Clonidine elicits a long-term depression in mucosal red cell flux

Objective: To evaluate the impact of clonidine on mucosal red cell flux during baseline sedation with propofol or sevoflurane, respectively. Materials and Methods:Six healthy, chronically instrumented dogs for the measurement of cardiac output (CO) were repeatedly studied. During baseline sedation with either propofol (15 mg kg ^-1 h ^-1) or sevoflurane (1.5 MAC), local tissue cell flux was assessed using laser Doppler flowmetry at the enoral mucosa. After baseline measurements, a bolus of clonidine (2.0 μ g/kg) was infused within 1 min. Data are presented as mean ± SEM; Statistics: ANOVA, Scheffé's post hoc test, p < 0.05. Results:Clonidine significantly reduced CO from 75 ± 4 and 75 ± 6 ml kg ^-1 min ^-1 (sedation with propofol or sevoflurane, respectively) to 40 ± 3 and 49 ± 5 ml kg ^-1 min ^-1 , however, with almost complete recovery to baseline after 30 min (70 ± 4 and 71 ± 6 ml kg ^-1 min ^-1 , NS from baseline). Similarly, clonidine decreased mucosal red cell flux by 44 ± 8% and 54 ± 4%. However, mucosal perfusion did not return to baseline (-25 ± 5% and -27 ± 3%). Conclusions:In spite of the rapid return to baseline in systemic perfusion, the mucosal red cell flux of the enoral mucosa remained markedly reduced after a single bolus of clonidine. Given the crucial role of preserved microcirculatory perfusion for an intact mucosal barrier function, our data suggest that clonidine might impair this important mechanism to prevent the translocation of bacteria and endotoxins into the systemic circulation.