Onset of and recovery from diving bradycardia in ducks

Abstract

SUMMARY1. No evidence was found of a 'postural reflex' in ducks. Neither the position of the head nor the water temperature affected the cardiac response to diving.2. In ducks with access to air through a tracheal cannula, submersion did not invariably cause apnoea until the water level reached the glottis. Heart rate was closely related to respiratory frequency, and bradycardia did not occur during submersion unless there was a reduction in respiratory frequency or a cessation of ventilation altogether.3. When apnoea and bradyeardia did occur during submersion, the first inspiration upon surfacing was 2-3 times larger than normal and was accompanied by an instantaneous rise in heart rate.4. Atropinization or cold block of the vagus abolished diving bradycardia. Only one vagal trunk was involved in cardiac chronotropic control at any one time. This vagal trunk also appeared to be more important in control of respiratory frequency.5. f8-adrenergic receptor blockade did not affect either diving bradycardia or post-dive tachycardia.6. The results show that the cardiac chronotropic response both during and after submergence is controlled solely by changes in parasympathetic vagal activity.

Heart rate regulation in diving sea lions: the vagus nerve rules

“…Cardiac accelerator fibers, as well as vagal fibers, are activated during the bradycardia induced by nasopharyngeal and cold face immersion stimulation of the neural pathways involved in the dive response (Houdi et al, 1995;Nalivaiko et al, 2003;Paton et al, 2005Paton et al, , 2006Tulppo et al, 2005). Maintenance of the activity of cardiac accelerator fibers during the dive response is also consistent with results from pharmacological blocker studies in experimental submersions of nutria (Myocastor coypus), muskrats (Ondatra zibethicus) and ducks, and in spontaneous dives of muskrats (Butler and Jones, 1968;Ferrante and Opdyke, 1969;Jones, 1981;Jones, 1995, 1996). Although partial withdrawal of sympathetic cardiac activity during spontaneous dives was proposed on the basis of decreases in heart rates of pharmacologically blocked harbor seals (Phoca vitulina) (Elliott et al, 2002), our review of control tests of the muscarinic ( parasympathetic) blockade in those seals suggests that such blockade was incomplete.…”

“…With inadequate muscarinic blockade, the vagus nerve could cause some decrease in heart rate during dives and make the interpretation of the results difficult. In contrast, no decreases from elevated pre-dive heart rates were observed in completely blocked muskrats, seals and ducks (Butler and Jones, 1968;McPhail and Jones, 1999;Murdaugh et al, 1961;Jones, 1995, 1996;Van Citters et al, 1965).…”

Respiratory and cardiovascular interactions in ducks: the effect of lung denervation on the initation of and recovery from some cardiovascular responses to submergence.

“…Certainly passive inflation with 8 % CO2 in nitrogen during a dive nearly always caused the animal to breathe voluntarily within 1-2 sec from the start of inflation which indicates respiratory neurone sensitivity to other inputs was increased by inflation, the resultant respiratory activity being sufficient to override water-initiated apnoea (Butler & Jones, 1968;Bamford & Jones, 1974). The fact that the degree of cardio-acceleration under our experimental conditions was similar whether caused by passive lung inflation or 'central irradiation' at least suggests that similar central nervous interconnexions are involved.…”

“…Heart rate was obtained from the e.c.g., the latter being recorded with bipolar copper wire electrodes (Butler & Jones, 1968) and after amplification the signal woo fed into an instantaneous heart-rate-meter to give pulse frequency. Electroncurograms were recorded from an intercostal nerve using bipolar platinum hook electrodes.…”

“…Respiratory motor neurone activity was monitored in an intercostal nerve of paralysed ducks either on unidirectional ventilation or during INTRODUCTION The initiation and maintenance of apnoea and concomitant cardiovascular adjustments to diving displayed by many air breathing vertebrates have been the subject of intensive investigation (Scholander, 1940;Anderson, 1966; Angell James & Daly, 1972a;Jones & Johansen, 1972). In ducks there is no bradycardia in the absence of apnoea (Butler & Jones, 1968) and Cohn, Krog & Shannon (1968) proposed that, in birds, cessation of thoracic motion was the initiating factor in the development ofthe cardiovascular responses to submergence. Undoubtedly generation of the diving responses in both birds and mammals is either prevented or reduced by continued rhythmic lung ventilation (Angell James & Daly, 1969;Drummond & Jones, 1972;Butler & Taylor, 1973) and Lin, Matsuura & Whittow (1972) even suggested that, in the California sea lion, diving bradycardia is solely the result of the lack of cardioacceleration normally caused by rhythmic lung inflation.…”