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. / Science, Faculty of / Zoology, Department of / Graduate

The hematological and rheological characteristics of blood from a number of vertebrates was compared to assess possible species differences in blood viscosity that may influence cardiovascular oxygen transport. Nucleated red blood cells (RBCs) were more viscous (measured by cone-plate viscometry) in comparison with enucleate (mammalian) RBCs at hematocrits greater than 40% when measured at equivalent temperatures. The lower viscosity of enucleate RBCs is attributed to an enhanced deformability of enucleate cells in comparison to nucleated cells.

When dabbling ducks are involuntarily submerged, arterial vasoconstriction produces a large increase in the peripheral resistance to blood flow which is balanced by a decrease in output of the heart, and arterial blood pressure is maintained. Arterial baroreceptors sense systemic blood pressure, and provide the afferent information to the baroreflex for pressure regulation. The effector limbs of the baroreflex are the same as those involved in the diving responses, and the baroreceptors are likely to be important in the integration of the cardiovascular responses to diving. The purpose of this study was to investigate the role of the arterial baroreceptors in maintaining blood pressure during diving, and in the initiation and maintenance of the diving responses. Baroreceptor function was studied by diving ducks at various times after barodenervation, and by electrically stimulating the central end of one baroreceptor nerve in baroreceptor-denervated animals to simulate a controlled baroreceptor input before and during submersion. Intact baroreceptor innervation was not necessary for the development of peripheral vasoconstriction, but loss of the baroreceptors modified the cardiac response to submersion by impairing the vagally mediated bradycardia. There was no effect of baroreceptor nerve stimulation on peripheral resistance during diving, and the baroreflex operated via the heart rate in modulating blood pressure early in the dive. Later in the dive, stimulation was ineffective in altering either heart rate or blood pressue. Strong chemoreceptor drive results from decreased blood oxygen and increased carbon dioxide levels in the dive, and the results of experiments to determine the mechanism of baroreflex attenuation showed that an interaction between chemoreceptor and baroreceptor inputs may be at least partly responsible for reducing baroreflex effectiveness. The main conclusion from this work is that the arterial baroreceptors contribute to the diving responses through modulation of heart rate, to help balance the fall in cardiac output against the baroreceptor-independent peripheral vasoconstriction in the first minute of forced dives. / Science, Faculty of / Zoology, Department of / Graduate