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

• Published in: Neuroscience letters Vol. 530; no. 1; pp. 69 - 74
• Main Authors: Pant, Jayanti, Pant, Mahendra K., Deshpande, Shripad B.
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 14.11.2012
• Subjects: 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; J-reflex; Pulmonary C reflex; Visceral reflexes; Vagal afferent activity; Toxic effects of BPA
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2012.09.046

► 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.