Baroreceptors and cardiopulmonary reflexes : afferent pathways and the influence of cold
A study was performed on decerebrate ferrets to define the contribution of vagal afferent non-myelinated fibres to the baroreceptor heart rate reflex produced by bolus i.v. injection of phenylephrine, using capsaicin as a selective C fibre blocker. Capsaicin blocked pulmonary chemoreflex substantially without any effects on bradycardia evoked by electrical stimulation of vagal efferent fibres to the heart. The significance of the contribution to bradycardia in response to marked increases in blood pressure by vagal C fibres are discussed in relation to findings in electrophysiological studies. A further study was performed on decerebrate ferrets and chloralose anaesthetised lambs. Baroreflex sensitivity was assessed by the relationship between cardiac interval changes and a rise in systolic blood pressure produced by bolus injection of phenylephrine and descending aorta occlusion. Moderate hypothermia (30-34oC) enhanced the baroreflex heart rate reflex substantially and was without effect on the sensitivity of pulmonary J receptor reflex pathways involved in the heart rate control. Action of vagal efferent fibres in altering heart rate was increased by moderate cooling. Such an effect may be partially responsible for the enhanced heart rate component of baroreflex response. Other possible mechanisms of enhanced baroreflex sensitivity are discussed. The consequence of enhanced vagal efferent fibre on heart was studied by electrical stimulation of the peripheral end of cervical vagus nerves in decerebrate ferrets and anaesthetised lambs. Moderate cooling substantially increases cardiac arrhythmias, such as sinus bradycardia, sinoatrial block, sinus arrest and A-V block. In addition vagal stimulation resulted in lethal ventricular arrythmia during infusion of noradrenaline. The possible mechanisms underlying the collapse and sudden death following rescue are discussed.