In-utero and neonatal exposure to secondhand smoke causes vascular dysfunction in newborn rats
Stuart J. Hutchison, MD, FRCP(C), FACCa,
Stanton A. Glantz, PhD, FACCa,
Bo-Qing Zhu, MDa,
Yi-Ping Sun, MDa,
Tony M. Chou, MD, FACCa,
Kanu Chatterjee, MB, FRCP, FACCa,
Prakash C. Deedwania, MD, FACCa,
William W. Parmley, MD, FACCa and
Krishnankutty Sudhir, MD, PhD, FRACPa
a Division of Cardiology, University of California, San Francisco, Moffitt Hospital Room 1186, San Francisco, California, USA
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Figure 1 (A) Dose–response curves of rat aortas exposed to Phe. The dose–response curves of the three groups of SHS-exposed rats are all shifted to the left of that of the control group, indicating greater sensitivity to adrenoceptor-mediated contraction. (B) EC50 values for Phe in the four groups of rats. Both in-utero and neonatal tobacco smoke exposure reduce the EC50 to Phe. SHSU = in-utero secondhand smoke exposure; SHSN = neonatal secondhand smoke exposure; SHSUN = in-utero and neonatal secondhand smoke exposure; Control = no secondhand smoke exposure.
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Figure 2 Endothelium-dependent relaxation. (A) Dose–response curves of rat aortas exposed to increasing concentration of acetylcholine. In-utero SHS exposure reduced maximal relaxation. (B) Dose–response curves of rat aortas exposed to increasing concentration of the calcium ionophore A23187. In-utero SHS tended to shift the EC50 of the response to the right, indicating reduced sensitivity.
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Figure 3 Endothelium-independent relaxation. (A) Dose–response curves of rat aortas exposed to nitroglycerin. The dose–response curves of the in-utero SHS exposed rats are all shifted to the right of the control and neonatal SHS groups. (B) Values of EC50 for nitroglycerin in the four groups of rats. In-utero tobacco smoke exposure increased the EC50 to nitroglycerin, indicating less sensitivity to endothelium-independent relaxation. Abbreviations as in Figure 1.
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