engleski

Effects of IV Remifentanil (Remi) on the discharge patterns of canine pre‐Botzinger complex (pBC) neurons

Mu-opioids at clinical doses typically produces bradypnea, which may be mediated by their effects on presynaptic neurons that supply inputs to pBC neurons. This study evaluated the effects of the rapid, short-acting mu-opioid Remi (IV) on the discharge patterns of pBC neuron subtypes in decerebrate, vagotomized, mechanically-ventilated, paralyzed dogs during hyperoxia. A NeuroNexus 16- electrode microprobe was used to simultaneously record from multiple pBC neurons before, during and after the IV infusion of Remi. Histograms (CTHs) triggered from the phrenic neurogram (PNG) were used to determine peak and time-averaged discharge frequency (Fn) and profiles. Remi (0.94 mcg/kg/min) increased TI and TE by 3% and 71% respectively, and decreased peak PNG by 55%. Depression (peak Fn) among subtypes was not different: I-aug (28±10% ; n=32), I-dec (22±10% ; n=18), E-aug (18±10% ; n=15), and E-dec (38±8% ; n=26). Depression based on average Fn was similar. The magnitude of neuronal depression was not related to TI and TE or control Fn. Differential depression between simultaneously recorded neurons was common. While the pBC neurons were much less depressed than the peak PNG, the similar degree of depression of neuron subtypes and response variability did not allow bradypnea to be assigned to any pBC neuron subtype. The mechanism for bradypnea may lie outside the pBC. Supported by VA Med. Res. and NIH GM059234 funds.

mu-opioids ; pBC region ; neuronal depression

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