Autonomic Function Evaluation in an Intermittent Lead Exposure Animal Model

Liana Shvachiy, Vera Geraldes, Mafalda Carvalho, Isabel Rocha

Abstract


Lead (Pb) is a toxic metal, which widespread use has resulted in environmental contamination, human exposure and significant public health problems. The autonomic nervous system, being a homeostatic controller, is impaired in acute and chronic lead exposure. In fact, sympathoexcitation associated to hypertension and tachypnea has been described together with baroreflex and chemoreflex dysfunction. However, up to date, no studies described the autonomic effects of an intermittent low-level lead exposure. In the present work, we addressed in vivo, autonomic behaviour in rats under chronic Pb exposure (control) and in rats under intermittent Pb exposure. For that, arterial blood pressure (BP) and ECG were recorded in 28 weeks old animal and low frequencies (LF) and high frequencies (HF) were determined (to estimate sympathetic and parasympathetic activities) using FisioSinal software with Wavelet module. Preliminary results: Rats intermittently exposed to lead showed a significant decrease in systolic BP (126 ± 4 vs 144 ± 3 mmHg) with no significant changes in LF, HF and LF/HF bands (1.5 ± 0.3 vs 1.7 ± 0.5 mmHg2, 1.9 ± 0.7 vs 2.8 ± 1.2 bpm2 and 1.2 ± 0.4 vs 1.1 ± 0.3 mmHg2/bpm2, respectively) when compared to chronically Pb exposed rats.
Our data suggests that the autonomic dysfunction induced by lead exposure is similar in a chronic and intermittent Pb exposure. Nevertheless, it seems that an intermittent exposure was no effect on systolic BP values.
The present study brings new insights on the environmental factors that influence autonomic and cardiovascular systems during development, which can help apprise public policy strategies to prevent and control the adverse effects of Pb toxicity.


Keywords


Lead toxicity, autonomic activity, Fisiosinal, Wavelet analysis, Heart Rate Variability

Full Text:

PDF

References


G. Flora, D. Gupta, and A. Tiwari (2012). Toxicity of lead: a review with recent updates. Interdiscip. Toxicol., vol. 5, no. 2, pp. 47–58. https://www.ncbi.nlm.nih.gov/pubmed/23118587

World Health Organization. Exposure to Lead: A major public health concern (2010). World Heal. Organ, p. 6. http://www.who.int/ipcs/features/lead..pdf?ua=1

A. Navas-Acien, E. Guallar, E. K. Silbergeld, and S. J. Rothenberg (2007). Lead exposure and cardiovascular disease - A systematic review Environ. Health Perspect., vol. 115, no. 3, pp. 472–482. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1849948/

N. D. Vaziri. Mechanisms of lead-induced hypertension and cardiovascular disease (2008). Am. J. Physiol. Heart Circ. Physiol., vol. 295, no. 2, pp. H454–H465. https://www.ncbi.nlm.nih.gov/pubmed/18567711

D. C. Basha, S. S. Basha, and G. R. Reddy (2012). Lead-induced cardiac and hematological alterations in aging Wistar male rats: Alleviating effects of nutrient metal mixture. Biogerontology, vol.13, no. 4,pp.359-368. https://www.ncbi.nlm.nih.gov/pubmed/22534743

N. a. Brown. Reproductive and developmental toxicity of styrene (1985). Reprod. Toxicol., vol. 5, pp. 3–29. https://www.ncbi.nlm.nih.gov/pubmed/1807534

M. Ahamed and M. K. J. Siddiqui (2007). Low level lead exposure and oxidative stress: Current opinions. Clin. Chim. Acta, vol. 383, no. 1–2, pp. 57–64. https://www.ncbi.nlm.nih.gov/pubmed/17573057

M. Loghman-Adham. Renal effects of environmental and occupational lead exposure (2008). Environ. Health Perspect., vol. 105, no. 3, pp. 103–106. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796746/

C. D. Toscano and T. R. Guilarte (2005). Lead neurotoxicity: From exposure to molecular effects. Brain Res. Rev., vol. 49, no. 3, pp. 529–554. https://www.ncbi.nlm.nih.gov/pubmed/16269318

Y. Finkelstein, M. E. Markowitz, and J. F. Rosen (1998). Low-level lead-induced neurotoxicity in children: An update on central nervous system effects. Brain Res. Rev., vol. 27, no. 2, pp. 168–176. https://www.ncbi.nlm.nih.gov/pubmed/9622620

V. Geraldes, M. Carvalho, N. Goncalves-Rosa, C. Tavares, S. Laranjo and I. Rocha (2016). Lead toxicity promotes autonomic dysfunction with increased chemoreceptor sensitivity. Neurotoxicology, 54,170-177. https://www.ncbi.nlm.nih.gov/pubmed/27133440

C. Tavares, R.M. Carneiro, S. Laranjo and I. Rocha (2011) Computational tools for assessing cardiovascular variability. IEEE/EMBS/ENBENG.2011.6026. http://ieeexplore.ieee.org/document/6026082/

H. Bielarczyk, X. Tian and J.B. Suszkiw (1996). Cholinergic denervation-like changes in rat hippocampus following developmental lead exposure. Brain Res 708, 108–115.https://www.ncbi.nlm.nih.gov/pubmed/8720865

N. Bourjeily and J. B. Suszkiw (1997). Developmental cholinotoxicity of lead: Loss of septal cholinergic neurons and long-term changes in cholinergic innervation of the hippocampus in perinatally lead-exposed rats. Brain Res 771, 319–328. https://www.ncbi.nlm.nih.gov/pubmed/9401752

B. J. Brockel and D. A. Cory-Slechta (1999). Lead-induced decrements in waiting behaviorinvolvement of D2-like dopamine receptors. Pharmacol Biochem Behav 63, 423–434. https://www.ncbi.nlm.nih.gov/pubmed/10418784




DOI: http://dx.doi.org/10.34629/ipl.isel.i-ETC.28

Refbacks

  • There are currently no refbacks.


Copyright (c) 2018 Liana Shvachiy, Vera Geraldes, Mafalda Carvalho, Isabel Rocha

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.