Respiratory depression produced by centrally administered taurine in the cat

The effects of taurine (0.8–64.8 umol) were studied on respiratory activity following intracisternal (cisterna magna) and intracerebroventicular (lateral ventricle) injections in cats anesthetized with alpha-chloralose. Respiratory activity was measured by using a Fleisch pneumotachograph and monitoring trachael airflow. The flow signal was integrated to obtain tidal volume (V T) and respiratory rate (f) was obtained by counting the number of V T excursions over one minute. Inspiratory (T I), expiratory (T E) and total (T TOT) cycle durations were also determined during this time period. In addition, end-tidal CO 2 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 (V̇ E). The maximal decrease in V̇ E was from 495 ± 59 to 64 ± 14 ml/min (p < 0.05), and was due to both decreases in V T (from 27 ± 3 to 5 ± 1 ml; p < 0.05) and f (from 18 ± 1 to 12 ± 2 breaths/min; p < 0.05). T E and T TOT were increased from 2.4 ± 0.4 to 4.5 ± 0.6 sec (p < 0.05) and from 3.7 ± 0.4 to 6.4 ± 0.8 sec (p < 0.05), respectively. Mean inspiratory flow (V T/T I), a measure of inspiratory drive, was decreased from 21 ± 4 to 4 ± 2 ml/sec (p < 0.05). Apnea occurred in 5 of 6 animals after the 64.8 umol 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< 0.05) in arterial pressure in doses that decreased V̇ E. 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.