Gatti P J, Souza J D, Namath I J, Da Silva A M, Holtman J R, Gillis R
J Pharmacol Exp Ther. 1985 Dec;235(3):820-8.
The purpose of our study was to determine whether taurine, like other naturally occurring central nervous system amino acid neurotransmitters (e.g., gamma-aminobutyric acid and glycine), act at the ventral surface of the medulla to influence cardiorespiratory activity. This was accomplished by monitoring cardiorespiratory activity. This was accomplished by monitoring cardiorespiratory activity in chloralose-anesthetized cats and then applying several doses of taurine locally to the ventral medullary surface chemosensitive areas. We found that 2 and 4 mumol of taurine applied to the intermediate area of the ventral surface produced cardiorespiratory depression, whereas taurine, in a similar dose range, produced only respiratory depression when applied to the rostral area. In contrast, taurine applied to the caudal area had no cardiorespiratory effects. Similar experiments with glycine revealed that this inhibitory amino acid elicited a similar pattern of cardiorespiratory depression as taurine. Furthermore, strychnine, an antagonist of glycine, counteracted the cardiorespiratory depressant effects of both taurine and glycine effectively. Pretreatment with strychnine prevented most of the cardiorespiratory depressant effects of taurine and glycine. 6-Aminomethyl-3-methyl-4H-1, 2,4-benzothiadiazine-1,1-dixoide, a putative antagonist of taurine, had antagonistic effects similar to those of strychnine in both treatment and pretreatment studies. 6-Aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide, per se, increased tidal volume when applied to the intermediate area; strychnine had no effect. These results indicate that taurine acts at the chemosensitive areas on the ventral surface of the medulla to produce cardiorespiratory depression, and these effects are due to an interaction of taurine with receptors similar to, but probably not identical with, glycine receptors.
我们研究的目的是确定牛磺酸是否像其他天然存在的中枢神经系统氨基酸神经递质(如γ-氨基丁酸和甘氨酸)一样,作用于延髓腹侧表面以影响心肺活动。这是通过监测心肺活动来实现的。具体做法是在水合氯醛麻醉的猫身上监测心肺活动,然后将几剂牛磺酸局部应用于延髓腹侧表面的化学敏感区域。我们发现,将2和4 μmol牛磺酸应用于腹侧表面的中间区域会导致心肺抑制,而在类似剂量范围内,牛磺酸应用于吻侧区域时仅产生呼吸抑制。相比之下,将牛磺酸应用于尾侧区域则没有心肺效应。用甘氨酸进行的类似实验表明,这种抑制性氨基酸引发了与牛磺酸类似的心肺抑制模式。此外,甘氨酸拮抗剂士的宁有效地抵消了牛磺酸和甘氨酸的心肺抑制作用。用士的宁预处理可预防牛磺酸和甘氨酸的大部分心肺抑制作用。6-氨甲基-3-甲基-4H-1,2,4-苯并噻二嗪-1,1-二氧化物,一种假定的牛磺酸拮抗剂,在治疗和预处理研究中都具有与士的宁类似的拮抗作用。6-氨甲基-3-甲基-4H-1,2,4-苯并噻二嗪-1,1-二氧化物本身应用于中间区域时会增加潮气量;士的宁则没有效果。这些结果表明,牛磺酸作用于延髓腹侧表面的化学敏感区域以产生心肺抑制,并且这些作用是由于牛磺酸与类似于但可能与甘氨酸受体不完全相同的受体相互作用所致。