Respiratory Control in Neonatal Rats Exposed to Prenatal Cigarette Smoke

Pendlebury, Jonathan; Wilson, Richard J. A.; Bano, Shehr; Lumb, Kathleen J.; Schneider, Jennifer M.; Hasan, Shabih U.

doi:10.1164/rccm.200711-1739oc

Cited by 31 publications

(42 citation statements)

References 47 publications

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“…As previously reported in similar studies (Carmines and Rajendran, 2008; Pendlebury et al, 2008; Tachi and Aoyama, 1983), the pups of the exposed mothers had lower body weight than that of the controls at birth (5.77 ± 0.15 g vs. 6.66 ± 0.12 g ( P < 0.0001) in the two litters of each group in which this was measured), and their growth over the first four postnatal days was slower as well (3.74 ± 0.17 g vs. 4.64 ± 0.25 g; P < 0.005).…”

Section: Resultssupporting

confidence: 84%

“…Several previous studies have shown that gestational exposure to cigarette smoke retards fetal growth, resulting in low birth weight in both rats and humans (Bailey and Byrom, 2007; Esposito et al, 2008; Gaworski et al, 2004; Pendlebury et al, 2008). Our data are consistent with this finding and also show some reduction in the rate of postnatal growth in pups of gestationally smoke-exposed dams.…”

Section: Discussionmentioning

confidence: 99%

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Gestational cigarette smoke exposure and hyperthermic enhancement of laryngeal chemoreflex in rat pups

Xia

Crane-Godreau

Leiter

et al. 2009

Respiratory Physiology & Neurobiology

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Laryngeal chemoreflex (LCR) apnea occurs in infant mammals of many species in response to water or other liquids in the laryngeal lumen. The apnea can last for many seconds, sometimes leading to dangerous hypoxemia, and has therefore been considered as a possible mechanism in the Sudden Infant Death Syndrome (SIDS). We have found recently that this reflex is markedly prolonged in decerebrate piglets and anesthetized rat pups that are warmed 1–3 °C above their normal body temperatures. We intermittently exposed pregnant rats to cigarette smoke and examined the LCR in their four- to fifteen-day-old offspring under general anesthesia, with and without whole body warming. During warming, pups of gestationally smoke-exposed dams had significantly longer LCR-induced respiratory disruption than similarly warmed control pups. The results may be significant for the pathogenesis and/or prevention of SIDS as maternal cigarette smoking during human pregnancy and heat stress in infants are known risk factors for SIDS.

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Section: Resultssupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Gestational cigarette smoke exposure and hyperthermic enhancement of laryngeal chemoreflex in rat pups

Xia

Crane-Godreau

Leiter

et al. 2009

Respiratory Physiology & Neurobiology

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“…Few urothelial cells like crystals, cast, necrotic debris, mild inflammatory cells, transitional epithelium and squamous epithelium were observed consistently in most of the urine smears in the control group who are non-cigarette smokers which is in agreement with [12]. According to [13], cigarette smoking has been one of the leading causes of preventable death and a major public health concern, cigarette smoking causes most of the commonly diseases affecting the heart, lungs and the renal system [14]. In this research study, High cellular turnover was detected among 140 (70%) of the test group, this is due to the fact that when smokers inhale some of the carcinogens (cancer causing chemicals) in cigarettes, smokes are absorbed from the lungs and get into the blood, and from the blood, they are filtered by the kidneys and they are concentrated in urine in the bladder, thereby damaging the cells that line the inside of the bladder, leading to high cellular turnover and eventually causing bladder cancer, depending on how often and how long an individual continues to engage in cigarettes smoking.…”

Section: Discussionsupporting

confidence: 71%

Cytology Analysis of Urine among Cigarette Smokers

Blessing¹,

Ikechi²,

Ayobami³

2016

Am. J. Biomed. Sci.

