What Factors Increase the Pulmonary Transvascular Fluid Flux

Pulmonary vascular permeability is regulated by several factors. Starling's equation tells us what is involved:

where Q is the net flux of fluid out of the microvasculature, K is the filtration coefficient (an index of microvascular permeability to small molecules), Pc and P; are the hydrostatic pressures in the capillary and interstitial spaces, respectively, pc and p are the corresponding colloid osmotic pressures, and s is the reflection coefficient; an index of the microvascular permeability to protein. The reflection coefficient is reduced when endothelial cells are injured and the permeability increases. The reflection coefficient is reduced and the pulmonary microvascular pressure is increased with ALI [3].

As we mentioned earlier, the blood flow to the lung is supplied by the pulmonary and bronchial arteries. In the normal condition, the bronchial arterial blood flow is approximately 1 percent of cardiac output. However, in the pathologic condition, it increases tenfold to fifteenfold. The marked reduction in bronchial vascular resistance results in an increase in microvascular pressure (Pc) and airway edema formation [3]. Some of the edema formed also leaks into the airway lumen. The airway fluid formed has a high protein content, suggesting that the bronchial microvas-culature has also become leaky to colloid. In our ovine ALI model with burn and smoke inhalation injury, the increase in bronchial blood flow was significantly inhibited by specific

Figure 1 Under normal conditions (left), microvascular blood flow is regulated by endothelial cells. Several anticoagulant mechanisms as well as PGI2 and NO production are involved in regulating microvascular circulation. When the endothelial cells are activated by inflammatory cytokines or endotoxin (right), adhesion molecules are expressed and neutrophils accumulate in the lung. Also, the activated neutrophil-induced endothelial injury causes an increase in vascular permeability, which results in edema formation. Exudates in the airways make clots and cause ventilation-perfusion mismatching. (see color insert)

Figure 1 Under normal conditions (left), microvascular blood flow is regulated by endothelial cells. Several anticoagulant mechanisms as well as PGI2 and NO production are involved in regulating microvascular circulation. When the endothelial cells are activated by inflammatory cytokines or endotoxin (right), adhesion molecules are expressed and neutrophils accumulate in the lung. Also, the activated neutrophil-induced endothelial injury causes an increase in vascular permeability, which results in edema formation. Exudates in the airways make clots and cause ventilation-perfusion mismatching. (see color insert)

iNOS and nNOS inhibitors, suggesting that the bronchial blood flow is regulated by both iNOS and nNOS [4, 5].

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Essentials of Human Physiology

Essentials of Human Physiology

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