The initiation and maintenance of bradycardia in a diving mammal, the muskrat, Ondatra zibethica.

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Abstract
The cardiac and respiratory responses of muskrats in unrestrained and restrained dives were compared with responses elicited by stimulation of a number of cardio-depressant receptor inputs, to determine which are most important in initiating and maintaining diving bradycardia. In unrestrained voluntary dives, heart rate fell from 310 .+-. 3 to 54 .+-. 3 beats/min in 1-2 s, which was significantly below that in dives by restrained unanesthetized or anesthetized animals. Pouring H2O on the external nares during maintained artificial ventilation caused heart rate to decline to 76 .+-. 12 beats/min after 1 s. hlowing water through the internal nares caused apnea, in the expiratory position, and bradycardia within 1/3 s. Heart rate fell to 20 .+-. 2 beats/min, 1 s after the start of H2O flow. Substituting saline for water reduced both the apneic and cardiac responses. Bilateral section of the maxillary branch of [cranial nerve] V and the inferior laryngeal (X) nerves completely abolished the cardiac and respiratory response to H2O flow. Artificial ventilation throughout periods of nasal stimulation with H2O or saline reduced the bradycardia, although even the saline-driven response could not be completely abolished. Lung deafferentation eliminated any direct effect of atrificial ventilation on heart rate during nasal stimulation. Lung deflation caused bradycardia within 0.97 .+-. 0.17 s, heart rate falling from 268 .+-. 7 to 59 .+-. 4 beats/min. Bradycardia also occurred during maintained lung inflation but it was delayed for a period which varied from 6.8 .+-. 1.8 s at an inflation pressure of 0.5 kPa [kilopascals] to 35 .+-. 7 s at 1.5 kPa. Bradycardia caused by nasal H2O flow or lung deflation was unaffected by bilateral section of the sinus nerve. Artificial ventilation of paralyzed muskrats with 5% CO2 in N2 caused bradycardia when PaO2 [arterial O2 tension] reached 8.4 .+-. 0.8 kPa and heart rate declined to 76 .+-. 7 beats/min at 4 kPa. Bilateral section of the sinus nerve delayed bradycardia until PaO2 reached 4.5 .+-. 0.5 kPa. Cardiac response to submergence could be the expression of input from nasal, lung and carotid chemoreceptors, although it is not clear how they interact to generate the cardiac responses displayed by unrestrained animals during submergence.