TY - JOUR
T1 - Deep venous contribution to hydrostatic blood volume change in the human leg
AU - Buckey, Jay C.
AU - Peshock, Ronald M
AU - Blomqvist, C. Gunnar
N1 - Funding Information:
From the Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research and the Harry S. Moss Heart Center, Department of Internal Medicine/Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas. This study was supported by grant NSG-9026 and Dr. Buckey’s Research Associate Award NAGW-70, both from the National Aeronautics and Space Administration, Washington, DC. Dr. Peshock is the recipient of Clinical Investigator Award HL-01 I57 from the National Institutes of Health, Bethesda, Maryland. Manuscript received February 12, 1988; revised manuscript received and accepted April 25, 1988.
PY - 1988/9/1
Y1 - 1988/9/1
N2 - The causes of orthostatic intolerance following prolonged bed rest, head-down tilt or exposure to zero gravity are not completely understood. One possible contributing mechanism is increased venous compliance and peripheral venous pooling. The present study attempted to determine what proportion of the increased calf volume during progressive venous occlusion is due to deep venous filling. Deep veins in the leg have little sympathetic innervation and scant vascular smooth muscle, so their compliance may be determined primarily by the surrounding skeletal muscle. If deep veins make a large contribution to total leg venous compliance, then disuse-related changes in skeletal muscle mass and tone could increase leg compliance and lead to decreased orthostatic tolerance. The increase in deep venous volume during progressive venous occlusion at the knee was measured in 6 normal subjects using calf cross-sectional images obtained with magnetic resonance imaging. Conventional plethysmography was used simultaneously to give an independent second measurement of leg volume and monitor the time course of the volume changes. Most of the volume change at all occlusion levels (20, 40, 60, 80 and 100 mm Hg) could be attributed to deep venous filling (90.2% at 40 mm Hg and 50.6% at 100 mm Hg). It is concluded that a large fraction of the calf volume change during venous occlusion is attributable to filling of the deep venous spaces. This finding supports theories postulating an important role for physiological mechanisms controlling skeletal muscle tone during orthostatic stress.
AB - The causes of orthostatic intolerance following prolonged bed rest, head-down tilt or exposure to zero gravity are not completely understood. One possible contributing mechanism is increased venous compliance and peripheral venous pooling. The present study attempted to determine what proportion of the increased calf volume during progressive venous occlusion is due to deep venous filling. Deep veins in the leg have little sympathetic innervation and scant vascular smooth muscle, so their compliance may be determined primarily by the surrounding skeletal muscle. If deep veins make a large contribution to total leg venous compliance, then disuse-related changes in skeletal muscle mass and tone could increase leg compliance and lead to decreased orthostatic tolerance. The increase in deep venous volume during progressive venous occlusion at the knee was measured in 6 normal subjects using calf cross-sectional images obtained with magnetic resonance imaging. Conventional plethysmography was used simultaneously to give an independent second measurement of leg volume and monitor the time course of the volume changes. Most of the volume change at all occlusion levels (20, 40, 60, 80 and 100 mm Hg) could be attributed to deep venous filling (90.2% at 40 mm Hg and 50.6% at 100 mm Hg). It is concluded that a large fraction of the calf volume change during venous occlusion is attributable to filling of the deep venous spaces. This finding supports theories postulating an important role for physiological mechanisms controlling skeletal muscle tone during orthostatic stress.
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U2 - 10.1016/0002-9149(88)90976-9
DO - 10.1016/0002-9149(88)90976-9
M3 - Article
C2 - 3414521
AN - SCOPUS:0023686369
SN - 0002-9149
VL - 62
SP - 449
EP - 453
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 7
ER -