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Introduction: This is a descriptive study carried out in Owo Town, Ondo State, during the period of February (2015) to August (2015). Aim: The main purpose of carrying out this research work is to evaluate the cytomorphological features of urine smears (using papanicoulaou stain) among cigarette smokers in Owo town, Ondo State, Nigeria. Materials and Method: 250 subjects were used for this research work, 200 subjects were cigarette smokers while 50 subjects were non-cigarette smokers. The numbers of years of cigarette smoking were different and the numbers of cigarette sticks smoked per day were also variable among the test group. Individuals with urinary tract infection were not included in this research work and individuals with less than five (5) years of cigarette smoking were also not included in this research work. From each urine sample collected, smears were obtained from the sediments after centrifuging and were immediately fixed with a cytology-spray fixative for at least 30 minutes, before staining smears with Papanicolaou stain. Results and Discussion: The stained smears were examined under a light microscope and revealed a high cellular turnover among 70% of the test group when compared with the control group which are nonsmokers, showing few normal urothelia cells. Enlargement in nuclear cytoplasm ratio, irregular nuclear borders, necrosis, cluster of cells showing dysplastic changes, moderate haemorrhage, heavy infiltrates of inflammatory cells, hyperchromatism, pleomorphysms and neoplastic transformation were among the features observed in smears of the test group. Conclusion: On the basis of this research work, cigarette smoking has been seen to be one of the leading causes of renal diseases.

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“…We hypothesized that, in mouse neonates, raphe neurons, which express functional nicotinic acetylcholine receptors (31,32), could be targeted by prenatal-perinatal nicotine exposure, affecting their activities, their electrical properties, and their chemosensitivities. We studied CF1 neonates at Postnatal Days 1 (P1) to P8, because it is known that, within this period, prenatal cigarette smoke disrupts eupneic breathing and the ventilatory response to hypoxia in rats (33), whereas prenatal-perinatal nicotine exposure impairs ventilatory responses to hypercapnia and depresses central respiratory chemoreception in mice (19,30). Therefore, we expect that the diminished hypercarbiainduced ventilatory responses that occur in nicotine-exposed mice at P1-P3 will be accompanied at the same time by changes in the electrical properties or CO 2 responsiveness of raphe neurons, including both the serotonergic and nonserotonergic populations.…”

mentioning

confidence: 99%

The Alteration of Neonatal Raphe Neurons by Prenatal–Perinatal Nicotine. Meaning for Sudden Infant Death Syndrome

Cerpa

Aylwin

Beltrán-Castillo

et al. 2015

Am J Respir Cell Mol Biol

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Nicotine may link maternal cigarette smoking with respiratory dysfunctions in sudden infant death syndrome (SIDS). Prenatal-perinatal nicotine exposure blunts ventilatory responses to hypercapnia and reduces central respiratory chemoreception in mouse neonates at Postnatal Days 0 (P0) to P3. This suggests that raphe neurons, which are altered in SIDS and contribute to central respiratory chemoreception, may be affected by nicotine. We therefore investigated whether prenatal-perinatal nicotine exposure affects the activity, electrical properties, and chemosensitivity of raphe obscurus (ROb) neurons in mouse neonates. Osmotic minipumps, implanted subcutaneously in 5-to 7-day-pregnant CF1 mice, delivered nicotine bitartrate (60 mg kg 21 d 21 ) or saline (control) for up to 28 days. In neonates, ventilation was recorded by head-out plethysmography, c-Fos (neuronal activity marker), or serotonin autoreceptors (5HT 1A R) were immunodetected using light microscopy, and patch-clamp recordings were made from raphe neurons in brainstem slices under normocarbia and hypercarbia. Prenatal-perinatal nicotine exposure decreased the hypercarbiainduced ventilatory responses at P1-P5, reduced both the number of c-Fos-positive ROb neurons during eucapnic normoxia at P1-P3 and their hypercapnia-induced recruitment at P3, increased 5HT 1A R immunolabeling of ROb neurons at P3-P5, and reduced the spontaneous firing frequency of ROb neurons at P3 without affecting their CO 2 sensitivity or their passive and active electrical properties. These findings reveal that prenatal-perinatal nicotine reduces the activity of neonatal ROb neurons, likely as a consequence of increased expression of 5HT 1A Rs. This hypoactivity may change the functional state of the respiratory neural network leading to breathing vulnerability and chemosensory failure as seen in SIDS.

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Respiratory Control in Neonatal Rats Exposed to Prenatal Cigarette Smoke

Cited by 31 publications

References 47 publications

Gestational cigarette smoke exposure and hyperthermic enhancement of laryngeal chemoreflex in rat pups

Gestational cigarette smoke exposure and hyperthermic enhancement of laryngeal chemoreflex in rat pups

Cytology Analysis of Urine among Cigarette Smokers

The Alteration of Neonatal Raphe Neurons by Prenatal–Perinatal Nicotine. Meaning for Sudden Infant Death Syndrome

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