The American surgeon
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Diffuse lung injury (acid aspiration) and a modest intravascular volume deficit (15% total blood volume) were produced in mongrel dogs. Replacement of lost volume was with shed blood plus an equal volume hydroxy ethyl starch (Group I) or shed blood plus balanced salt solution (3 ml/ml shed blood). Extravascular lung value (EVLW) measurements were used to quantitate edema formation and alveolar arterial oxygen gradient (A-a and O2) was monitored on a reflection of hypoxia. No significant differences were observed in A-a and O2 between groups despite a significantly larger amount of pulmonary edema in Group I (hydroxy ethyl starch).
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The American surgeon · Dec 1983
Measurement of extravascular lung water in sheep during colloid and crystalloid resuscitation from smoke inhalation.
The pathophysiology of pulmonary inhalation injury, a major cause of morbidity and mortality from fires, is poorly understood. To examine the effects of colloid and crystalloid resuscitation on extravascular lung water (EVLW) during a standard smoke inhalation injury, we subjected 12 sheep to 8 minutes of cool pine smoke inhalation. The animals were then resuscitated to a pulmonary capillary wedge pressure (PCWP) of 10 +/- 1.5 mm Hg with either lactated Ringer's solution or plasma protein derivative. ⋯ The increases in EVLW were associated with progressive hypoxia, which was worse in the crystalloid group. In the crystalloid group, COP decreased from 27.3 +/- 0.9 to 14.2 +/- 0.4 mm Hg and intravascular driving force (COP-PCWP) dropped from 17.6 to 3.26 +/- 1.5 mm Hg; COP and COP-PCWP were maintained in the colloid group. These data demonstrate that supporting serum COP minimizes the increase in EVLW with smoke inhalation injury and suggests that smoke inhalation does not lead to a dramatic increase in alveolar capillary membrane permeability to protein.