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Open Access Research article

Sidestream cigarette smoke effects on cardiovascular responses in conscious rats: involvement of oxidative stress in the fourth cerebral ventricle

Vitor E Valenti15*, Luiz Carlos de Abreu2, Monica A Sato2, Celso Ferreira2, Fernando Adami2, Fernando LA Fonseca2, Valdelias Xavier2, Moacir Godoy3, Carlos B Monteiro2, Luiz Carlos M Vanderlei1 and Paulo HN Saldiva4

Author Affiliations

1 Programa de Pós-Graduação em Fisioterapia, Faculdade de Ciências e Tecnologia, Universidade Estadual Paulista, UNESP, Presidente Prudente, SP, Brazil

2 Departamento de Morfologia e Fisiologia, Faculdade de Medicina do ABC, Santo André, SP, Brazil

3 Departamento de Cardiologia e Cirurgia Cardiovascular, Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto, São Paulo, Brasil

4 Departamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil

5 Departamento de Fonoaudiologia, Faculdade de Filosofia e Ciências, Universidade Estadual Paulista, UNESP, Av. Higyno Muzzi Filho, 737, Marília, SP 17525-900, Brazil

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BMC Cardiovascular Disorders 2012, 12:22  doi:10.1186/1471-2261-12-22

Published: 30 March 2012

Abstract

Background

Cigarette exposure increases brain oxidative stress. The literature showed that increased brain oxidative stress affects cardiovascular regulation. However, no previous study investigated the involvement of brain oxidative stress in animals exposed to cigarette and its relationship with cardiovascular regulation. We aimed to evaluate the effects of central catalase inhibition on baroreflex and cardiovascular responses in rats exposed to sidestream cigarette smoke (SSCS).

Methods

We evaluated males Wistar rats (320-370 g), which were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4th V). Femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. Rats were exposed to SSCS during three weeks, 180 minutes, 5 days/week (CO: 100-300 ppm). Baroreflex was tested with a pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) to induce bradycardic reflex and a depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus) to induce tachycardic reflex. Cardiovascular responses were evaluated before, 5, 15, 30 and 60 minutes after 3-amino-1,2,4-triazole (ATZ, catalase inhibitor, 0.001 g/100 μL) injection into the 4th V.

Results

Central catalase inhibition increased basal HR in the control group during the first 5 minutes. SSCS exposure increased basal HR and attenuated bradycardic peak during the first 15 minutes.

Conclusion

We suggest that SSCS exposure affects cardiovascular regulation through its influence on catalase activity.