© 1998 American Heart Association, Inc.
Original Contributions |
Endogenous Nitric Oxide Protects Against Thromboembolism in Venules But Not in Arterioles
From the Departments of Physiology (M.A.W.B., G.-J.T., R.S.R., M.G.A. oude E.) and Biophysics (D.W.S.), Cardiovascular Research Institute Maastricht, Maastricht University; and the Laboratory for Physiology, Institute for Cardiovascular Research, Free University, Amsterdam (G.-J.T.), the Netherlands.
Correspondence to M.G.A. oude Egbrink, PhD, Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50, PO Box 616, 6200 MD Maastricht, the Netherlands. E-mail m.oudeegbrink{at}fys.unimaas.nl
Abstract—Because nitric oxide (NO)
inhibits aggregation and adhesion of blood platelets, NO may play a
role in platelet–vessel wall interactions. Therefore, the purpose
of this study was to investigate the involvement of
endogenous NO in thromboembolic processes, as induced by
wall puncture, in rabbit mesenteric arterioles and venules (diameters
20 to 43 µm). In venules, inhibition of NO synthase by
superfusion of the mesentery with
N
-nitro-L-arginine (L-NA;
0.1 mmol/L) significantly increased the duration of embolization
(from 50 seconds to 511 seconds) and the number of emboli produced
(from 2 to 11 emboli per vessel), while the median period of time
needed to produce an embolus was not influenced. On the contrary, in
arterioles, L-NA had no significant effect on embolization (duration of
embolization: 426 seconds in the control and 382 seconds in the L-NA
group, with 20 and 12 emboli per vessel, respectively). Addition to the
L-NA superfusate of L-arginine (L-ARG; 1 mmol/L), the
active precursor for endogenous NO synthesis, resulted in a
complete reversal of the L-NA effects in venules, while addition of the
inactive D-arginine (D-ARG; 1 mmol/L) had no effect. Addition of
L-ARG and D-ARG had no significant effect in arterioles. Addition to
the L-NA superfusate of the exogenous NO donor sodium
nitroprusside (0.1 µmol/L) also resulted in reversal of the L-NA
effects in venules, while in arterioles, it slightly but significantly
decreased embolization duration. The differences in effect of L-NA on
embolization between arterioles and venules were not caused by
differences in fluid dynamic conditions. It is concluded that the role
of endogenous NO in inhibiting thromboembolic processes is
more important in venules than in arterioles.
Key Words: vessel wall injury • thromboembolism pathophysiology • nitric oxide • intravital microscopy • microcirculation
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