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Article
March 1988

Pulmonary Microvascular Changes Following Fluid Resuscitation in an Ovine Model of Endotoxemia

Author Affiliations

From the Departments of Anesthesiology (Drs Lubbesmeyer, Irei, and Traber, and Ms Traber) and Surgery (Dr Herndon), University of Texas Medical Branch, and the Departments of Anesthesia Research (Drs Lubbesmeyer, Kimura, and Traber, and Ms Traber) and Surgery (Drs Maguire and Herndon), Shriners Burns Institute, Galveston; Department of Plastic Surgery, Tokyo Women's Medical College (Dr Kimura); and Department of Anesthesiology and Intensive Care Medicine, Westfalian Wilhelms University, Münster, West Germany (Dr Lubbesmeyer).

Arch Surg. 1988;123(3):345-350. doi:10.1001/archsurg.1988.01400270079012
Abstract

• Fluid resuscitation is complicated in hypotensive septic patients by their susceptibility to pulmonary edema. This problem was evaluated in the ovine model of endotoxemia with a chronic lung lymph fistula. Escherichia coli endotoxin (lipopolysaccharide, 1.5 μg/kg) was given intravenously over 30 minutes. Group M (n=9) continued to receive baseline fluids (2 mL/kg/h), while group R (n=6) received 7 mL/kg/h of Ringer's lactate. After an initial drop in cardiac index, animals in both groups developed a hyperdynamic state. The fall in mean arterial pressure seen in group M was absent from group R. The higher fluid volume resulted in a rise in left atrial pressure and pulmonary microvascular pressure. The lung lymph flow and permeability index were elevated in both groups but were higher in group R. The calculated filtration coefficient showed a threefold increase in both groups. Augmented fluid resuscitation during endotoxemia resulted in an elevated interstitial fluid flux and permeability index secondary to an increase in pulmonary microvascular pressure and greater surface area of the injured microvascular beds being perfused.

(Arch Surg 1988;123:345-350)

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