Camacho M T, Totapally B R, Torbati D, Wolfsdorf J
Division of Critical Care Medicine, Miami Children's Hospital, Miami, FL 33155-3009, USA.
Chest. 2001 Nov;120(5):1655-62. doi: 10.1378/chest.120.5.1655.
We tested the hypothesis that an increase in the blood colloid osmotic pressure (COP) that is maintained during early-stage endotoxemia may decrease fluid flux across capillaries and may reduce pulmonary and multiple-organ edema.
Prospective study.
Research laboratory in a hospital.
Male albino Sprague-Dawley rats.
Rats were anesthetized with pentobarbital, underwent tracheotomies, were cannulated in the femoral vein and artery, and were randomly assigned to the following four groups comprising 11 rats each: group I, controls (saline solution treatment); group II, albumin treatment (three doses of 1 g/kg 25% human albumin every 2 h); group III, endotoxin treatment with a single IV dose of 4 mg/kg endotoxin; and group IV, endotoxin and albumin-treatment (4 mg/kg endotoxin plus albumin treatment). Experiments lasted for 6 h while fluid intake was equally maintained in all groups.
COP and other variables were measured every 2 h. To determine the water content of an organ, after the rat was killed, the lung, heart, kidney, intestine, and liver were removed. Albumin treatment alone (group II) generated significant increases in COP (maximum, 58% from the baseline measurement) but did not change the water content of the organ, compared with saline solution-treated controls. Endotoxin-treated rats (group III) developed significant reductions in COP, with significant increases in pulmonary, renal, and heart water content compared with controls. Albumin treatment in endotoxemic rats (group IV) significantly increased the COP without improving the endotoxemia-induced organ edema. Pulmonary edema, however, was increased further, compared with endotoxemia alone.
COP elevation by albumin administration during the early stage of endotoxemia does not ameliorate pulmonary or multiple-organ edema and may aggravate pulmonary edema.
我们检验了这样一个假设,即在早期内毒素血症期间维持的血胶体渗透压(COP)升高可能会减少跨毛细血管的液体通量,并可能减轻肺部和多器官水肿。
前瞻性研究。
医院的研究实验室。
雄性白化病斯普拉格 - 道利大鼠。
大鼠用戊巴比妥麻醉,进行气管切开术,在股静脉和动脉插管,并随机分为以下四组,每组11只大鼠:第一组,对照组(生理盐水治疗);第二组,白蛋白治疗组(每2小时给予三剂1 g/kg 25%人白蛋白);第三组,单次静脉注射4 mg/kg内毒素进行内毒素治疗组;第四组,内毒素和白蛋白治疗组(4 mg/kg内毒素加白蛋白治疗)。实验持续6小时,同时所有组的液体摄入量均保持相等。
每2小时测量一次COP和其他变量。为了确定器官的含水量,在大鼠处死后,取出肺、心脏、肾脏、肠道和肝脏。与生理盐水治疗的对照组相比,单独白蛋白治疗(第二组)使COP显著升高(最高比基线测量值增加58%),但未改变器官的含水量。与对照组相比,内毒素治疗的大鼠(第三组)COP显著降低,肺、肾和心脏含水量显著增加。内毒素血症大鼠的白蛋白治疗(第四组)显著提高了COP,但并未改善内毒素血症引起的器官水肿。然而,与单独内毒素血症相比,肺水肿进一步加重。
在内毒素血症早期通过给予白蛋白提高COP并不能改善肺部或多器官水肿,反而可能加重肺水肿。