Bisphenol A attenuates phenylbiguanide-induced cardio-respiratory reflexes in anaesthetized rats

► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ► Acute intravenous injection of BPA also attenuated PBG-reflex response. ► Attenuation of PBG-reflex by BPA was seen with decreased vagal affere...

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Published inNeuroscience letters Vol. 530; no. 1; pp. 69 - 74
Main Authors Pant, Jayanti, Pant, Mahendra K., Deshpande, Shripad B.
Format Journal Article
LanguageEnglish
Published Ireland Elsevier Ireland Ltd 14.11.2012
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Abstract ► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ► Acute intravenous injection of BPA also attenuated PBG-reflex response. ► Attenuation of PBG-reflex by BPA was seen with decreased vagal afferent activity. ► BPA by attenuating the visceral reflexes may produce cardio-respiratory changes. Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2μg/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50–65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35mg/kg body weight) for 30min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity.
AbstractList Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2 mu g/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50a65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35 mg/kg body weight) for 30 min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity.
Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2 μg/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50-65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35 mg/kg body weight) for 30 min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity.
► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ► Acute intravenous injection of BPA also attenuated PBG-reflex response. ► Attenuation of PBG-reflex by BPA was seen with decreased vagal afferent activity. ► BPA by attenuating the visceral reflexes may produce cardio-respiratory changes. Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2μg/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50–65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35mg/kg body weight) for 30min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity.
Author Pant, Jayanti
Pant, Mahendra K.
Deshpande, Shripad B.
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Keywords J-reflex
Pulmonary C reflex
Visceral reflexes
Vagal afferent activity
Toxic effects of BPA
Language English
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Snippet ► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ►...
Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex...
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StartPage 69
SubjectTerms Air Pollutants, Occupational - toxicity
Analgesics - pharmacology
Anesthesia
Animals
Apnea
Benzhydryl Compounds - toxicity
Biguanides - pharmacology
Bisphenol A
Blood pressure
Blood Pressure - drug effects
Body weight
Bradycardia
Central Nervous System Depressants - pharmacology
Drug Interactions
EKG
Electrocardiography - drug effects
Ethanol
Ethanol - pharmacology
Female
Heart rate
Heart Rate - drug effects
Hypotension
J-reflex
Jugular vein
Nervous system
Neurons, Afferent - drug effects
Phenols - toxicity
phenylbiguanide
Plasticity
Plastics - toxicity
Pulmonary C reflex
Rats
Rats, Inbred Strains
Reflex - drug effects
Reflexes
Respiration
Respiratory Mechanics - drug effects
Sensory neurons
Sleep disorders
Toxic effects of BPA
Vagal afferent activity
Vagus nerve
Vagus Nerve - drug effects
Visceral reflexes
Title Bisphenol A attenuates phenylbiguanide-induced cardio-respiratory reflexes in anaesthetized rats
URI https://dx.doi.org/10.1016/j.neulet.2012.09.046
https://www.ncbi.nlm.nih.gov/pubmed/23041044
https://search.proquest.com/docview/1257735908
Volume 530
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