本研究目的在探討貓延腦背側對膈神經及舌下神經呼吸活動的影響。
成貓在麻醉狀態下去大腦，切斷兩側迷走神經，以肌肉痳痹劑痳痹後，由人工呼吸機維持生命。在高氧二氧化碳濃度正常及／或高氧二氧化碳濃度增加狀態下，以化學方法注射麩胺酸鈉（50mM，20~50nl）興奮延腦背側，觀察膈神經及舌下神經呼吸活動的反應。
在呼氣末二氧化碳濃度正常（4%~5%）的狀態下，在貓延腦背側進行1.0、1.5和2.0nmole三種不同劑量麩胺酸鈉刺激，結果得兩種反應類型：
第一類型，膈神經活動高度分別降低為刺激前的79.7%（p<0.05）、61.9%（p<0.05）和36.7%（p<0.01），舌下神經吸氣活動的高度分別降低為刺激前的47.3%（p<0.05）、33.2%（p<0.01）和17.7%（p<0.01）。
第二類型，膈神經活動高度不具顯著性變化，舌下神經吸氣活動的高度分別降低為刺激前的68.7%（p<0.05）、48.7%（p<0.01）和21.2%（p<0.01）。
提高呼氣末二氧化碳濃度至8%可減弱延腦背側對膈神經及舌下神經呼吸活動的抑制作用：
在呼氣末二氧化碳濃度正常狀態下，麩胺酸鈉（50mM，20~50nl）注射，第一類型結果為，膈神經活動高度降低為刺激前的62.6%（p<0.05），舌下神經吸氣活動降低為刺激前的31.2%（p<0.01），第二類型結果為膈神經活動高度不具顯著性變化，舌下神經吸氣活動降低為刺激前的35.6%（p<0.05）。將呼氣末二氧化碳濃度調為8%狀態下，同一位置進行化學刺激，膈神經及舌下神經吸氣活動高度的兩種類型結果均不具顯著性差異。
由以上的結果可知：
刺激延腦背側對膈神經、舌下神經呼吸活動的抑制作用了隨著不同的注射劑量而有dose dependent的趨勢。
刺激延腦背側對膈神經、舌下神經呼吸活動具有兩種反應類型；第一類型為膈神經及舌下神經呼吸活動均受抑制，第二類型為膈神經不具顯著性變化，舌下神經吸氣活動受到抑制。提高呼氣末二氧化碳濃度可減弱延腦背側對膈神經及舌下神經的抑制作用，推論延腦背側對上呼吸道的暢通可能扮演重要的角色。

The purpose of the present study was to examine the influence of the dorsal medulla (DM) on respiratory-related hypoglossal activity in cats. The adult cat was decerebrated under halothane and then vagotomized, paralyzed and ventialted artificially. Activites of both the phrenic (PN) and hypoglossal nerves (HN) were monitored. End-tidal fractional concentration of gas was maintain at normocapnia and/or hypercapnia in hyperoxia. Microinjection of glutamate ( 50 mM, 20 ~ nl) into the DM was performed to evaluate the changes of PN and HN activities.
In response to varied dose of 1.0, 1,5, and 2.0 nmole of glutamate microinjection into the DM at nomocapnia, there were two types of results according to PN activity; the first response type showed that PN activities were reduced to 79.7% ( p<0.05), 61.9% ( p<0.05) and 36.7% (p<0.01) of control respectively while HN a ctivities were reduced to 47.3% ( p<0.05), 33.2% (0.01) and 17.7% (p<0.01) of control respectively. The second response type showed that PN activities were uneffected whereas HN activities were reduced to 68.7% ( p<0.05), 48.7% (p<0.01) and 21.1% (p<0.01) of control respectively. These inhibitions of the DM upon PN and HN activities were attenuated by hypercapnia. Hence, in the first type of response glutamate microinjection (50 mM, 20 ~ 50nl ) into the DM produced a decrease of PN activities to 62.6% (p<0.05) and HN activities to 31.2% (p<0.01). In contrsat, reductions in both PN and HN activities were not affected significantly when end -tidal fractional concentration of CO2 was raised to 8%. In the second type of response significant reduction (35.6% of control) of HN in response to DM activation at normocapnia was not observed at hypercapnia.
These results suggest that neurons in the dorsal medulla may play a role in the modulation of upper airway patency by reducing respiratory-related hypoglossal nerve discharge.