Cardiovascular responses to underwater submersion change little after disrupting the RVLM with anti‐DBH‐saporin.

Abstract

Two groups of bulbospinal neurons in the RVLM respond to nasal stimulation with ammonia vapors. One group is slowly‐conducting neurons, probably catecholaminergic, while another involves faster‐conducting neurons, probably noncatecholaminergic. We investigated the C1 catecholaminergic neurons located in the RVLM of rats, and their role in changes of heart rate (HR) and arterial blood pressure (AP) to either diving underwater or nasal stimulation with ammonia vapors. The toxin anti‐DBH‐saporin was injected either directly into the RVLM (20ng/200nl, bilaterally) of one group or into theT2‐T4 spinal cord of another group of rats trained to dive underwater; rats survived for 3–6wks. The dramatic bradycardia (avg. = ~80%) and the increase in BP (avg. =~10%) usually seen in diving rats persisted in both groups. The lesser bradycardia usually seen with nasal stimulation of rats after anesthesia was similar to that after either spinal or medullary injections. However, AP fell −14% in rats with spinal injections, but rose 3% in rats receiving medullary injections. The brains were sectioned and immunostained for tyrosine hydroxylase; positive C1 neurons were counted. The results are discussed in terms of the drop in AP seen after nasal stimulation and spinal injections, the route of injection, and the correlation of physiological data with the loss of C1 neurons. Supported by SLU School of Medicine.