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Vol. 284, Issue 2, 693-699, February 1998
Cardiovascular Research Institute and Department of Anatomy,
University of California, San Francisco, California (P.B., D.M.McD.)
and
School of Public Health, University of California, Berkeley,
California (N.W.F., H.A.T., E.T.W.)
Mystixins are synthetic peptides that inhibit plasma leakage after
tissue injury. We sought to determine the mechanism of the antileakage
effect of mystixins, with particular reference to the formation of
endothelial gaps in postcapillary venules. Intravenous administration
of mystixin-7, a prototype heptapeptide (p-anisoyl-Arg-Lys-Leu-Leu-D-Thi-Ile-D-Leu-NH2),
decreased Evans blue leakage induced by substance P (5 µg/kg i.v.)
with an ED50 (95% confidence limits) of 130 (76-211)
µg/kg in trachea and 52 (27-100) µg/kg in skin of anesthetized
F344 rats. Leakage was decreased without a reduction in the number or
size of endothelial gaps, visualized by silver deposits after silver
nitrate staining. The number of silver deposits per tracheal
endothelial cell was 11.4 ± 0.2 (mean ± S.E.) after vehicle
pretreatment vs. 13.0 ± 0.8 after mystixin-7
pretreatment (100 µg/kg i.v.). Silver deposit diameter was unchanged
at 1.4 ± 0.1 µm. Mean arterial blood pressure dropped by a
maximum of 38% from baseline for approximately 10 min after mystixin-7
(100 µg/kg i.v.), then recovered to a plateau at about 13% below
baseline. The antileakage effect of mystixin-7 pretreatment in
vivo was also demonstrated in aldehyde-fixed vessels perfused
in situ with Evans blue at constant flow (skin, 79%
reduction; trachea, 49% reduction), which suggests that mystixin can
reduce leakage independent of its hypotensive effect. We conclude that the antileakage effect of mystixin does not depend on reducing the
number or size of endothelial gaps, but instead could be caused by
residual hypotension, which reduces the negative interstitial fluid
pressure toward zero, or clogging of endothelial gaps.
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