Holtman J R, Buller A L, Taveira Da Silva A M, Hamosh P, Gillis R A
Life Sci. 1983 May 16;32(20):2313-20. doi: 10.1016/0024-3205(83)90760-9.
The effects of taurine (0.8-64.8 mumol) were studied on respiratory activity following intracisternal (cisterna magna) and intracerebroventricular (lateral ventricle) injections in cats anesthetized with alpha-chloralose. Respiratory activity was measured by using a Fleisch pneumotachograph and monitoring tracheal airflow. The flow signal was integrated to obtain tidal volume (VT) and respiratory rate (f) was obtained by counting the number of VT excursions over one minute. Inspiratory (TI), expiratory (TE) and total (TTOT) cycle durations were also determined during this time period. In addition, end-tidal CO2 was continuously monitored. Associated changes in arterial pressure (femoral artery cannula) and heart rate were also determined. After injections into the cisterna magna, taurine caused dose-related decreases in minute ventilation (VE). The maximal decrease in VE was from 495 +/- 59 to 64 +/- 14 ml/min (p less than 0.05), and was due to both decreases in VT (from 27 +/- 3 to 5 +/- 1 ml; p less than 0.05) and f (from 18 +/- 1 to 12 +/- 2 breaths/min; p less than 0.05). TE and TTOT were increased from 2.4 +/- 0.4 to 4.5 +/- 0.6 sec (p less than 0.05) and from 3.7 +/- 0.4 to 6.4 +/- 0.8 sec (p less than 0.05), respectively. Mean inspiratory flow (VT/TI), a measure of inspiratory drive, was decreased from 21 +/- 4 to 4 +/- 2 ml/sec (p less than 0.05). Apnea occurred in 5 of 6 animals after the 64.8 mumol dose. This respiratory depression occurred without any significant change in arterial pressure. After lateral ventricle injections, taurine also caused dose-related, but not as pronounced, decreases in respiratory activity. In addition, taurine caused significant decreases (p less than 0.05) in arterial pressure in doses that decreased VE. Taurine administered intravenously had no significant cardiorespiratory depressant effects. These data indicate that centrally administered taurine produces respiratory depression and, depending on the route of CNS administration, also produces hypotension.
研究了牛磺酸（0.8 - 64.8微摩尔）对用α-氯醛糖麻醉的猫进行脑池内（小脑延髓池）和脑室内（侧脑室）注射后呼吸活动的影响。通过使用Fleisch呼吸流速计并监测气管气流来测量呼吸活动。对气流信号进行积分以获得潮气量（VT），通过计算一分钟内VT波动的次数来获得呼吸频率（f）。在此时间段内还测定吸气（TI）、呼气（TE）和总周期时长（TTOT）。此外，持续监测呼气末二氧化碳。还测定了动脉压（股动脉插管）和心率的相关变化。脑池内注射后，牛磺酸导致每分通气量（VE）呈剂量依赖性降低。VE的最大降幅为从495±59降至64±14毫升/分钟（p<0.05），这是由于VT（从27±3降至5±1毫升；p<0.05）和f（从18±1降至12±2次/分钟；p<0.05）均降低所致。TE和TTOT分别从2.4±0.4秒增加至4.5±0.6秒（p<0.05）和从3.7±0.4秒增加至6.4±0.8秒（p<0.05）。平均吸气流量（VT/TI），一种吸气驱动力的指标，从21±4降至4±2毫升/秒（p<0.05）。64.8微摩尔剂量后6只动物中有五只出现呼吸暂停。这种呼吸抑制在动脉压无任何显著变化的情况下发生。侧脑室注射后，牛磺酸也导致呼吸活动呈剂量依赖性降低，但程度不如前者明显。此外，在降低VE的剂量下，牛磺酸导致动脉压显著降低（p<0.05）。静脉注射牛磺酸无显著的心肺抑制作用。这些数据表明，中枢给予牛磺酸会产生呼吸抑制，并且根据中枢神经系统给药途径的不同，还会产生低血压。
