Delpierre S, Jammes Y
Laboratoire de Physiologie Respiratoire, Faculté de Médecine Timone, Marseille, France.
Neurosci Lett. 1997 Apr 25;226(2):83-6. doi: 10.1016/s0304-3940(97)00240-1.
We hypothesized that hypoventilation induced by resistive loaded breathing may result in part from the inhibition of central respiratory-related structures by gamma-aminobutyric acid (GABA), through the stimulation of GABA(B) receptors. In that case, ventilatory depression should be minimized by GABA(B) receptor blockade. To test this assumption, the ventilatory effects of a GABA(B) receptor antagonist (CGP 35348) were evaluated in two groups of urethane anesthetized rabbits, breathing either through an inspiratory resistive load (IRL group) or not (Control group). CGP 35348 did not modify baseline ventilation in the Control group. On the other hand, it partially reversed IRL-induced hypoventilation through a higher respiratory rate and central inspiratory drive. These data suggest that, unlike GABA(A) receptors, GABA(B) receptors would not play a part in eupneic breathing, but that they could participate in the hypoventilation resulting from an acute increase in the work of breathing.
我们推测，由阻力负荷呼吸诱导的通气不足可能部分是由于γ-氨基丁酸（GABA）通过刺激GABA（B）受体对中枢呼吸相关结构的抑制作用所致。在这种情况下，通气抑制应通过GABA（B）受体阻断作用而减至最小。为验证这一假设，在两组经氨基甲酸乙酯麻醉的家兔中评估了GABA（B）受体拮抗剂（CGP 35348）的通气效应，一组通过吸气阻力负荷呼吸（IRL组），另一组则无此负荷（对照组）。CGP 35348对对照组的基础通气无影响。另一方面，它通过提高呼吸频率和中枢吸气驱动，部分逆转了IRL诱导的通气不足。这些数据表明，与GABA（A）受体不同，GABA（B）受体在平静呼吸中不起作用，但它们可能参与了因呼吸功急性增加而导致的通气不足。
