 ± 3.0 years old, arterial pressure 133.8 ± 6.8/80.0 ± 5.0 mmHg, time on dialysis 55.0 ± 16.6 months, immediately before and after a hemodialysis session, and 10 healthy controls matched for age and gender. Endothelial function was assessed by the dorsal hand vein technique using graded local infusion of acetylcholine (endothelium-dependent venodilation, EDV) and sodium nitroprusside (endothelium-independent venodilation). Oxidative stress was evaluated by measuring protein oxidative damage (carbonyls) and antioxidant defense (total radical trapping antioxidant potential - TRAP) in blood samples. All patients were receiving recombinant human erythropoietin for at least 3 months and were not taking nitrates or a-receptor antagonists. EDV was significantly lower in ESRD patients before hemodialysis (65.6 ± 10.5) vs controls (109.6 ± 10.8; P = 0.010) and after hemodialysis (106.6 ± 15.7; P = 0.045). Endothelium-independent venodilation was similar in all comparisons performed. The hemodialysis session significantly decreased TRAP (402.0 ± 53.5 vs 157.1 ± 28.3 U Trolox/µL plasma; P = 0.001). There was no difference in protein damage comparing ESRD patients before and after hemodialysis. The magnitude of change in the EDV was correlated negatively with the magnitude of change in TRAP (r = -0.70; P = 0.037). These results suggest that a hemodialysis session improves endothelial venous function, in association with an antioxidant effect.

Evaluation of two different oxygen inspiratory fractions on the hemodynamic effects of No-nitro-L-arginine methyl ester in anesthetized dogs

The effect of two different oxygen inspiratory fractions (FiO2 = 21 percent and 100 percent) on the hemodynamic responses induced by N(omega)-nitro-L-arginine methyl ester (L-NAME) was investigated in anesthetized dogs. L-NAME (0.01-10.0 mg/kg), but not D-NAME, induced dose-dependent changes in the hemodynamic parameters of the animals. At the highest dose, L-NAME increased mean arterial blood pressure in both room air (from 86.2 +/- 3.2 to 125.1 +/- 7.8 mmHg) and pure oxygen (from 100.0 +/- 7.5 to 139.0 +/- 3.2 mmHg) ventilated animals. L-NAME also increased systemic and pulmonary vascular resistances. These effects were accompanied by a decrease in cardiac output and bradycardia (37 percent and 31 percent decreases for pure oxygen and room air, respectively). However, there were no significant differences in the responses to L-NAME between the dogs ventilated with FiO2 = 21 percent and those ventilated with FiO2 = 100 percent. L-NAME did not modify blood gas analyses, despite the expected difference in PO2 levels between the two experimental groups of animals (3 times higher in the animals ventilated with pure oxygen). These results indicate that nitric oxide release accounts for the maintenance of hemodynamic function in the anesthetized dog, and that L-NAME-induced effects are not affected by hyperoxemia.