UBC Theses and Dissertations
Neural control of the cardiac response of the Pekin duck (Anas platyrhynchos) to forced submersion Gabbott, Geoffrey Roy Julian
Cardiovascular responses evoked during forced submersion enable the Pekin duck (Anas platyrhynchos) to survive protracted periods of asphyxia. The responses include an extraordinary bradycardia and intense peripheral vasoconstriction with the result that blood flow is favoured to those organs most susceptible to lack of oxygen. These adjustments appear to be mediated via the caudal brainstem following stimulation of peripheral and central arterial chemoreceptors. The minor role that baroreceptors play in the generation of these responses was demonstrated by the persistence of the cardiovascular changes following peripheral arterial baroreceptor denervation. Isolation of the cephalic circulation from the systemic circulation enabled a series of experiments to assess the relative contributions from peripheral chemoreceptors, located in the carotid bodies, and from unidentified central chemoreceptors within the cranial circulation. A declining arterial P0₂ in the systemic circulation appeared especially potent in evoking bradycardia during submersion. Increased arterial PC0₂, likewise, resulted in a reduced heart rate. Similar changes in the blood gas levels of the cephalic circulation did not elicit significant bradycardia. However, both receptor groups responded to arterial hypoxic hypercapnia by activating substantial reduction in peripheral blood flow, as reflected by the rise in hind limb vascular resistance. Although baroreceptors may continue to mitigate changes in arterial blood pressure and cause some change in heart rate and vascular resistance, chemoreceptors appear to be predominantly responsible for the changes during submersion. The cardiac response to chemoreceptor stimulation during submersion was discovered to habituate following repetitive diving. Habituation was so pronounced in some ducks that after several training sessions the bradycardia during 40-second forced dives was abolished. Habituation of the cardiac response appeared dependent on the intensity of chemoreceptor stimulation. With severe arterial hypoxia, produced by either prolonging dive times or by reducing the pre-dive inspired oxygen content, little or no cardiac habituation was observed. Tests were conducted to demonstrate efficacy of the cardioinhibitory efferent discharge. Maintained sensitivity of chemoreceptors was suggested by the lack of change in oxygen breathing tests before and after training. Furthermore, the persistence of stimulus intensity was established and these observations led to the suggestion that the locus of habituation is within the CNS. The demonstration that the level of bradycardia was dependent on arterial P0₂ in both naive and habituated animals argues against the contention that the diving response is a fear response. Further evidence against this view was provided by the demonstration that the diving response remains essentially intact following transection in the rostral mesencephalon below the level of the hypothalamus. It is concluded that chemoreceptor-driven cardiovascular changes evoked as part of the diving response are mediated by regions of the CNS below the rostral brainstem. Modification of these responses can be produced in the intact animal by simple forms of learning. However, it remains uncertain at what level this influence arises.