Heterogeneity of Multimedia Exposures to Neurotoxic Elements (Al, As, Cd, Pb, Mn, and Hg) in Breastfed Infants from Porto Velho, Brazil.

Infant exposure to neurotoxic elements is a public health issue that needs monitoring with regard to breast milk composition. We studied six neurotoxic elements in breast milk samples at different stages of lactation in mothers from Porto Velho, Brazil. We used a flow-injection mercury system (FIMS) to determine total Hg concentrations and an inductively coupled plasma optical emission spectrometer (ICP-OES) to determine the concentrations of Al, As, Cd, Pb, and Mn in 106 donors of a human milk bank. Association rules analyses were applied to determine the pattern of binary and ternary mixtures of the measured exposants. The metal concentration was mostly below the limit of detection (LOD) for Cd (99%), Pb (84%), and Hg (72%), and it was above the LOD for As (53%), Mn (60%), and Al (82%), respectively. Median concentrations (dry weight) of Al, As, Hg, Mn, and Pb were 1.81 µg/g, 13.8 ng/g, 7.1 ng/g, 51.1 ng/g, and 0.43 µg/g, respectively. Al is singly the most frequent element to which infants are exposed. Occurring binary combination (> LOD) was 56% for Al-Mn, 41% for Al-As, 22% for Al-Hg, and 13% for Al-Pb. In 100% of neonates, exposure to Al-ethylmercury (EtHg) occurred through immunization with thimerosal-containing vaccines (TCV). Association rules analysis revealed that Al was present in all of the multilevel combinations and hierarchical levels and that it showed a strong link with other neurotoxic elements (especially with Mn, As, and Hg). (a) Nursing infants are exposed to combinations of neurotoxicants by different routes, dosages, and at different stages of development; (b) In breastfed infants, the binary exposures to Al and total Hg can occur through breast milk and additionally through TCV (EtHg and Al);

Cardiovascular effects of partial sleep deprivation in healthy volunteers.

Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.

Bradykinin or acetylcholine as vasodilators to test endothelial venous function in healthy subjects.

INTRODUCTION: The evaluation of endothelial function has been performed in the arterial bed, but recently evaluation within the venous system has also been explored. Endothelial function studies employ different drugs that act as endothelium-dependent vasodilatory response inductors. OBJECTIVES: The aim of this study is to compare the endothelium-dependent venous vasodilator response mediated by either acetylcholine or bradykinin in healthy volunteers. METHODS AND RESULTS: Changes in vein diameter after phenylephrine-induced venoconstriction were measured to compare venodilation induced by acetylcholine or bradykinin (linear variable differential transformer dorsal hand vein technique). We studied 23 healthy volunteers; 31% were male, and the subject had a mean age of 33 +/- 8 years and a mean body mass index of 23 +/- 2 kg/m(2). The maximum endothelium-dependent venodilation was similar for both drugs (p = 0.13), as well as the mean responses for each dose of both drugs (r = 0.96). The maximum responses to acetylcholine and bradykinin also had good agreement. CONCLUSION: There were no differences between acetylcholine and bradykinin as venodilators in this endothelial venous function investigation.

Bradykinin or acetylcholine as vasodilators to test endothelial venous function in healthy subjects

INTRODUCTION: The evaluation of endothelial function has been performed in the arterial bed, but recently evaluation within the venous system has also been explored. Endothelial function studies employ different drugs that act as endothelium-dependent vasodilatory response inductors. OBJECTIVES: The aim of this study is to compare the endothelium-dependent venous vasodilator response mediated by either acetylcholine or bradykinin in healthy volunteers. METHODS AND RESULTS: Changes in vein diameter after phenylephrine-induced venoconstriction were measured to compare venodilation induced by acetylcholine or bradykinin (linear variable differential transformer dorsal hand vein technique). We studied 23 healthy volunteers; 31 percent were male, and the subject had a mean age of 33 ± 8 years and a mean body mass index of 23 ± 2 kg/m². The maximum endothelium-dependent venodilation was similar for both drugs (p = 0.13), as well as the mean responses for each dose of both drugs (r = 0.96). The maximum responses to acetylcholine and bradykinin also had good agreement. CONCLUSION: There were no differences between acetylcholine and bradykinin as venodilators in this endothelial venous function investigation.

