Moore Jonathan P, Hainsworth Roger, Drinkhill Mark J
Institute for Cardiovascular Research, The School of Medicine, University of Leeds, Leeds LS2 9JT, UK.
J Physiol. 2004 Mar 16;555(Pt 3):805-14. doi: 10.1113/jphysiol.2003.057919. Epub 2004 Jan 23.
Distension of the main pulmonary artery and its bifurcation are known to result in a reflex vasoconstriction and increased respiratory drive; however, these responses are observed at abnormally high distending pressures. In this study we recorded afferent activity from pulmonary arterial baroreceptors to investigate their stimulus-response characteristics and to determine whether they are influenced by physiological changes in intrathoracic pressure. In chloralose-anaesthetized dogs, a cardiopulmonary bypass was established, the pulmonary trunk and its main branches were vascularly isolated and perfused with venous blood at pulsatile pressures designed to simulate the normal pulmonary arterial pressure waveform. Afferent slips of a cervical vagus were dissected and nerve fibres identified that displayed discharge patterns with characteristics expected from pulmonary arterial baroreceptors. Recordings were obtained with (a) chest open (b) chest closed and resealed, and (c) with phasic negative intrathoracic pressures in the resealed chest. Pressure-discharge characteristics obtained in the open-chest animals indicated that the threshold pulmonary pressure (corresponding to 5% of the overall response) was 17.1 +/- 2.9 and the inflexion point of the curve was 29.2 +/- 3.3 mmHg (mean +/-S.E.M). In closed-chest animals the threshold and inflexion pressures were reduced to 12.0 +/- 1.7 and 20.7 +/- 1.8 mmHg. Application of phasic negative intrathoracic pressures further reduced the threshold and inflexion pressures to 9.5 +/- 1.2 mmHg (P < 0.05 vs. open) and 14.7 +/- 0.8 mmHg (P < 0.003 vs. open and P < 0.02 vs. atmospheric). These results indicate that under physiological conditions, with closed-chest and phasic negative intrathoracic pressure changes similar to those associated with normal breathing, activity from pulmonary baroreceptors is obtained at physiological pulmonary arterial pressures in intact animals.
已知主肺动脉及其分叉处的扩张会导致反射性血管收缩和呼吸驱动增加;然而,这些反应是在异常高的扩张压力下观察到的。在本研究中,我们记录了肺动脉压力感受器的传入活动,以研究其刺激-反应特性,并确定它们是否受胸内压生理变化的影响。在水合氯醛麻醉的犬中,建立体外循环,将肺动脉干及其主要分支进行血管分离,并用脉动压力的静脉血灌注,该脉动压力旨在模拟正常肺动脉压力波形。解剖颈迷走神经的传入分支,识别出显示出肺动脉压力感受器预期特征放电模式的神经纤维。在以下三种情况下进行记录:(a) 开胸;(b) 开胸后关闭并重新缝合;(c) 重新缝合胸腔时施加阶段性胸内负压。开胸动物获得的压力-放电特性表明,阈值肺动脉压(对应于总反应的5%)为17.1±2.9,曲线拐点为29.2±3.3 mmHg(平均值±标准误)。在闭胸动物中,阈值和拐点压力分别降至12.0±1.7和20.7±1.8 mmHg。施加阶段性胸内负压进一步将阈值和拐点压力分别降至9.5±1.2 mmHg(与开胸相比P<0.05)和14.7±0.8 mmHg(与开胸相比P<0.003,与大气压相比P<0.02)。这些结果表明,在生理条件下,当胸壁闭合且胸内压阶段性负压变化类似于正常呼吸相关变化时,在完整动物的生理肺动脉压下可获得来自肺压力感受器的活动。