Properties of sympathetic neuron responses to cerebral ischemia and to systemic hypoxia or hypercapnia which suggest mediation by central chemosensitive mechanisms

This thesis concerns the possible existence of central nervous system (CNS) chemosensitive mechanisms influencing sympathetic activity. The thesis is based on observations of sympathetic neuron and cardiovascular responses to CNS ischemia, systemic hypoxia and systemic hypercapnia. Investigation of the pressor response to cerebral ischemia in the cat indicates that it is mediated by superficial regions of the ventral medulla also involved in the pressor response to central hypercapnia. Experiments concerning the sympathetic response to systemic hypoxia in the CNS-intact sino-aortic denervated cat revealed a two-component response of the firing rates of single sympathetic preganglionic neurons (SPN), the mass activity of the cervical sympathetic trunk, and the neurogenic component of hindlink vascular resistance (N-HLVR). The response consisted of: (i) an increase of all three variables during extreme hypoxia, and (ii) a decrease during moderate hypoxia. The hypoxic sympatho-depression resulted from loss of central respiratory input to SPNs as well as of respiration-independent input. The hypoxic sympatho-excitation involved only the latter input. Investigation of the sympathetic response to systemic hypercapnia in the acute C$ sb1$ spinal cat demonstrated a direct relationship between SPN firing rate or N-HLVR and arterial PCO$ sb2$ between normocapnia and severe hypercapnia. N-HLVR also increased in this preparation during systemic hypoxia