| Summary: | 碩士 === 國立臺灣師範大學 === 生物研究所 === 91 === The aim of the present study was to examine the effects of Arg8-vasopressin (AVP) which was microinjected into ventrolateral medulla (VLM) on phrenic nerve activity and respiratory-related facial nerve discharge. In addition, we further identified whether these effects of AVP on cardiopulmonary functions were mediated by AVP V1A receptor.
Adult male Wistar rats (250-350 g) were used. Under urethane (1.2g/kg i.p.) anesthesia, tracheotomy was performed and femoral artery and vein were catheterized. The animal was placed in a prone position on a stereotaxic instrument. The phrenic and facial nerves on one side was isolated and cut distally. Activities of both nerves were recorded via an amplifier and then integrated. Ends-tidal fractional concentration of gas was maintained at normncapnia or hypercapnia in hyperoxia. AVP and AVP V1A antagonist were microinjected into the VLM to observe the responses of phrenic and facial nerve activity.
The results revealed that：(1) AVP microinjected into the medial portion of the VLM produced apnea, decreases in phrenic and facial nerve activities without change in blood pressure (Type I response). (2) AVP microinjected into the lateral portion of the VLM produced apnea, decrease in phrenic and facial nerve activities and concomitant pressor effect (Type II response). (3) These inhibitions of AVP upon phrenic and respiratory-related facial nerves were partially attenuated by hypercapnia. (4) These cardiopulmonary responses could be totally abolished by treatment of vasopressin V1A antagonist ([β-Mercapto-β, β-cyclopentamethyl enepropionyl1,-O-Me-Tyr2-Arg8]-vasopressin). (5) Pretreatment with phentolamine could abolish the pressor effect but not affect the inhibitory action on PNA evoked by AVP. These results implied that the modulatory effects of an endogenous vasopressinergic pathway on cardiopulmonary functions were mediated by vasopressin V1A receptor located on the neurons within the VLM. In addition, this pathway may also influence upper airway patency by the modulation on respiratory-related facial nerve.
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