Objectives: 

Bacterial infection might represent one of primary etiological agents inducing atherosclerosis and heart injury. Both are linked with endothelial dysfunction (ED) characterized by reduced NO availability and increased endothelial permeability. We studied the effect of bacterial endotoxin (LPS) on: 1) micro- and macro-vascular endothelial structure, 2) coronary flow of the rat heart before and after ischemia/reperfusion (I/R).

Materials: 

Inflammation was induced by a single dose of LPS (E.coli, 1 mg/kg, i.p.) in adult male Wistar rats (W). 10 days after LPS administration, tissues of left ventricle (LV) and aorta were processed for electron-microscopy. Changes in coronary flow, induced by 25-min ischemia followed by 25-min reperfusion in Langendorff perfused hearts and NO-dependent relaxation of aorta were studied in control and endotoxemic rats. Myocardial and aortic NOS activities were measured as well. At the end of experiments, selected biomarkers (NAGA, MDA, C-RP) were measured in plasma.

Results: 

LPS significantly increased levels of biomarkers, indicating cell injury, oxidative stress and inflammation. Local heterogeneous subcellular abnormalities of endothelial cells (EC) were seen in LV and the aorta, characterizing ED and changes in endothelial permeability. Correlating, enhanced NOS activity was demonstrated in tissue of LV and aorta of endotoxemic rats compared to controls. In addition, some structural alterations of EC observed in the heart indicate presence of angiogenesis. Reduced coronary flow by 31% before I/R and by 20% after I/R and impaired NO-dependent relaxation of aorta demonstrate prevalence of degradative processes in endotoxemic rats.

Conclusions: 

The results indicate that a single bacterial insult can induce the structural abnormalities of vascular endothelial monolayer, which may contribute to injury of aortic function as well as to increased predisposition of the heart to I/R. Supported by VEGA 2/0108/10.