The effect of vasopressin on respiratory-related hypoglossal nerve activity in rats

碩士 === 國立臺灣師範大學 === 生物研究所 === 89 === 英文摘要 The purpose of the present study was to examine the influence of the arginine vasopressin (AVP) on respiratory-related hypoglossal activity in rats. The rat was anesthetized by urethane (1.2 g/kg, i.p.).Tracheotomy, and catheterization...

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Bibliographic Details
Main Authors: Ching-Wen Chuang, 莊菁雯
Other Authors: Ji-Chuu Hwang
Format: Others
Language:zh-TW
Published: 2001
Online Access:http://ndltd.ncl.edu.tw/handle/91826488499169679164
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Summary:碩士 === 國立臺灣師範大學 === 生物研究所 === 89 === 英文摘要 The purpose of the present study was to examine the influence of the arginine vasopressin (AVP) on respiratory-related hypoglossal activity in rats. The rat was anesthetized by urethane (1.2 g/kg, i.p.).Tracheotomy, and catheterization of the femoral artery and vein were performed. The animal was then paralyzed with gallamine triethiodide (5 mg/kg) and ventilated artificially. End-tidal fractional concentration of gas was maintained at normocapnia in hyperoxia. Activities of both the phrenic and hypoglossal nerves were monitored Arginine vasopressin (AVP) was microinjected into a specific area of the ventrolateral medulla (VLM) to evaluate the response of the phrenic and the hypoglossal nerve. There were two types of response with AVP administration. In type I response, activities of the phrenic nerve (PNA) and the hypoglossal nerve (HNA) showed apnea and then recovered gradually. Mean period of apnea in response to low dose (1.5x10-8 IU) and high dose (3.0x10-8 IU) of AVP was 3.24 and 5.28 seconds respectively (p < 0.05) . Average PNA of the first neurogram after recovery from AVP treatment with low and high dose was 75.61 % and 58.21 % (p < 0.01) while HNA was 68.92 % annd 46.45 % of control. Blood pressure was unchanged. In type II response, mean period of apnea with a dosage of 3.0x10-8 IU was 4.22 seconds (p < 0.05). Average PNA of the first neurogram flowing AVP administration was 63.71 % of control whereas HNA was 80 %.These inhibitions of AVP upon PNA and HNA were attenuated by hypercapnia. Thus PNA was reduced to 85.19 % and 70.94 % of control in type I response whereas to 93.97 % of control in type II response. HNA was 88.70 % and 74.00 % of contral in type I response but to 88.99 % in type II response. These results suggest that AVP may play a role in the modulation of respiration and upper airway patency by direct action upon the neurons in the VLM.