Fauroux B, Isabey D, Desmarais G, Brochard L, Harf A, Lofaso F
Service de Physiologie, Explorations Fonctionnelles, Institut National de la Santé et de la Recherche Médicale U 492, Hôpital Henri Mondor, 94010 Créteil, France.
J Appl Physiol (1985). 1998 Dec;85(6):2169-75. doi: 10.1152/jappl.1998.85.6.2169.
To determine whether nonchemical inhibition of respiratory activity occurs during inspiratory pressure support (IPS) ventilation (IPSV), respiratory motor output (in 9 subjects), obtained by calculating transdiaphragmatic pressure-time products, and central respiratory output (in 5 subjects), obtained by integrating the electromyographic activity of the diaphragm (EMGdi) during mechanical inspiratory time, EMGdi per minute, and electrical inspiratory time, as determined from onset to peak EMGdi, were compared during spontaneous ventilation (control) and IPSV with (IPS+CO2) and without (IPS) correction of hypocapnia. Both IPS and IPS+CO2 induced significant decreases in transdiaphragmatic pressure-time products (46 +/- 31 and 53 +/- 23%, respectively), EMGdi during mechanical inspiratory time (49 +/- 12 and 57 +/- 14%, respectively), EMGdi per minute (65 +/- 22 and 69 +/- 15%, respectively), and electrical inspiratory time (73 +/- 8 and 65 +/- 6%, respectively). Because correction of hypocapnia failed to eliminate the marked inhibition of both respiratory and central motor output seen with IPS, we conclude that nonchemical inhibition of respiratory activity occurs during IPSV.
为了确定在吸气压力支持(IPS)通气(IPSV)过程中是否会出现呼吸活动的非化学性抑制,我们比较了在自主通气(对照)以及伴有(IPS+CO2)和不伴有(IPS)低碳酸血症校正的IPSV期间,通过计算跨膈压-时间乘积获得的呼吸运动输出(9名受试者),以及通过在机械吸气时间内整合膈肌肌电图活动(EMGdi)、每分钟EMGdi以及从EMGdi起始到峰值确定的电吸气时间获得的中枢呼吸输出(5名受试者)。IPS和IPS+CO2均导致跨膈压-时间乘积(分别为46±31%和53±23%)、机械吸气时间内的EMGdi(分别为49±12%和57±14%)、每分钟EMGdi(分别为65±22%和69±15%)以及电吸气时间(分别为73±8%和65±6%)显著降低。由于低碳酸血症的校正未能消除IPS所见的对呼吸和中枢运动输出的明显抑制,我们得出结论,在IPSV期间会出现呼吸活动的非化学性抑制。