From the Sorbonne Universités, UPMC Univ Paris-06, UMRS INSERM 1166, IHU ICAN (P.M., J.A., B.R.), UMRS INSERM 1158 (A.D.), UMRS INSERM 974, Centre de Recherche en Myologie (C.C.), Paris, France; Department of Emergency Medicine and Surgery (B.R.), and Department of Anesthesiology and Critical Care (S.C., O.L.), Groupe hospitalier Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, Paris, France; Université de la Méditerranée, Department of Emergency Medicine and Surgery, Hôpital de la Timone, Assistance Publique-Hôpitaux de Marseille, Marseille, France (P.M.).
Anesthesiology. 2015 Apr;122(4):876-83. doi: 10.1097/ALN.0000000000000574.
Acute respiratory acidosis is associated with alterations in diaphragm performance. The authors compared the effects of respiratory acidosis and metabolic acidosis in the rat diaphragm in vitro.
Diaphragmatic strips were stimulated in vitro, and mechanical and energetic variables were measured, cross-bridge kinetics calculated, and the effects of fatigue evaluated. An extracellular pH of 7.00 was obtained by increasing carbon dioxide tension (from 25 to 104 mmHg) in the respiratory acidosis group (n = 12) or lowering bicarbonate concentration (from 24.5 to 5.5 mM) in the metabolic acidosis group (n = 12) and the results compared with a control group (n = 12, pH = 7.40) after 20-min exposure.
Respiratory acidosis induced a significant decrease in maximum shortening velocity (-33%, P < 0.001), active isometric force (-36%, P < 0.001), and peak power output (-59%, P < 0.001), slowed relaxation, and decreased the number of cross-bridges (-35%, P < 0.001) but not the force per cross-bridge, and impaired recovery from fatigue. Respiratory acidosis impaired more relaxation than contraction, as shown by impairment in contraction-relaxation coupling under isotonic (-26%, P < 0.001) or isometric (-44%, P < 0.001) conditions. In contrast, no significant differences in diaphragmatic contraction, relaxation, or contraction-relaxation coupling were observed in the metabolic acidosis group.
In rat diaphragm, acute (20 min) respiratory acidosis induced a marked decrease in the diaphragm contractility, which was not observed in metabolic acidosis.
急性呼吸性酸中毒与膈肌功能改变有关。作者比较了大鼠膈肌体外呼吸性酸中毒和代谢性酸中毒的影响。
体外刺激膈神经,测量力学和能量学变量,计算横桥动力学,并评估疲劳的影响。呼吸性酸中毒组(n = 12)通过增加二氧化碳分压(从 25 至 104mmHg),将细胞外 pH 调节至 7.00;代谢性酸中毒组(n = 12)通过降低碳酸氢盐浓度(从 24.5 至 5.5mM),将细胞外 pH 调节至 7.00,并与对照组(n = 12,pH = 7.40)比较 20 分钟后的结果。
呼吸性酸中毒显著降低了最大缩短速度(-33%,P < 0.001)、主动等长力(-36%,P < 0.001)和峰值功率输出(-59%,P < 0.001),减慢了舒张,并减少了横桥数量(-35%,P < 0.001),但不影响每根横桥的力,并损害了疲劳的恢复。与代谢性酸中毒组相比,呼吸性酸中毒组舒张受损更为严重,表现为等张(-26%,P < 0.001)或等长(-44%,P < 0.001)条件下的收缩-舒张偶联受损。相反,代谢性酸中毒组的膈神经收缩、舒张或收缩-舒张偶联无明显差异。
在大鼠膈肌中,急性(20 分钟)呼吸性酸中毒引起膈肌收缩力明显下降,而代谢性酸中毒则未观察到。