Abstract
The discharges of single phrenic units were examined in anesthetized, paralyzed, vagotomized and artificially ventilated dogs during hypothermia and during local cooling of the cervical spinal cord. The following results were obtained for individual phrenic motoneurons during hypothermia. The average frequency of impulses during discharge decreased with decreasing blood temperature. This effect was in principle independent of the arterial CO2 pressure (PaCO2). In some animals recruitment of additional units occurred with falling blood temperature. The response of phrenic units to CO2 stimulation was qualitatively identical at normal and at decreased blood temperatures, but was less pronounced during hypothermia. However, the thresholds of activation by PaCO2 of single phrenic motoneurons were lowered by hypothermia. The results suggest that the observed changes of phrenic motoneuron responses induced by hypothermia are caused by temperature effects on the respiratory output at both the central and the spinal level. An inhibitory influence of lowered blood temperature on the respiratory center is indicated by the reduced response to CO2 stimulation. On the other hand, the recruitment of motor units during hypothermia suggests a stimulating effect of cold on the phrenic motoneurons. The reduced discharge frequency of the single units during hypothermia may be ascribed to effects at the central and spinal levels. The effects of cold at the spinal level on the discharges of single phrenic units were evaluated by local cooling of the cervical spinal cord by about 4°C. During the experiments body temperature and PaCO2 were kept at normal levels. The results indicate that the frequency of the bursts of phrenic nerve discharge, which is equivalent to respiratory frequency, remained constant. The average impulse frequency within the single burst decreased significantly. Recruitment of additional units was frequently observed. It is suggested that the observed effects of local spinal cooling on phrenic nerve discharge are caused by a prolongation of the excitatory and inhibitory synaptic processes.
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