Cardioprotective effect of glucose-insulin on acute propafenone toxicity in rat.

OBJECTIVE: We recently observed a case of propafenone self-poisoning in which the patient was initially unresponsive to conventional therapies such as sodium bicarbonate, dopamine, and norepinephrine but recovered with intravenous glucose-insulin infusion. We raised the hypothesis that insulin may have a cardioprotective effect in acute propafenone toxicity. METHODS: We evaluated the effect of glucose-insulin infusion on mortality and electrocardiographic abnormalities during acute propafenone toxicity in rats. After measurements of basal mean arterial pressure, heart rate, PR interval, and QRS duration, rats received intravenous propafenone (36 mg/kg per hour) for 12 minutes. Two minutes after the induction of toxicity, the rats (n=10 per group) received either normal saline solution (NSS) or insulin with glucose. Rats in the insulin-treated (Insulin group) and the NSS-treated (NSS group) groups received an intravenous infusion of 36 mg/kg per hour of propafenone until death occurred. Rats receiving only NSS intravenously without propafenone toxicity served as control (Control group, n=10). RESULTS: Insulin treatment improved survival and delayed the hemodynamic and electrocardiographic consequences of propafenone toxicity. Survival was significantly greater in the insulin group than that in the NSS group (P<.001). Insulin prevented the decline in mean arterial pressure and heart rate (P<.05). Insulin also prevented the increase of the PR interval and the QRS duration (P<.05). CONCLUSION: Glucose-insulin infusion delayed the abnormalities in cardiac conduction and improved rat survival after acute propafenone toxicity. These results suggest a cardioprotective effect of glucose-insulin in acute propafenone toxicity.

Effects of Fine Particulate Matter on Pseudomonas aeruginosa Adhesion and Biofilm Formation In Vitro.

Respiratory infections of Pseudomonas aeruginosa are a major cause of mortality and morbidity for hospitalized patients. Fine particulate matter (FPM) is known to have interactions with some bacterial infection in the respiratory system. In this report, we investigate the effect of different concentration of FPM on P. aeruginosa attachment and biofilm formation using in vitro cell culture systems. P. aeruginosa were cultured to form mature biofilms on hydroxyapatite-coated peg and the number of bacteria in the biofilms was enumerated. Morphology of biofilm was imaged with scanning electron microscopy and confocal laser scanning microscopy. Bacterial affinity change to the cell membrane was evaluated with attached colony counting and fluorescence microscopy images. Alteration of bacterial surface hydrophobicity and S100A4 protein concentration were explored as mechanisms of P. aeruginosa adhesion to human cells. There were a concentration-dependent increase of thickness and surface roughness of biofilm mass. P. aeruginosa adherence to respiratory epithelial cells was increased after FPM treatment. Bacterial surface hydrophobicity and S1000A4 protein concentration were increased with proportionally the dose of FPM in media. FPM in the airway could enhance both the adhesion of P. aeruginosa to epithelial cells and biofilm formation. Bacterial surface hydrophobicity and human cell plasma membrane injury are associated with binding of P. aeruginosa on airway epithelial cells and biofilm formation.