Guyenet P G, Darnall R A, Riley T A
Department of Pharmacology, University of Virginia School of Medicine, Charlottesville 22908.
Am J Physiol. 1990 Nov;259(5 Pt 2):R1063-74. doi: 10.1152/ajpregu.1990.259.5.R1063.
The respiratory modulation of the lumbar sympathetic nerve discharge (LSND) was examined in halothane-anesthetized, paralyzed, and vagotomized rats by means of phrenic nerve discharge (PND)-triggered histograms. The respiratory modulation was 1) proportional to PND amplitude during chemoreceptor activation with CO2 and 2) reduced at elevated arterial pressure. Bilateral injections of bicuculline [gamma-aminobutyric acid (GABA)A receptor antagonist, n = 5] into the rostral ventrolateral medulla (RVLM), but not into medullary raphe, reversibly increased mean arterial pressure (MAP) and resting LSND, decreased the baroreflex, reduced PND amplitude and central respiratory rate, and greatly magnified the respiratory modulation of LSND. Injections of strychnine (glycine receptor antagonist, n = 5) or phaclofen (GABAB receptor antagonist, n = 2) into RVLM were without effect. Injections of kynurenic acid (excitatory amino acid receptor antagonist) into RVLM (n = 8), but not raphe (n = 3), reduced PND amplitude, increased central respiratory rate, reduced MAP, elevated resting LSND slightly, and greatly reduced the respiratory modulation of LSND. These data suggest that the rostral tip of the ventrolateral medulla represents a critical link between the central respiratory rhythm generator and the vasomotor outflow. Also, it indicates that the respiratory modulation of SND does not involve a gating of the activity of the medullary neurons that convey baroreceptor information to RVLM sympathoexcitatory neurons.
通过膈神经放电（PND）触发直方图，在氟烷麻醉、麻痹和迷走神经切断的大鼠中检测腰交感神经放电（LSND）的呼吸调制。呼吸调制表现为：1）在二氧化碳激活化学感受器期间，与PND幅度成比例；2）在动脉压升高时降低。向延髓头端腹外侧（RVLM）双侧注射荷包牡丹碱（γ-氨基丁酸（GABA）A受体拮抗剂，n = 5），而不是向中缝髓质注射，可使平均动脉压（MAP）和静息LSND可逆性升高，压力反射降低，PND幅度和中枢呼吸频率降低，并极大地放大了LSND的呼吸调制。向RVLM注射士的宁（甘氨酸受体拮抗剂，n = 5）或巴氯芬（GABAB受体拮抗剂，n = 2）无效。向RVLM（n = 8）而非中缝髓质（n = 3）注射犬尿氨酸（兴奋性氨基酸受体拮抗剂），可降低PND幅度，增加中枢呼吸频率，降低MAP，轻微升高静息LSND，并极大地降低LSND的呼吸调制。这些数据表明，延髓腹外侧的头端是中枢呼吸节律发生器与血管运动输出之间的关键联系。此外，这表明SND的呼吸调制不涉及将压力感受器信息传递给RVLM交感兴奋神经元的髓质神经元活动的门控。
