Ischemia-Reperfusion Impairs Ascending Vasodilation in Feed Arteries of Hamster Skeletal Muscle

• Published in: Microcirculation (New York, N.Y. 1994) Vol. 12; no. 7; pp. 551 - 561
• Main Authors: de With, Miriam C. J., Haug, Sara J., Brigitte van der Heijden, E. P. A., Segal, Steven S.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Informa UK Ltd 01.10.2005; Blackwell Publishing Ltd
• Subjects: acetylcholine; Acetylcholine - pharmacology; Animals; Arteries - physiopathology; Blood Flow Velocity - drug effects; conduction; Cricetinae; Endothelial Cells - metabolism; endothelium; Endothelium - physiopathology; Male; Mesocricetus; muscle blood flow; Muscle, Skeletal - blood supply; Muscle, Skeletal - physiopathology; Reperfusion Injury - physiopathology; signal transduction; Vasodilation; Vasodilator Agents - pharmacology
• ISSN: 1073-9688; 1549-8719
• DOI: 10.1080/10739680500253451

Objective: Vasodilation originating within the microcirculation ascends into proximal feed arteries during muscle contraction to attain peak levels of muscle blood flow. Ascending vasodilation (AVD) requires an intact endothelium, as does conducted vasodilation in response to acetylcholine (ACh). Whereas ischemia-reperfusion (I-R) can affect endothelial cell function, the effect of I-R on AVD is unknown. The authors tested the hypothesis that I-R (1h-1h) would impair AVD. Methods: Using the retractor muscle of anesthetized hamsters, contractions were evoked using field stimulation (200 ms at 40 Hz every 2 s for 1 min) and ACh was delivered using microiontophoresis (1 μm tip, 500-4000 ms pulse at 800 nA). Feed artery responses were monitored 500-1500 μm upstream. Results: Neither resting (51 ± 4 μm) nor maximal diameter (81 ± 5 μm; 10 μm sodium nitroprusside) following I-R (n = 8) were different from time-matched controls (n = 10). With peak active tension of 23 ± 4 mN · mm−2, control AVD was 26 ± 2 μm. Following I-R, active tension fell by 48% (p < .05) and AVD by 57% (p < .05). Stimulation at 70 Hz restored active tension but AVD remained depressed by nearly half (p < .05), as did local and conducted responses to ACh. Nevertheless, control responses to 500 ms ACh were restored by increasing stimulus duration to 4000 ms. Conclusions: Ischemia-reperfusion impairs the initiation of feed artery dilation with muscle contraction and with ACh while conduction along the vessel wall is preserved. Respective components of endothelial cell signaling events may differ in their susceptibility to I-R.