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Results: 5

1.
Figure 5.

Figure 5. From: Life-long Programming Implications of Exposure to Tobacco Smoking and Nicotine Before and Soon After Birth: Evidence for Altered Lung Development.

The effect of nicotine exposure via the mother during pregnancy and lactation on the parenchyma of the lung tissue of adult offspring. The alveoli of the control lungs (A) are smaller than those of the lungs that were exposed to nicotine (B).

Gert S. Maritz, et al. Int J Environ Res Public Health. 2011 March;8(3):875-898.
2.
Figure 2.

Figure 2. From: Life-long Programming Implications of Exposure to Tobacco Smoking and Nicotine Before and Soon After Birth: Evidence for Altered Lung Development.

Diagram to illustrate the factors that induce premature aging of the lung parenchyma of rats exposed to nicotine via tobacco smoke or nicotine replacement therapy (NRT) via the placenta and mother’s milk. Premature aging of the lung is associated with an increased propensity for emphysema.

Gert S. Maritz, et al. Int J Environ Res Public Health. 2011 March;8(3):875-898.
3.
Figure 3.

Figure 3. From: Life-long Programming Implications of Exposure to Tobacco Smoking and Nicotine Before and Soon After Birth: Evidence for Altered Lung Development.

Effect of maternal nicotine exposure during pregnancy and lactation in rats on the connective tissue framework (stained black) of the lung of adult offspring. Note that the connective tissue framework of the control lungs (A) is more extensive than that of the offspring that were exposed to nicotine via the mother (B) [102].

Gert S. Maritz, et al. Int J Environ Res Public Health. 2011 March;8(3):875-898.
4.
Figure 4.

Figure 4. From: Life-long Programming Implications of Exposure to Tobacco Smoking and Nicotine Before and Soon After Birth: Evidence for Altered Lung Development.

Scanning electron micrographs of the alveolar surface in postnatal rats showing (A) control lung, (B) blebbing of the alveolar type I cell membrane in a nicotine exposed animal and (C) rupture of the alveolar surface to reveal the underlying capillary filled with red blood cells in a nicotine exposed animal. The nicotine exposed rats received nicotine during gestation and lactation. All animals were sacrificed on postnatal day 21 and lung tissue processed for scanning electron microscopy [102].

Gert S. Maritz, et al. Int J Environ Res Public Health. 2011 March;8(3):875-898.
5.
Figure 1.

Figure 1. From: Life-long Programming Implications of Exposure to Tobacco Smoking and Nicotine Before and Soon After Birth: Evidence for Altered Lung Development.

The influence of maternal nicotine exposure during gestation and lactation on: (A) glucose (Control vs. Experimental groups: P < 0.001), (B) glycogen utilization (Control vs. Experimental groups: P < 0.001) and (C) lactate production (Control vs. Experimental groups: P < 0.01) by lung tissue of the offspring.
Hatched bars show data from Control offspring (postnatal days 21 and 42 data combined); Grey bars show data from Nicotine exposed offspring killed at postnatal day 21; Black bars show data from a Withdrawal group at postnatal day 42. In the Withdrawal group, nicotine was not available from weaning on postnatal age 21 until the animals were killed at day 42; a period of 21 days of nicotine withdrawal was allowed to establish the longer term effect of nicotine exposure on carbohydrate metabolism by lung tissue of the offspring. Age-matched Control tissue was used in each case [68,71]. Data are presented as mean ± SEM.

Gert S. Maritz, et al. Int J Environ Res Public Health. 2011 March;8(3):875-898.

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