Hypertension, Vol 5, 927-934, Copyright © 1983 by American Heart Association
CH Baker, FR Wilmoth and ET Sutton
Alterations in the structure, number, reactivity, contractility and
sensitivity of resistance vessels of hypertensive animals have been
reported. If the etiology of hypertension is due to one or a combination of
these factors, it could logically be expected that the distribution of
blood flow from the arterial to venous circulation through parallel
microcirculatory circuits could be affected. The right cremaster muscles of
pentabarbital anesthetized Wistar-Kyoto (WKY) rats and spontaneously
hypertensive rats (SHR) (6-8 weeks old) were exposed and prepared for
fluorescent videomicroscopy. The right iliac artery was cannulated with
PE-10 tubing, the tip of which was placed at the aortic bifurcation for
bolus injections of FITC-dextran (70,000 molecular weight) and arterial
pressure measurement. Passage of the indicator through the microcirculation
was recorded on videotape during control and during vasodilation by topical
application of adenosine (0.2 M). Time-concentration curves were recorded
by means of dual window videodensitometry upon replay of the tape. Arterial
pressure averaged 85 +/ 3 mm Hg in WKY rats and 110 +/- 5 mm Hg in SHR.
Arteriolar flow velocity varied directly with small arteriolar diameter.
Dilation significantly reduced the venular appearance (ta), mean transit
time (t), and curve width time (tE) in WKY and SHR. The ta was
significantly more reduced in SHR than WKY. This would suggest that, in
WKY, dilation may have opened some new parallel circuits but principally
increased flow velocity through existing circuits. In SHR, new shorter
and/or higher velocity circuits were opened as evidenced by the reduced ta
with the longer and/or lower velocity circuits largely unaffected.(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
Effects of vasodilation on plasma distribution in SHR cremaster muscle microvessels
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