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

Abstract

SUMMARY1. The cardiac and respiratory responses shown by muskrats in both unrestrained and restrained dives have been compared with responses elicited by stimulation of a number of cardio-depressant receptor inputs, in an attempt to determine which are most important in initiating and maintaining diving bradyeardia.2. In unrestrained voluntary dives heart rate fell from 310 + 3 to 54+3 beats min-in 1 to 2 sec, which was significantly below that seen in dives by restrained unanaesthetized or anaesthetized animals. 3. Pouring water on the external nares during maintained artificial ventilation caused heart rate to decline to 76 + 12 beats minm-after 1 sec. Flowing water through the internal nares caused apnoea, in the expiratory position, and bradycardia within one third of a second. Heart rate fell to 20 + 2 beats min-, 1 sec after the start of water flow. Substituting saline for water reduced both the apnoeic and cardiac responses. Bilateral section of the maxillary branch of V and the inferior laryngeal (X) nerves completely abolished the cardiac and respiratory response to water flow.4. Artificial ventilation throughout periods of nasal stimulation with water or saline reduced the bradycardia, although even the saline driven response could not be completely abolished. Lung deafferentation eliminated any direct effect of artificial ventilation on heart rate during nasal stimulation.5. Lung deflation caused bradycardia within 0-97 + 0-17 sec, heart rate falling from 268 + 7 to 59 + 4 beats min-. Bradyeardia also occurred during maintained lung inflation but it was delayed for a period which varied from 6-8 + 1-8 sec at an inflation pressure of 0-5 kPa to 35 + 7 sec at 1-5 kPa.6. Bradyeardia caused by nasal water flow or lung deflation was unaffected by bilateral section of the sinus nerve.7. Artificial ventilation of paralysed muskrats with 5 % CO2 in N2 caused bradycardia when Pa°2 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 Pa o, reached 4-5 + 0-5 kPa.8. These results suggest that the cardiac response to submergence could be the expression of input from three groups of receptors, nasal, lung and carotid chemoreceptors, although it is not clear how they interact with one another to generate the cardiac responses displayed by unrestrained animals during submergence.

The diving response in man: effects on sympathetic activity in muscle and skin nerve fascicles.

“…Thus, impulses from facial receptors and effects of apnoea seem to act by mutual reinforcement in evoking the diving response. Similar mechanisms have been reported to underlie diving bradyeardia in the duck (Andersen, 1963b) and the diving muskrat (Drummond & Jones, 1979). Whether chemoreceptors or any other effects of apnoea cause the reinforcement cannot be concluded from the present results.…”

The effects of breathing different levels of O2 and CO2 on the diving responses of ducks (Anas platyrhynchos) and cormorants (Phalacrocorax auritus)

“…Obviously, in cormorants, bradycardia is initiated and probably maintained by other mechanisms which may involve receptors in the beak, or both central and peripheral respiratory related nervous activities. Certainly, these mechanisms can predominate in mammals (Dykes 1974a, b;Drummond and Jones 1979) and have been claimed to have some effect on the development of bradycardia in ducks (Andersen 1963;Jones and Butler 1982).…”

The cold face test: A non-baroreflex mediated test of cardiac vagal function

“…[4]. The trigeminal reflex is paramount in eliciting the diving bradycardia [3,6,7,20]; however, at present the specific role of the other reflexogenic areas is uncertain.…”