Acute reduction of ventricular volume decreases QT interval dispersion in elderly subjects with and without heart failure.

To evaluate the effects of acute reduction in ventricular volume (VV) on QT interval dispersion (QTd), 14 men with heart failure (HF; 74.5 +/- 2 yr of age) and 11 healthy male control subjects (68 +/- 2 yr of age) were studied. For 15 min, lower body negative pressure (LBNP) was applied at -15 and -40 mmHg to reduce venous return. At baseline and during LBNP application, QTd was measured with an 87-lead, body-surface-mapping device; chamber volumes were assessed by radioisotope ventriculography; blood pressure (BP) and heart rate (HR) were continuously monitored; and blood samples were obtained for assessment of norepinephrine (Nor) levels. At -15 mmHg, LNBP application induced a significant decrease in VV but did not change BP and HR in both groups. In addition, Nor levels increased significantly (P < or = 0.05) in the control group (from 286.7 +/- 31.5 to 388.8 +/- 41.2 pg/ml) and in HF patients (from 405.8 +/- 56 to 477.6 +/- 47 pg/ml), and QTd was significantly (P < or = 0.05) decreased in the control group (57.2 +/- 3.8 vs. 49.1 +/- 3.4 ms) and in HF patients (67.8 +/- 6 vs. 63.7 +/- 5.9 ms). No additional decreases in VV or QTd were produced by -40 mmHg LNBP, but Nor levels did increase in both groups and reach 475.5 +/- 34 and 586.5 +/- 60 pg/ml (P < 0.05) in the control and HF groups, respectively; BP did not change, but HR also increased in both groups. In conclusion, an acute LBNP-induced reduction in VV caused a decrease in the QTd of elderly men regardless of the existence of HF. Because increased sympathetic activity with more intense LBNP was not accompanied by additional changes in QTd, altered QTd may be better related to changes in VV than to autonomic nervous system activity.

Endothelial function is preserved in Chagas' heart disease patients without heart failure.

Endothelium may be damaged, especially at the coronary microcirculation, in animal models of Chagas' disease by several mechanisms. Endothelial dysfunction has been reported in chronic Chagas' heart disease patients with heart failure. Nevertheless, peripheral endothelial function has never been studied in patients with Chagas' heart disease without heart failure and other conditions that could per se alter the endothelial function. Endothelial function was evaluated in 9 patients with Chagas' heart disease (44.8 +/- 1.5 years, 5 females, left ventricular ejection fraction > or = 60%) and 10 healthy matched controls (38.6 +/- 5.5 years, 5 females). Extreme caution was exercised to select patients with no other conditions that could per se alter the endothelial function. Forearm blood flow was measured at baseline and during intra-brachial artery infusion of crescent doses of acetylcholine (0.75, 5, and 15 microg/100 mL tissue/min) and nitroprusside (1, 2, and 4 microg/ 100 mL tissue/min), an endothelium-dependent and an endothelium-independent vasoactive drug, respectively. At baseline, blood pressure and heart rate (continuously recorded with Finapress) and the forearm blood flow were similar in both groups. Acetylcholine (ACh) and sodium nitroprusside (SNP) caused significant and similar dose-dependent increases in forearm blood flow of all subjects: maximum ACh response of 24.8 versus 23.7, and maximum SNP response 24.4 versus 23.7 mL/100 mL tissue/min, respectively, for control and chagasic Groups. No significant systemic hemodynamic changes were observed during the intra-arterial infusion of the drugs. The authors conclude that the peripheral endothelial function is preserved in Chagas' heart disease patients without heart failure.