Background: In our previous study, adrenomedullin (AM) overexpression could limit the arterial intimal hyperplasia induced by cuff injury in rats. However, it remains to be elucidated whether endogenous AM plays a role against vascular injury.
Methods And Results: We used the AM knockout mice to investigate the effect of endogenous AM.
Adrenomedullin (AM) inhibits vascular smooth muscle cell proliferation stimulated by fetal calf serum and platelet-derived growth factor in vitro. In this study, an adenovirus expressing AM (AxCAAM) was created to examine the in vivo action of AM. Femoral arteries of Wistar rats were wrapped with a silicone cuff and treated with adenovirus expressing Escherichia coli beta-galactosidase (AxCALacZ) or AxCAAM.
View Article and Find Full Text PDFBecause both vasodilation induced by adrenomedullin (AM) and that induced by calcitonin gene-related peptide (CGRP) may occur via the same receptor, the two peptides might play similar roles in circulation. To examine this possibility, we used the colored microsphere technique and an ultrasonic flowmeter to investigate the systemic and regional effects of an equivalent dose (650 pmol/l) of AM and CGRP in conscious Wistar rats. AM significantly decreased mean arterial pressure and peripheral resistance but increased heart rate and cardiac index (CI).
View Article and Find Full Text PDFTo investigate whether hyperthermic preconditioning can actually protect skin flaps against ischemia/reperfusion injury, the authors first developed a new skin-flap model in 15 mice, a dorsal bipedicle island skin-flap model. Then, another 75 mice were separated into five groups. Mice in Groups 1 to 4 received the same hyperthermic preconditioning, but had different recovery times of 6 hr, 24 hr, 48 hr, and 72 hr, respectively.
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