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Mechanisms of bacterial resistance to fluoro-quinolones may be grouped into three principal categories: gene mutations of DNA topoisomerase Ⅱ (GyrA or GyrB), DNA topoisomerase Ⅳ (ParC or ParE), decrease of outer membrane permeation and upregulation of multi-drug efflux pump (active efflux system).1 Efflux pumps are transport proteins removing toxic substrates (including virtually all classes of clinically relevant antibiotics) from cells to the extal environment. These proteins exist in both Gram positive bacteria and Gram negative bacteria as well as in fungi and mammalian (tumour) cells.2-4 It has been reported that alkaloid reserpine and carbonyl cyanide m-chlorophenylhydrazone (CCCP) can inhibit NorA multi-drug efflux.5,6 In order to explore the universality of drug efflux in microorganisms, 85 strains of Acinetobacter baumannii (A. Baumannii) were tested using reserpine and CCCP. The quinolone-resistant-determining region (QRDR) of gyrA and parC genes in 35 isolates of A. Baumannii were amplified by polymerase chain reaction (PCR) and sequenced by DNA sequencer. The correlation between resistant mutation regularity and bacterial drug efflux were analysed.