Tobin Antony E, Pellizzer Anne-Marie, Santamaria John D
Intensive Care Unit, St Vincent's Hospital, Melbourne, Victoria, Australia.
Respirology. 2006 Mar;11(2):182-7. doi: 10.1111/j.1440-1843.2006.00832.x.
Salbutamol (SAL) has systemic effects that may adversely influence ventilation in asthmatic patients. The authors sought to determine the magnitude of this effect and mechanisms by which i.v. SAL affects ventilation.
A prospective study of nine healthy subjects (eight men, one woman; age 23 +/- 1.4 years (SD)) was undertaken. Each subject received i.v. SAL at 5, 10 and 20 microg/min each for 30 min at each dose and was observed for 1 h post infusion. Minute ventilation ((VE)), oxygen consumption (VO(2)), CO(2) production (VCO(2)), occlusion pressure (P(0.1)), heart rate, blood pressure, respiratory rate, glucose, arterial blood gases, lactate and potassium (K(+)) were recorded at baseline and at 30-min intervals. The effect of 100% oxygen on (VE) and P(0.1) during SAL infusion at 20 microg/min was observed. Results are expressed as mean +/- SEM.
V(E) was significantly increased at 20 microg/min SAL (37.8 +/- 12.1%, P = 0.01), as were VO(2) (22.5 +/- 5.1%, P < 0.01) and VCO(2) (40.9 +/- 10.6%, P < 0.01). Ventilation was in excess of metabolic needs as demonstrated by a rise in the respiratory exchange ratio (0.87 +/- 0.03 to 0.99 +/- 0.04, P < 0.05). Serum lactate rose by 124 +/- 30.4% from baseline to 20 microg/min (1.1 +/- 0.1 to 2.3 +/- 0.25 mmol/L, P < 0.01) and base excess decreased (0.89 +/- 0.56 to vs. -1.75 +/- 0.52 mmol/L, P < 0.01) consistent with a lactic acidosis contributing to the excess ventilation. There was no significant differences in (VE) or P(0.1) with F(I)O(2) = 1.0, suggesting peripheral chemoreceptor stimulation was not responsible for the rise in (VE). At 20 microg/min SAL, K(+) fell significantly from baseline (3.8 +/- 0.06 to 2.8 +/- 0.09 mmol/L, P < 0.001).
Systemic SAL imposes ventilatory demands by increasing metabolic rate and serum lactate. This may adversely affect patients with severe asthma with limited ventilatory reserve.
沙丁胺醇（SAL）具有全身效应，可能对哮喘患者的通气产生不利影响。作者试图确定这种效应的程度以及静脉注射SAL影响通气的机制。
对9名健康受试者（8名男性，1名女性；年龄23±1.4岁（标准差））进行了一项前瞻性研究。每名受试者分别以5、10和20微克/分钟的速度静脉注射SAL，每种剂量持续30分钟，注射后观察1小时。在基线和每隔30分钟记录分钟通气量（（VE））、耗氧量（VO(2)）、二氧化碳产生量（VCO(2)）、阻断压（P(0.1)）、心率、血压、呼吸频率、血糖、动脉血气、乳酸和钾（K(+)）。观察在以20微克/分钟的速度注射SAL期间100%氧气对（VE）和P(0.1)的影响。结果以平均值±标准误表示。
在20微克/分钟的SAL剂量下，V(E)显著增加（37.8±12.1%，P = 0.01），VO(2)（22.5±5.1%，P < 0.01）和VCO(2)（40.9±10.6%，P < 0.01）也显著增加。呼吸交换率升高（从0.87±0.03升至0.99±0.04，P < 0.05）表明通气超过了代谢需求。血清乳酸从基线到20微克/分钟时升高了124±30.4%（从1.1±0.1升至2.3±0.25毫摩尔/升，P < 0.01），碱剩余降低（从0.89±0.56降至-1.75±0.52毫摩尔/升，P < 0.01），这与乳酸酸中毒导致通气过度一致。当F(I)O(2)=1.0时，（VE）或P(0.1)没有显著差异，表明外周化学感受器刺激不是（VE）升高的原因。在20微克/分钟的SAL剂量下，K(+)从基线显著下降（从3.8±0.06降至2.8±0.09毫摩尔/升，P < 0.001）。
全身性SAL通过提高代谢率和血清乳酸来增加通气需求。这可能对通气储备有限的重度哮喘患者产生不利影响。
