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Vol. 84, Issue 3, 837-844, March 1998
A. C. Burton Vascular Biology Laboratory, Victoria Hospital Research Institute, and Departments of Medical Biophysics and Pharmacology and Toxicology, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Although sepsis is
known to affect vascular function, little is known about changes at the
capillary level. We hypothesized that sepsis attenuates the
"upstream" arteriolar response to vasoactive agents applied
locally to capillaries. Sepsis in rats was induced by cecal ligation
and perforation. After 24 h, extensor digitorum longus muscle was
prepared for intravital microscopy. Phenylephrine (PE, 10 mM) and
acetylcholine (ACh, 10 mM) were applied iontophoretically on terminal
arterioles and on their downstream daughter capillaries (300 µm from
arteriole). There was no significant difference between control and
septic rats in baseline arteriolar diameters [8.0 ± 0.6 vs.
9.8 ± 0.8 (SE) µm] or baseline red blood cell
velocity (VRBC)
in perfused daughter capillaries (255 ± 10 vs. 264 ± 13 µm/s). Application of PE onto arterioles resulted in comparable constrictions (i.e., 
22% diameter change) and
VRBC reductions (100%) in control and septic rats. In contrast, arteriolar
diameter and VRBC
increases after application of ACh were attenuated in sepsis (diameter:
from 41 to 14%;
VRBC: from 67 to
24%). Application of PE onto the capillary reduced
VRBC to the same
level (100%) in both groups, whereas application of ACh
increased VRBC
less in septic than in control rats (20 vs. 73%). On the basis of
arteriolar-capillary pair stimulations, sepsis affected
VRBC responses to
ACh more in the capillary than in the arteriole. When the adenosine
analog 5'-N-ethylcarboxamidoadenosine
(0.1 mM) was used instead of ACh, similar effects of sepsis were seen.
To test for a possible involvement of inducible NO synthase (iNOS) in
sepsis-induced attenuated ACh responses, arterioles and capillaries in
septic animals were locally pretreated with the iNOS blocker
aminoguanidine (10 mM). In both microvessels, aminoguanidine restored
the ACh response to the control level. We conclude that impaired
capillary VRBC
and arteriolar diameter responses to vasodilators applied to
capillaries in septic rat skeletal muscle were due to dysfunction at
arteriolar and capillary levels. The study underscores the significant
role iNOS/NO may play in sepsis-induced alteration of vascular
reactivity in vivo.
capillary; skeletal muscle; nitric oxide
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