Bacteremic sepsis disturbs alveolar perfusion distribution in the lungs of rats

Sepsis often leads to lung injury, although the mechanisms that initiate this are unclear. One preinjury phenomenon that has not been explored previously is the effect of bacterial (nonlipopolysaccharide) sepsis on the distribution of alveolar perfusion. The goals of our studies were to measure this.

Randomized, controlled, prospective animal study.

University animal laboratory.

Male Sprague-Dawley rats (450-550 g).

We induced sepsis by placing gelatin capsules containing Escherichia coli and Bacteroides fragilis into the abdomens of rats (n = 9). Empty capsules (n = 6) were placed into the abdomens of controls. After 24 hrs, 4-microm-diameter fluorescent latex particles (2 x 10(8)) were infused into the pulmonary circulation. Sepsis was induced in additional rats and controls to assess lung injury, as follows: Lung histology was performed on eight septic rats and on seven controls; lung lavage was performed on three septic rats and three controls after their plasma albumin had been labeled with Evans blue dye.

Confocal microscopy was used to prepare digital maps of latex particle trapping patterns (eight per lung). Analysis of these patterns revealed statistically more clustering (perfusion inhomogeneity) down to tissue volumes less than that of ten alveoli in septic lungs compared with controls (p < or = .05). Bacterial counts and neutrophil counts were significantly higher in the circulation of septic rats (p < or = .05). Blood pressures and arterial PO2s were unchanged. Cell counts in histological images were three-fold higher in septic lungs than in controls (p < or = .05). Lung lavage revealed 0.41 +/- 0.03 mL of plasma in the lungs of septic rats, and 0.06 +/- 0.05 mL in the lungs of controls (p < or = .05).

Bacterial sepsis caused significant maldistribution of interalveolar perfusion in the lungs of rats in the absence of significant lung injury.