International angiology : a journal of the International Union of Angiology · 2010
Medical compression: effects on pulsatile leg blood flow.
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Mayrovitz H N, Macdonald J M
Аннотация
AIM: Leg compression bandaging is the mainstay of venous ulcer treatment, yet little is known about the impact of therapeutic compression levels on arterial haemodynamics. In this study, the effect of foot-to-knee, four-layer compression bandaging on below-knee arterial pulsatile blood flow was assessed by nuclear magnetic resonance flowmetry.
METHODS: In 14 healthy supine subjects, bilateral pulsatile blood flow measured at five below-knee sites without compression; and during compression of one leg to an average malleolar sub-bandage pressure of 40.7±4.0 mmHg.
RESULTS: The forefoot-to-knee compression bandaging caused a highly significant (P<0.001) increase in the bandaged leg pulsatile blood flow due to increases in both peak flow and pulse width.
CONCLUSION: It is hypothesized that arteriolar vasodilatation, induced either myogenically by reduced transmural pressure or by vasodilatory substance release triggered by increased venous shear stress and veno-arterial interactions, possibly combined with altered vascular compliance, produce the observed compression-related phenomenon. Whatever the mechanism(s), the finding of a compression-associated pulsatile flow increase suggests an arterial linkage, which may play a role in the well-documented beneficial effects of compression bandaging in venous ulcer and lymphedema treatment. Possible beneficial effects of the arterial flow-pulse increase on venous ulcer outcome may be related to a decrease in leukocyte effects in the distal microvasculature.
METHODS: In 14 healthy supine subjects, bilateral pulsatile blood flow measured at five below-knee sites without compression; and during compression of one leg to an average malleolar sub-bandage pressure of 40.7±4.0 mmHg.
RESULTS: The forefoot-to-knee compression bandaging caused a highly significant (P<0.001) increase in the bandaged leg pulsatile blood flow due to increases in both peak flow and pulse width.
CONCLUSION: It is hypothesized that arteriolar vasodilatation, induced either myogenically by reduced transmural pressure or by vasodilatory substance release triggered by increased venous shear stress and veno-arterial interactions, possibly combined with altered vascular compliance, produce the observed compression-related phenomenon. Whatever the mechanism(s), the finding of a compression-associated pulsatile flow increase suggests an arterial linkage, which may play a role in the well-documented beneficial effects of compression bandaging in venous ulcer and lymphedema treatment. Possible beneficial effects of the arterial flow-pulse increase on venous ulcer outcome may be related to a decrease in leukocyte effects in the distal microvasculature.