Dextromethorphan affects ventilation differently in male and female rats.
Dextromethorphan affects ventilation differently in male and female rats.
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右美沙芬对雄性和雌性大鼠通气的影响不同。
DOI：
10.1152/jappl.1996.81.5.1911
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Schlenker,EH
中科院分区：
文献类型：
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作者：
Schlenker,EH
Schlenker，Evelyn H.右美沙芬对雄性和雌性大鼠通气的影响不同。J. Appl. Physiol.81（5）：1911-1916，1996。天冬氨酸皮下给药可导致雄性大鼠长期但可逆的通气抑制，但在雌性大鼠中不存在。天冬氨酸作用于N-甲基-d-天冬氨酸受体。本研究验证了一种非竞争性N-甲基-d-天冬氨酸受体拮抗剂，美沙芬（Dex），将抑制雌性大鼠的通气和刺激它在雄性大鼠的假设。此外，Dex先于天冬氨酸给药可预防天冬氨酸诱导的雄性大鼠通气抑制。在雌性大鼠中，Dex在5和10 mg/kg时引起相对于生理盐水30%的通气抑制（P< 0.01），但在最高剂量（20 mg/kg）时没有。在雄性大鼠中，Dex对通气没有影响。在20 mg/kg剂量下，在给药后45和60 min，雌性大鼠（P< 0.001）和雄性大鼠在所有时间点的耗氧量均降低至生理盐水值的50%。Dex抑制雌性大鼠通气和耗氧量的时间点不同，表明通气抑制不是耗氧量抑制的结果。在高碳酸血症激发（7% CO2）期间，与生理盐水处理相比，5和10 mg/kg Dex处理的雌性大鼠表现出较小的排便反应增加。20 mg/kg剂量组雄性大鼠的高碳酸血症反应性（85.8 ± 8.95 ml/min）明显高于生理盐水组（50.6 ± 9.14 ml/min;P< 0.001）。最后，在天冬氨酸之前给予Dex防止了天冬氨酸诱导的雄性大鼠通气抑制。因此，在大鼠中，Dex对通气具有性别特异性影响，这些影响与耗氧量变化无关。
Schlenker, Evelyn H.Dextromethorphan affects ventilation differently in male and female rats.J. Appl. Physiol.81(5): 1911–1916, 1996.—Subcutaneous administration of aspartic acid results in a long-lasting but reversible depression of ventilation in male but not in female rats. Aspartic acid acts onN-methyl-d-aspartate receptors. The present study tested the hypothesis that a noncompetitiveN-methyl-d-aspartate-receptor antagonist, dextromethorphan (Dex), would depress ventilation in female rats and stimulate it in male rats. Moreover, Dex administered prior to aspartic acid should prevent the aspartic acid-induced depression of ventilation in male rats. In female rats, Dex caused a 30% depression of ventilation relative to saline at 5 and 10 mg/kg (P< 0.01) but not at the highest dose (20 mg/kg). In male rats, Dex had no effect on ventilation. At a dose of 20 mg/kg, Dex depressed oxygen consumption to 50% of the saline value at all time points in female rats (P< 0.001) and in male rats 45 and 60 min after administration. The time points when Dex depressed ventilation and oxygen consumption were different in female rats, suggesting that the depression of ventilation was not the result of a depression in oxygen consumption. During a hypercapnic challenge (7% CO2), female rats treated with 5 and 10 mg/kg of Dex exhibited a smaller increase in ventilatory response relative to saline treatment. At a dose of 20 mg/kg, the hypercapnic responsiveness of male rats was markedly stimulated (85.8 ± 8.95 ml/min) relative to saline (50.6 ± 9.14 ml/min;P< 0.001). Finally, Dex administered before aspartic acid prevented the aspartic acid-induced depression of ventilation in male rats. Thus, in rats, Dex has gender-specific effects on ventilation and these effects are not associated with changes in oxygen consumption.