The effects of omeprazole on polymorphonuclear neutrophil (PMN) chemotaxis, superoxide generation, degranulation and translocation of cytochrome b-245 were investigated. Omeprazole (106-5x0X-3 mol/l) reduced chemotaxis under agarose in a dose dependent manner, and the effect was irreversible. Superoxide anion generation was inhibited 50% at a concentration of 255X 0-5 mol/l and completely abolished at 5X 10-3 mol 1. Acid degraded omeprazole also inhibited 02 generation. Omeprazole did not scavenge 02 generated in a celi free xanthin-xanthine oxidase system. Degranulation by PMNs was inhibited only by omeprazole in concentrations above 10-4 moW. Translocation of cytochrome b-245, essential for generation of 02-, was not affected by omeprazole. In conclusion, the anti-ulcer agent omeprazole in concentrations obtained during intravenous administration may inhibit the function of PMNs in vitro.

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Polymorphonuclear leucocyte (PMN) ingestion of particles coated with lipopolysaccharide (LPS) from Escherichia coli was compared to other PMN functions in seven patients with insulin dependent diabetes mellitus (IDDM) during short-term controlled metabolic changes from normo- to hyperglycemia without ketoacidosis. Factors known to interfere with PMN functions were excluded. PMN ingestion of particles coated with both LPS and bovine serum albumin became reduced from normo- to hyperglycemia. PMN motility was impaired in IDDM, but did not seem to be affected by short-term changes in metabolic control. PMN metabolism did not change from normo-to hyperglycemia. Particle-uptake by diabetic PMN is impaired after short term hyperglycemia in the range normally occurring in diabetics in every-day life.

In patients in the early phase of acute bacterial meningitis, CBF autoregulation is impaired. With recovery from meningitis, the cerebral vasculature regains the ability to maintain cerebral perfusion at a constant level despite variations in MAP.