Nitazoxanide (NTZ), a synthesized drug of the nitrothiazolide class, was initially developed as an antiparasitic compound. This compound has recently been shown to have antibacterial activities against some bacterial pathogens. In the present study, NTZ and its main metabolite tizoxanide (TIZ) were found to have strong minimum inhibitory concentrations (MICs) against both metronidazole (MTZ)-resistant strains and sensitive clinical isolates of Helicobacter pylori. The MIC90 of both NTZ and TIZ against 37 clinical isolates was 8 microg/ml. Vacuolating toxin activity of H. pylori assayed by HeLa cell vacuole formation was inhibited by NTZ at a sub-MIC. In contrast, urease production by H. pylori was not specifically affected by the sub-MIC of NTZ. An acidic pH (pH 5.0) medium reduced the antimicrobial activity of the drug in terms of growth inhibition due to the low growth rate of the bacteria, but killing activity of NTZ against the bacteria was still observed. Thus, it was apparent that both NTZ and TIZ are highly effective against H. pylori, even when the bacteria are resistant to MTZ.

Anti-Bacterial Agents↗

PubMedDate not supplied

Chronotropic effect of the antithrombotic agent cilostazol in a patient with sick sinus syndrome and syncope.

In this case report we describe an 80-year-old man with sick sinus syndrome (SSS) who developed syncope attacks. The diagnosis of SSS was based on electrocardiographic evidence of markedly prolonged sinus arrests associated with syncope attacks while in hospital. The patient was given cilostazol, an antithrombotic agent that selectively inhibits cyclic nucleotide phosphodiesterase type 3, at a dose of 100 mg twice daily. The syncope attacks ceased, and an electrocardiogram obtained 1 week after the start of cilostazol administration showed no evidence of sinus arrest. The outcome of this case suggests that cilostazol may be useful in patients with syncope attacks due to SSS, although the long-term chronotropic effects of cilostazol need to be evaluated.

Aged↗

PubMedDate not supplied

Cardioprotective effect of edaravone against ischaemia-reperfusion injury in the rabbit heart before, during and after reperfusion treatment.

The free radical scavenger edaravone is able to stimulate prostacyclin release and inhibit the lipoxygenase pathway in the arachidonic acid cascade. The effect of edaravone administration on myocardial damage in rabbit hearts subjected to ischaemia-reperfusion was examined at different times relative to reperfusion. All rabbits underwent sustained coronary artery occlusion for 30 min followed by 3 h of reperfusion. Rabbits were divided into the following groups: control; early (3 mg/kg edaravone IV 10 min before reperfusion); immediate (3 mg/kg edaravone IV immediately after the start of reperfusion); and late (3, 6 or 10 mg/kg edaravone IV 5 min after the start of reperfusion). Single bolus administration of edaravone 10 min before reperfusion or immediately upon initiation of reperfusion appears to be associated with reductions in infarction size and the percentage of apoptotic cells, but treatment with edaravone 5 min after initiation of reperfusion does not appear to have this protective effect.

Animals↗