Propofol bolus injection has been reported to influence cardiovascular functions. However, the detailed mechanism underlying this action has not been elucidated. This study was designed to investigate the effects of propofol i.v. bolus on the left ventricular function, the myocardial β-adrenoceptor (β-AR) binding-site density (Bmax) and Kd (apparent dissociation constant) in a 30-minute period. One hundred and four male Wistar rats were randomly divided into four groups: group C (control group), group I (intralipid group), group P1 (5mg/kg propofol) and group P2 (10 mg/kg propofol). The results showed a significant downregulation of HR, LVSP, +dp/dt(subscript max) and -dp/dt(subscript max) in both groups P1 and P2 (especially after bolus injection in 7 min) than those of group C (P<0.05), whereas no significant difference was found between the P1 and P2 groups (P>0.05). Likely, Bmax was remarkably upregulated in both groups P1 and P2 (P<0.05, vs. groups C and I), and there was no significant difference between these two groups (P>0.05). Of note, the Kd value in group P2 (10 mg/kg propofol) was found dramatically increased in 30 min than that in the low-dose propofol-treated group (group P1) as well as in groups C and I (P<0.05). In conclusion, these results indicate that intravenous injection of propofol bolus can inhibit the cardiac function partially via upregulation of Bmax and downregulation of the β-AR affinity at higher-dose injection of propofol bolus.
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