Effects of endotoxemia on pulmonary vascular resistances in unanesthetized sheep

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Abstract
Ten experiments were conducted on nine sheep to determine the effects of endotoxemia (1.0 .mu.g/kg iv over 15 min) on the vascular resistances of two segments of the pulmonary circulation. The first segment (S1) was from the main pulmonary artery to the site in the pulmonary veins corresponding to the pressure measured with a deflated and wedged 7-Fr Swan-Ganz catheter. The second segment (S2) was from the wedge pressure measurement site to the left atrium. Endotoxemia caused both pulmonary arterial pressure and pulmonary arterial wedge pressure to increase significantly during early (phase 1) and late (phase 2) periods of response; left atrial pressure was significantly decreased during both phases. Normalized cardiac output decreased significantly at 35 and 180 min but not at 240 min after starting endotoxin infusion. The calculated resistance of S1 significantly increased from a base-line value of 3.03 .+-. 0.31 (cmH2O .cntdot. l-1 .cntdot. min) to 7.60 .+-. 0.71, 6.34 .+-. 1.22, and 6.66 .+-. 1.35 at 35, 180, and 240 min, respectively. Calculated resistance of S2 was 1.32 .+-. 0.14 at base line and increased significantly to 11.43 .+-. 1.66 at 35 min, 4.45 .+-. 0.47 at 180 min, and 3.32 .+-. 0.61 at 240 min. The calculated percent of total pulmonary resistance in S2 increased significantly from $ 31 to 59% during phase 1 and remained significantly increased at 41% from 90 to 180 min after endotoxin. Hematocrit increased by 40% at 35 min, whereas plasma total protein concentration increased by only 8% at 35 min. We conclude that endotoxemia caused intense pulmonary venoconstriction during phase 1, and venoconstriction persisted at a lesser degree during phase 2. The resulting increased pressure in lung microvessels would contribute to increased filtration of fluid into the lungs during endotoxemia.