Wareing T H, Gruber M A, Brigham K L, Hammon J W
Department of Cardiac and Thoracic Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
J Surg Res. 1989 Jan;46(1):29-34. doi: 10.1016/0022-4804(89)90178-9.
Hydrostatic and oncotic pressures are the primary determinants of fluid movement across the pulmonary vascular membrane. The precise role of oncotic pressure in regulating transvascular fluid exchange especially when hydrostatic pressure is high is not known. Awake, adult sheep were instrumented for pressure monitoring and the collection of pulmonary lymph. A left atrial (LA) balloon catheter was utilized to control LA pressure. Statistically significant increases in lymph protein flux were seen with infusion of saline and elevated pulmonary microvascular pressure (Pmv) over elevated Pmv alone (15.3 +/- 1.23 versus 11.2 +/- 1.09 mg/min) concomitant with a decrease in plasma colloid oncotic pressure (COP) (14.9 +/- 0.5 versus 16.9 +/- 0.5 mm/Hg). The protein flux seen with elevated Pmv and saline infusion was blunted when plasma was infused (13.8 +/- 1.58 mg/min) and the plasma COP augmented (18.1 +/- 0.05 mg Hg) but was not statistically different. We conclude that under conditions of stable membrane permeability and elevated Pmv, the plasma COP appears to be an important mechanism for protection against pulmonary edema.
流体静力压和胶体渗透压是液体通过肺血管膜移动的主要决定因素。胶体渗透压在调节跨血管液体交换中的精确作用，尤其是在流体静力压较高时，尚不清楚。对清醒的成年绵羊进行仪器安装，用于压力监测和肺淋巴液的收集。使用左心房（LA）球囊导管控制左心房压力。与单独升高肺微血管压力（Pmv）相比，输注生理盐水并升高Pmv时，淋巴蛋白通量有统计学意义的增加（15.3±1.23对11.2±1.09毫克/分钟），同时血浆胶体渗透压（COP）降低（14.9±0.5对16.9±0.5毫米汞柱）。当输注血浆时，Pmv升高和生理盐水输注时所见的蛋白通量减弱（13.8±1.58毫克/分钟），血浆COP升高（18.1±0.05毫米汞柱），但无统计学差异。我们得出结论，在膜通透性稳定和Pmv升高的情况下，血浆COP似乎是预防肺水肿的重要机制。
