Pedersen Michael, Brandt Christian T, Knudsen Gitte M, Ostergaard Christian, Skinhøj Peter, Skovsted Ian C, Frimodt-Møller Niels, Møller Kirsten
Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
J Cereb Blood Flow Metab. 2008 Jan;28(1):126-34. doi: 10.1038/sj.jcbfm.9600514. Epub 2007 Jun 13.
In the present study, we studied the effect of bacteremia on cerebral blood flow (CBF) autoregulation in a rat model of pneumococcal bacteremia and meningitis. Anesthetized rats were divided into five groups (A to E) and inoculated with pneumococci intravenously and normal saline intracisternally (group A, N=10); saline intravenously and pneumococci intracisternally (group B, N=10); pneumococci intravenously and pneumococci intracisternally (group C, N=5); saline intravenously, antipneumococcal antibody intravenously (to prevent bacteremia), and pneumococci intracisternally (group D, N=10); or saline intravenously and saline intracisternally (group E, N=10), respectively. Positive cultures occurred in the blood for all rats in groups A, B, and C, and in the cerebrospinal fluid for all rats in groups D and E. Twenty-four hours after inoculation, CBF was measured with laser-Doppler ultrasound during incremental reductions in cerebral perfusion pressure (CPP) by controlled hemorrhage. Autoregulation was preserved in all rats without meningitis (groups A and E) and was lost in 24 of 25 meningitis rats (groups B, C, and D) (P<0.01). In group A, the lower limit was higher than that of group E (P<0.05). The slope of the CBF/CPP regression line differed between the meningitis groups (P<0.001), being steeper for group B than groups C and D, with no difference between these two groups. The results suggest that pneumococcal bacteremia in rats triggers cerebral vasodilation, which right shifts the lower limit of, but does not entirely abolish, CBF autoregulation in the absence of meningitis, and which may further aggravate the vasoparalysis induced by concomitant pneumococcal meningitis.
在本研究中,我们在肺炎球菌菌血症和脑膜炎大鼠模型中研究了菌血症对脑血流量(CBF)自动调节的影响。将麻醉的大鼠分为五组(A至E组),分别静脉注射肺炎球菌并脑池内注射生理盐水(A组,N = 10);静脉注射生理盐水并脑池内注射肺炎球菌(B组,N = 10);静脉注射肺炎球菌并脑池内注射肺炎球菌(C组,N = 5);静脉注射生理盐水、静脉注射抗肺炎球菌抗体(以预防菌血症)并脑池内注射肺炎球菌(D组,N = 10);或静脉注射生理盐水并脑池内注射生理盐水(E组,N = 10)。A、B和C组所有大鼠的血液培养呈阳性,D和E组所有大鼠的脑脊液培养呈阳性。接种24小时后,通过控制性出血使脑灌注压(CPP)逐渐降低,同时用激光多普勒超声测量CBF。所有无脑膜炎的大鼠(A组和E组)的自动调节功能得以保留,而25只脑膜炎大鼠中的24只(B、C和D组)的自动调节功能丧失(P<0.01)。A组的下限高于E组(P<0.05)。脑膜炎组之间CBF/CPP回归线的斜率不同(P<0.001),B组比C组和D组更陡,这两组之间无差异。结果表明,大鼠肺炎球菌菌血症引发脑血管舒张,在无脑膜炎的情况下,这会使CBF自动调节的下限右移,但不会完全消除,并且可能会进一步加重由伴随的肺炎球菌脑膜炎引起的血管麻痹。