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New insight into abnormal muscle vasodilatory responses in aged hypertensive rats by in vivo nuclear magnetic resonance imaging of perfusion.

作者信息

Bertoldi Didier, Parzy Elodie, Fromes Yves, Wary Claire, Leroy-Willig Anne, Carlier Pierre G

机构信息

NMR Laboratory, AFM-CEA, Institute of Myology, IFR 14, Pitié-Salpêtrière University Hospital, Paris, France.

出版信息

J Vasc Res. 2006;43(2):149-56. doi: 10.1159/000090944. Epub 2006 Jan 11.

Abstract

OBJECTIVE

Increased peripheral arterial resistances and decreased maximum vasodilation are characteristic features of chronic hypertension. However, little data are available in the literature regarding the possible alterations in the temporal patterns of vasodilatory responses elicited by various stimuli.

DESIGN

This question was addressed by measuring skeletal muscle perfusion using nuclear magnetic resonance imaging combined with arterial spin labeling.

METHODS

Ninety-week-old male spontaneously hypertensive (SHR; n = 7) and normotensive Wistar Kyoto (WKY; n = 8) rats were studied, and calf muscle perfusion was measured at rest and during reactive hyperemia following total ischemia of 5 and 30 min duration.

RESULTS

Reactive hyperemia profiles differed according to duration of ischemia. In WKY rats, 5 min of ischemia induced a short peak of hyperemia lasting no more than 63 s, while 30 min of ischemia were followed by a prolonged hyperemic response of 261 s. In SHRs, after 5 min of ischemia, peak muscle arterial conductance was decreased to 0.5 +/- 0.3 versus 0.9 +/- 0.3 ml.min(-1).100 g(-1).mm Hg(-1) in the WKY rats (p < 0.05), as expected. After 30 min of ischemia, there was, in addition, a shortening of the hyperemic response duration. Time to post-ischemic half normalization of arterial conductance was 38 +/- 24 s in the SHRs versus 149 +/- 58 s in the WKY rats (p < 0.001).

CONCLUSION

In vivo perfusion measurement not only confirmed the existence of a reduced maximum peripheral vasodilation in chronically hypertensive rats, it revealed a blunted hyperemic response after prolonged ischemia in the SHRs, which might be an important contributing factor to the increased sensitivity to ischemia in hypertension.

摘要

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