Cardiorespiratory changes induced by vertebral artery injection of sodium cyanide in cats

Brain stem hypoxia caused by vertebral artery injection of sodium cyanide (NaCN) (1-20 micrograms) in artificially ventilated cats depressed phrenic and stimulated sympathetic nerve activity with a simultaneous increase in arterial blood pressure. Larger doses of NaCN caused greater effects. Hypercapnia produced by inhalation of 7% CO2 in O2 tended to reduce NaCN-induced responses on phrenic activity but not on blood pressure or sympathetic activity. Infusion into the vertebral artery with hypoxic saline (3% CO2 in N2) altered blood pressure, also affecting phrenic and sympathetic nerves similarly to NaCN administration. However, washout of CO2 by infusion of 100% O2 bubbled saline at high flow rates (3.6 ml/min) depressed phrenic as well as sympathetic activity and blood pressure. Spinal transection at the first cervical level eliminated sympathetic excitatory response to intravertebral cyanide injection. However, a large dose of NaCN (600 micrograms) given intravenously in spinal animal excited sympathetic activity. We conclude that intravertebral injection of NaCN can be used to study the effects of local hypoxia of the brain stem on cardiorespiratory responses and that hypoxia acts at both these sites (brain stem and spinal cord) to stimulate sympathetic excitation.