Autonomic Cardiovascular Effects of Nasal Inhalation of Cigarette Smoke in the Rabbit

Summary Nasopharyngeal stimulation by cigarette smoke in unanaesthetised rabbits evokes apnoea in expiration, bradycardia (to 30% of control), a rise in mean arterial (to 110%) and right atrial pressure (by 6 mm Hg) and a fall in cardiac output (to 41% of control) and systemic conductance (to 36%). Blood flow (measured by Doppler flowmeter) and conductance in the mesenteric, renal, hind limb and car beds falls uniformly between beds and to the extent that, on occasions, flow in all these beds ceases. Sagittal sinus flow and conductance, in contrast, do not change or rise. The cardiovascular response is mediated predominantly through cardiac vagal and peripheral sympathetic vasoconstrictor nervous pathways. PνO 2 in animals with intact autonomic reflex mechanisms falls by 10 ± 0·4 mm Hg 25 see after the onset of apnoea, but in animals with either combined or selective blockade of vagal and sympathoadrenal pathways peripheral flow is not reduced as in animals with intact autonomic pathways, and PνO 2 falls by a significantly greater but equal amount in each (av. 15 ± 0·6 mm Hg, P diff < 0·001). The circulatory changes thus appear to conserve body oxygen stores during the induced apnoea, an effect dependent on the integration of evoked vagal and sympathetic autonomic activity.