VULNERABILITY OF VASCULAR ENDOTHELIUM IN LIPOPOLYSACCHARIDE TOXICITY - EFFECT OF (ACYL) CARNITINE ON ENDOTHELIAL STABILITY

THE literature presented illustrates that lipopolysaccharide (LPS), fr om bacterial cell walls, induces tumour necrosis factor (TNF) synthesi s in macrophages. TNF affects a number of cell types, amongst which ar e endothelial cells, within a few hours. Its inj ection has been shown to produce all symptoms of the toxic syndrome. In the present communi cation the vulnerability of endothelial cells will be stressed. These cells require carnitine not only for fatty acid oxidation but also for membrane protection and repair. As endothelial cells lose carnitine d uring hypoperfusion, it is speculated that the supply of carnitine dur ing the early phase of LPS toxicity in rats might delay or avoid loss of endothelial functions. Earlier it was observed that hearts from rat s, injected 3 h previously with LPS, showed strongly increased interst itial fluid production compared to hearts from control rats, even when TNF was present during a 3 h in vitro perfusion. It showed that LPS i n vivo generates factors other than TNF, such as platelet activating f actor (PAF), that are responsible for the increased capillary permeabi lity.