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The initiation of and recovery from diving bradycardia in the muskrat

University of British Columbia

Heart rate was found to be significantly lower in unrestrained diving muskrats than in those which were forced to dive. The response in the unrestrained animal represents a heart rate of about 9% of the resting rate and is similar to the cardiac responses recorded in freely diving pinnipeds. Apnea and bradycardia were initiated by water lapping the nares of the conscious animal. Anaesthesia abolished this narial reflex to submersion. In anaesthetized muskrats water was drawn into the nasal cavity causing transient apnea and prominent bradycardia by stimulating receptors located principally in the glottal and pharyngeal areas. Nerve blockade by reversible cooling and section demonstrated that these nasal receptors are innervated by the maxillary and inferior, laryngeal nerves. In the conscious animal trigeminal neurotomy failed to affect the course of the response confirming that the muskrat has a number of external sensory mechanisms capable of initiating the diving reflexes. Respiratory activity was shown to have a marked effect on heart rate when the muskrat was at rest and when water was passed through the nares. Cardioacceleration during nasal stimulation resulted from a central component and from neural input originating in fast adapting pulmonary receptors. Artificial ventilation not only increased heart rate but often tended to restore normal respiratory activity. Pulmonary deafferentation by steaming eliminated the Hering-Breuer reflex to maintained lung inflation as well as the cardioacceleration seen in response to artificial ventilation during nasal stimulation. The loss of the Hering-Breuer reflex occurred first suggesting that different receptors are involved. Lung deflation per se caused a reflex bradycardia but it appears that this does not potentiate the narial reflex since nasal bradycardia was not reduced when lung inflation was maintained. Central and peripheral components arising from respiratory activity have their greatest effect during the recovery period. Elimination of the carotid bodies delayed but did not abolish chemoreceptor driven bradycardia demonstrating that these are the most chemosensitive units but not the only ones responding to changes in blood gas tensions. No role however, has been found for the arterial baroreceptors. The barostatic reflex brought on by drug induced hypertension was triggered at a lower pressure than that found in the seal but it appears that this pressure would not be exceeded in the muskrat if heart rate remained low during a dive. It is concluded that the cardiac response to submersion in the muskrat results from at least three reflex arcs. These reflexes originate from the nares, the lungs and from peripheral chemoreceptors. Although the chemoreceptors act to maintain the prevailing diving responses, it is likely that the external narial reflex accounts for almost all of the cardiovascular adjustment brought about in normal foraging dives since these are usually of short duration. The chemoreflex could play a significant role in dives exceeding one minute by prompting the animal to resurface when oxygen stores are depleted.

Text

2010-03-23

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http://hdl.handle.net/2429/22344

Zoology

University of British Columbia

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