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ASGSB 1998 Annual Meeting Abstracts
[41]
HINDLIMB SUSPENSION ALTERS ARTERIAL MORPHOLOGY IN RAT HINDLIMB SKELETAL MUSCLE.
P.N. Colleran1, J.M. Delp2, M.K. Wilkerson1,
and M.D. Delp1. Depts. of Health and Kinesiology, 1Texas A&M
University, College Station, TX, and 2Sam Houston State University, Huntsville,
TX.
Simulated microgravity diminishes the force producing capacity of large conduit vessels in rats. It has been hypothesized that this attenuation in vasoconstrictor force may be due to smooth muscle atrophy. Therefore, the purpose of this study was to determine if the cross sectional area (CSA) and thickness of the medial layer of rat skeletal muscle feed arteries and 1A arterioles is altered by hindlimb suspension. Vessels from control (n=7) and hindlimb suspended (n=6) rats were dissected free and cannulated on glass micropipets. Luminal pressure was set at 60 cm H20, and the vessels were dilated with sodium nitroprusside (10-4 M), fixed with paraformaldehyde, and embedded in paraffin. Vessel cross sections were cut 5 ?m thick and stained with hematoxylin and eosin. Medial layer CSA and thickness were measured with a BioQuant image analysis system. Hindlimb suspension (14 day) reduced medial layer CSA and thickness in gastrocnemius muscle feed arteries and 1A arterioles (P < .05), but did not alter the number of smooth muscle cell nuclei. Medial layer CSA was also reduced in soleus muscle feed arteries and 1A arterioles (P ???05), but medial thickness was unaltered. In addition, hindlimb suspension did not alter medial CSA, thickness, or the number of smooth muscle cell nuclei in triceps muscle feed arteries in the forelimb. These data suggest that the simulated microgravity-induced reduction in the vasoconstrictor responsiveness of the resistance vasculature in hindlimb muscle may be due to a decrease in the thickness of the medial layer that results from smooth muscle cell atrophy. These data have important implications in regard to the regulation of muscle blood flow and vascular resistance.
(Supported by NASA grants NAGW-4842 and NAG5-3754 and NSBRI grant NCC-9-58.)
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