Prenatal cigarette smoke exposure: Pregnancy outcome and gestational changes in plasma nicotine concentration, hematocrit, and carboxyhemoglobin in a newly standardized rat model

2006 ◽  
Vol 214 (2) ◽  
pp. 118-125 ◽  
Author(s):  
Svetlana Farkas ◽  
Jabeen Hussein ◽  
Robert E. Ariano ◽  
Daniel S. Sitar ◽  
Shabih U. Hasan
2004 ◽  
Vol 28 (7) ◽  
pp. 1120-1128 ◽  
Author(s):  
Martha J. Gentry-Nielsen ◽  
Elizabeth Vander Top ◽  
Mary U. Snitily ◽  
Carol A. Casey ◽  
Laurel C. Preheim

2015 ◽  
Vol 37 (5) ◽  
pp. 1712-1724 ◽  
Author(s):  
Xue Jiang ◽  
LinDong Yuan ◽  
Peng Li ◽  
Jia Wang ◽  
Pengyu Wang ◽  
...  

Background/Aims: To investigaterole of serotonin (5-HT) and serotonin transporter (5-HTT) in a rat model of cigarette smoke-induced pulmonary artery hypertension (PAH) and the effect of statins on regulating 5HT and 5-HTT. Methods: A rat model of COPD comorbid with PAH was established by cigarette smoke exposure with or without simvastatin administration. The smoking and the simvastatin plus smoking groups were exposed to cigarette smoke daily, and the latter received simvastatin at 5mg/kg, once a day. After 16 weeks of cigarette smoke exposure, body weight and mean pulmonary arterial pressure (mPAP) were measured, bronchoalveolar lavage (BAL) was performed, and lung tissues and blood samples were collected to determine cardiopulmonary pathology, physiological indices, blood levelof 5-HT and expression of 5-HTT in the lung. Results: In addition to alveolar structural damage (COPD-like injury), chronic cigarette smoke exposure lead to pulmonary artery remodeling and PAH as evidenced by significant elevation of mPAP, RVHI, WT%and WA%. Cigarette smoke exposure resulted in significant reduction in animal body weight, and simvastatin significantly prevented smoke-induced weight loss. The number of inflammatory cells in BALF was dramatically increased in smoke exposed rats, and simvastatin dampened the number of leukocytes, neutrophils, lymphocytes, and macrophages. In addition, circulating 5-HTand expression of 5-HTT in the lung were significantly increased in the smoked rats compared to control rats, and it was significantly reduced by simvastatin. Alteration of BALF inflammatory cells, 5-HT and 5-HTT was significantly correlated with changes of mPAP, RVHI, WT% and WA%. Conclusions: Cigarette smoke exposure could result in not only COPD, but also PAH, which may attribute to the alteration of blood 5-HT and lung tissue 5-HTT. Simvastatin could significantly inhibited 5-HT and 5-HTT expression, and by which mechanism, it may protect animals from development of PAH.


2009 ◽  
Vol 18 (4) ◽  
pp. 562-567 ◽  
Author(s):  
Maricelma da Silva Soares de Souza ◽  
Paula Helena Ortiz Lima ◽  
Yuri Karen Sinzato ◽  
Marilza Vieira Cunha Rudge ◽  
Oduvaldo Câmara Marques Pereira ◽  
...  

2013 ◽  
Vol 27 (6) ◽  
pp. 791-800 ◽  
Author(s):  
Rodrigo Gibin Jaldin ◽  
Édson Castardelli ◽  
Juliana Elaine Perobelli ◽  
Winston Bonetti Yoshida ◽  
Antônio de Castro Rodrigues ◽  
...  

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 302A-302A
Author(s):  
Svetlana Farkas-Cubra ◽  
Jabeen Hussein ◽  
Yolanda MacKinnon ◽  
Ather Bano ◽  
Shabih U Hasan

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