Walley Keith R, McDonald Treena E, Wang Yingjin, Dai Shelley, Russell James A
University of British Columbia McDonald Research Laboratories/iCAPTURE Center, Vancouver, Canada.
Crit Care Med. 2003 Jan;31(1):187-94. doi: 10.1097/00003246-200301000-00029.
Hypotension and hypoperfusion during septic shock may contribute to tissue hypoxia and the intramyocardial inflammatory response that results in myocardial dysfunction. Therefore, we hypothesized that crystalloid or colloid resuscitation may alter myocardial dysfunction.
Randomized, controlled, prospective animal study.
University animal laboratory.
Sprague-Dawley rats (250-300 g, n = 6/group).
Rats received an intraperitoneal injection of 10 mg/kg lipopolysaccharide or control. One hour later, rats were randomized to intravenous resuscitation and received either 30 mL/kg normal saline, 10 mL/kg 10% pentastarch, 10 mL/kg 5% rat albumin, or no volume.
We measured fractional shortening of cardiomyocytes isolated 5 hrs after lipopolysaccharide or control injection. In separate identical experiments, we measured myocardial interleukin-6, macrophage inhibitory protein-2, and nitric oxide synthase II protein and messenger RNA expression. Control fractional shortening of 24.1 +/- 2.2% was decreased by lipopolysaccharide to 18.8 +/- 1.2% (p <.001). Volume resuscitation after lipopolysaccharide significantly improved fractional shortening (p <.001). In particular, albumin resuscitation increased fractional shortening to 23.5 +/- 0.9%, which was more than either saline (fractional shortening 20.1 +/- 1.7%,p <.01) or pentastarch (fractional shortening 21.4 +/- 0.9%,p <.01). Myocardial macrophage inhibitory protein-2 protein and interleukin-6 and macrophage inhibitory protein-2 messenger RNA expression and neutrophil content were elevated following lipopolysaccharide (p <.05) but were not altered by volume resuscitation. Myocardial nitric oxide synthase II protein and messenger RNA expression increased following lipopolysaccharide (p <.01) and decreased with albumin resuscitation.
We conclude that following lipopolysaccharide injection, volume resuscitation improves cardiomyocyte fractional shortening. Albumin resuscitation is particularly beneficial in preventing reduced cardiomyocyte contractility, and this benefit may be related to an albumin-induced reduction in nitric oxide synthase II protein and messenger RNA expression following endotoxin injection.
脓毒性休克期间的低血压和低灌注可能导致组织缺氧以及引起心肌功能障碍的心肌内炎症反应。因此，我们推测晶体液或胶体液复苏可能会改变心肌功能障碍。
随机、对照、前瞻性动物研究。
大学动物实验室。
斯普拉格-道利大鼠（250 - 300克，每组n = 6只）。
大鼠腹腔注射10毫克/千克脂多糖或对照物。1小时后，将大鼠随机分组进行静脉复苏，分别给予30毫升/千克生理盐水、10毫升/千克10% 羟乙基淀粉、10毫升/千克5% 大鼠白蛋白，或不给予液体。
我们测量了脂多糖或对照物注射5小时后分离出的心肌细胞的缩短分数。在单独的相同实验中，我们测量了心肌白细胞介素-6、巨噬细胞抑制蛋白-2以及一氧化氮合酶II的蛋白和信使核糖核酸表达。脂多糖使对照的缩短分数从24.1±2.2%降至18.8±1.2%（p <.001）。脂多糖注射后的液体复苏显著改善了缩短分数（p <.001）。特别是，白蛋白复苏使缩短分数增加到23.5±0.9%，高于生理盐水组（缩短分数20.1±1.7%，p <.01）或羟乙基淀粉组（缩短分数21.4±0.9%，p <.01）。脂多糖注射后心肌巨噬细胞抑制蛋白-2蛋白、白细胞介素-6以及巨噬细胞抑制蛋白-2信使核糖核酸表达和中性粒细胞含量升高（p <.05），但液体复苏未改变这些指标。脂多糖注射后心肌一氧化氮合酶II蛋白和信使核糖核酸表达增加（p <.01），而白蛋白复苏使其降低。
我们得出结论，脂多糖注射后，液体复苏可改善心肌细胞缩短分数。白蛋白复苏在预防心肌细胞收缩力降低方面特别有益，这种益处可能与内毒素注射后白蛋白诱导一氧化氮合酶II蛋白和信使核糖核酸表达降低有关。
