Effects of vasodilation on plasma distribution in SHR cremaster muscle microvessels.
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)
- Copyright © 1983 by American Heart Association