Gnidec A G, Finley R R, Sibbald W J
Richard Ivey Critical Care Trauma Centre, Victoria Hospital, London, Ontario, Canada.
Chest. 1988 Jan;93(1):180-6. doi: 10.1378/chest.93.1.180.
The effect on pulmonary fluid balance of adrenergic receptor agonist agents commonly employed in clinical sepsis has not been well characterized. Therefore, we tested the hypothesis that dobutamine would increase pulmonary microvasular fluid flux in experimental sepsis-induced lung injury. To define the effects of this synthetic catecholamine on pulmonary lymph flow (QL), we infused dobutamine in sheep at two doses in sequence (5 micrograms/kg/min and 10 micrograms/kg/min) before and after the induction of intraperitoneal sepsis which resulted in the development of lung microvascular injury. In the nonseptic state, cardiac output increased at both 5 micrograms/kg/min and 10 micrograms/kg/min (22 and 36 percent, respectively), while QL was unchanged from baseline (for 5 micrograms, delta QL = +0.44 +/- 1.35 ml/15 min; not significant) (for 10 micrograms, delta QL = -0.20 +/- 1.0 ml/15 min; not significant). Values for the ratio of lymph/plasma total protein levels [( L/P]TP) fell modestly in the nonseptic study at both doses (p less than 0.05). With established sepsis syndrome, QL increased from the nonseptic baseline study (2.99 +/- 1.8 to 7.01 +/- 3.95 ml/15 min; p less than 0.05), without change in [L/P]TP ratios or the calculated microvascular hydrostatic pressure. (Pmv) During sepsis, dobutamine infusion was again associated with an increase in cardiac output at both the 5 micrograms/kg/min (+29 percent) and 10 micrograms/kg/min (+33 percent) doses, while QL increased modestly only with the lower dose of dobutamine infused (5 micrograms/kg/min, delta QL = 1.80 +/- 2.2 ml/15 min; p less than 0.05). In this model of sepsis-induced lung injury, dobutamine increased systemic flow without substantially augmenting QL.
临床脓毒症中常用的肾上腺素能受体激动剂对肺液体平衡的影响尚未得到充分阐明。因此,我们检验了以下假设:多巴酚丁胺会增加实验性脓毒症诱导的肺损伤中的肺微血管液体通量。为了确定这种合成儿茶酚胺对肺淋巴流量(QL)的影响,我们在腹腔内脓毒症诱导并导致肺微血管损伤前后,按顺序以两种剂量(5微克/千克/分钟和10微克/千克/分钟)给绵羊输注多巴酚丁胺。在非脓毒症状态下,5微克/千克/分钟和10微克/千克/分钟剂量时心输出量均增加(分别增加22%和36%),而QL与基线相比无变化(5微克时,ΔQL = +0.44±1.35毫升/15分钟;无显著差异)(10微克时,ΔQL = -0.20±1.0毫升/15分钟;无显著差异)。在非脓毒症研究中,两种剂量下淋巴/血浆总蛋白水平比值[(L/P)TP]均略有下降(p<0.05)。在已确立脓毒症综合征时,QL从非脓毒症基线研究时增加(2.99±1.8至7.01±3.95毫升/15分钟;p<0.05),而(L/P)TP比值或计算出的微血管静水压(Pmv)无变化。在脓毒症期间,输注多巴酚丁胺在5微克/千克/分钟(增加29%)和10微克/千克/分钟(增加33%)剂量时再次与心输出量增加相关,而仅在输注较低剂量多巴酚丁胺(5微克/千克/分钟)时QL适度增加(ΔQL = 1.80±2.2毫升/15分钟;p<0.05)。在这种脓毒症诱导的肺损伤模型中,多巴酚丁胺增加了全身血流,但未显著增加QL。