1. We have studied the time course of the numbers of arterial monocytes and their superoxide anion (O2) production in a chronically instrumented sheep model of subacute endotoxaemia induced by a continuous intravenous infusion of Escherichia coli lipopolysaccharide (20 ng min−1 kg−1).

2. Four out of 11 animals died from irreversible respiratory and cardiovascular failure within 21 h of the start of lipopolysaccharide administration ('non-survivors'), whereas in the seven surviving sheep ('survivors') there was a persistence of decreased systemic vascular resistance, systemic hypotension, pulmonary hypertension, anorexia and lethargy.

3. O2 generation by isolated monocytes was measured by the O2 dismutase-inhibitable reduction of ferricytochrome c after stimulation with phorbol myristate acetate (100 ng/ml) or opsonized zymosan (3 mg/ml). Basal mean value of phorbol myristate acetate-stimulated O2 production was significantly (P = 0.008) higher for non-survivors (31.3 ± 8.8 nmol 30 min−1 10−6 cells; n = 4) than for survivors (6.2 ± 2.3 nmol 30 min−1 10−6 cells; n = 7).

4. For both survivors and non-survivors, monocyte counts and phorbol myristate acetate-stimulated O2 production increased over time to reach in survivors a plateau after 2 days of continuous lipopolysaccharide infusion. Similar results were obtained when monocytes were stimulated for O2 production with opsonized zymosan.

5. These results suggest that (1) increased O2 production by monocytes and monocytosis appear with a precise, delayed time course during the development of subacute endotoxaemia in sheep; and (2) a high stimulated O2 production by monocytes before lipopolysaccharide administration may represent a predictive factor for the subsequent respiratory failure and outcome of endotoxaemia.

This content is only available as a PDF.
You do not currently have access to this content.