Moore Jonathan P, Hainsworth Roger, Drinkhill Mark J
Institute for Cardiovascular Research, School of Medicine, University of Leeds, Leeds LS2 9JT, UK.
J Physiol. 2004 Mar 16;555(Pt 3):815-24. doi: 10.1113/jphysiol.2003.057968. Epub 2004 Jan 14.
We investigated whether the reflex responses to stimulation of pulmonary arterial baroreceptors were altered by intrathoracic pressure changes similar to those encountered during normal breathing. Dogs were anaesthetized with alpha-chloralose, a cardiopulmonary bypass was established, and the pulmonary trunk and its main branches as far as the first lobar arteries were vascularly isolated and perfused with venous blood. The chest was closed following connection to the perfusion circuit and pressures distending the aortic arch, carotid sinus and coronary artery baroreceptors were controlled. Changes in the descending aortic (systemic) perfusion pressure (SPP; flow constant) were used to assess changes in systemic vascular resistance. Values of SPP were plotted against mean pulmonary arterial pressure (PAP) and sigmoid functions applied. From these curves we derived the threshold pressures (corresponding to 5% of the overall response of SPP), the maximum slopes (equivalent to peak gain) and the corresponding PAP (equivalent to 'set point'). Stimulus-response curves were compared between data obtained with intrathoracic pressure at atmospheric and with a phasic intrathoracic pressure ranging from atmospheric to around -10 mmHg (18 cycles min(-1)). Results were obtained from seven dogs and are given as means +/-S.E.M. Compared to the values obtained when intrathoracic pressure was at atmospheric, the phasic intrathoracic pressure decreased the pulmonary arterial threshold pressure in five dogs; average change from 28.4 +/- 5.9 to 19.3 +/- 5.9 mmHg (P > 0.05). The inflexion pressure was significantly reduced from 37.8 +/- 4.8 to 27.4 +/- 4.0 mmHg (P < 0.03), but the slopes of the curves were not consistently changed. These results have shown that a phasic intrathoracic pressure, which simulates respiratory oscillations, displaces the stimulus-response curve of the pulmonary arterial baroreceptors to lower pressures so that it lies within a physiological range of pressures.
我们研究了肺动脉压力感受器对刺激的反射反应是否会因胸腔内压力变化而改变，这种压力变化类似于正常呼吸时所遇到的情况。用α-氯醛糖麻醉狗，建立体外循环，将肺动脉干及其主要分支直至第一叶动脉进行血管分离，并用静脉血灌注。连接到灌注回路后关闭胸腔，并控制扩张主动脉弓、颈动脉窦和冠状动脉压力感受器的压力。通过降主动脉（全身）灌注压力（SPP；流量恒定）的变化来评估全身血管阻力的变化。将SPP值与平均肺动脉压（PAP）绘制在一起，并应用S形函数。从这些曲线中，我们得出阈值压力（相当于SPP总体反应的5%）、最大斜率（相当于峰值增益）以及相应的PAP（相当于“设定点”）。比较了胸腔内压力处于大气压时和胸腔内压力在大气压至约-10 mmHg（18次/分钟）范围内波动时所获得的数据之间的刺激-反应曲线。结果来自7只狗，以平均值±标准误表示。与胸腔内压力处于大气压时获得的值相比，胸腔内压力波动使5只狗的肺动脉阈值压力降低；平均变化从28.4±5.9 mmHg降至19.3±5.9 mmHg（P>0.05）。拐点压力从37.8±4.8 mmHg显著降低至27.4±4.0 mmHg（P<0.03），但曲线斜率并未持续改变。这些结果表明，模拟呼吸振荡的胸腔内压力波动会使肺动脉压力感受器的刺激-反应曲线向更低压力方向移动，从而使其处于生理压力范围内。
