Static magnetic fields alter arteriolar tone in vivo.
This study was designed to directly quantify the effect of localized static magnetic field (SMF) exposure on the diameter of microvessels in adult rat skeletal muscle in vivo. Microvascular networks in the exteriorized rat spinotrapezius microvasculature were exposed to a localized, uniform 70 mT SMF for 15 min. Arteriolar vessel diameters were measured; and the extent of vessel contraction, microvascular tone, was calculated before exposure, immediately after exposure, and 15 and 30 min after removal of the field. A calculated value of high tone corresponds to vessels that are vasoconstricted and a calculated value of low tone refers to vessels that are vasodilated. Vessels with initial tone <15% showed an increasing trend in tone and, conversely, vessels with initial tone >15% showed a significant (P < 0.05) decrease in tone 15 and 30 min following application, respectively. Further classification of the data with regards to the initial vessel diameter demonstrated that vessels with initial diameters <30 microm and initial tone <15%, smaller diameter vessels that are initially vasodilated, showed significant (P < 0.05) increase in tone immediately, 15 and 30 min following SMF exposure. Additionally, <30 microm vessels with >15% initial tone, smaller diameter vessels that are initially vasoconstricted, demonstrated a significant (P < 0.05) decrease in tone 30 min after SMF exposure. Vessels with initial diameters >30 microm had no significant response to the SMF. These results imply that SMF exposure influences arteriolar diameters, and therefore microvascular tone, in a restorative fashion acting to normalize the tone to the median tone value of 15% following exposure. Because this response occurs primarily in the resistance arterioles, which significantly influence tissue perfusion, SMF application could be efficacious for the treatment of both ischemic and edematous tissue disorders involving compromised microvascular function.
Morris
Cassandra
C
Department of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Skalak
Thomas
T
D000222:Adaptation, Physiological / Q000187:drug effects / Q000528:radiation effects; D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000166:cytology / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D004574:Electromagnetic Fields; D005260:Female; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects*; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects*; D011829:Radiation Dosage; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D014665:Vasodilator Agents / Q000494:pharmacology
D014665:Vasodilator Agents; D000241:Adenosine