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Electromagnetic Fields in Biological Systems
effects on capillary flow of red blood cells (RBCs) in unanesthetized Syrian golden hamsters, using a skinfold chamber technique for intravital fluorescence microscopy. Capillary
RBC velocities (v RBC ), capillary diameters (D), arteriolar diameters (D art ), and functional
vessel densities (FVDs) were measured in striated skin muscle at different magnetic flux
densities. Exposure above a threshold level of about 500 mT resulted in a significant reduction of v RBC in capillaries compared with the baseline value. At the maximum field strength
of 587 mT, v RBC was reduced (40%). Flow reduction was reversible when the field strength
was decreased below the threshold level. In contrast, mean values determined at different
exposure levels for the parameters D, D art , and FVD did not vary (5%). Blood flow through
capillary networks is affected by SMFs directed perpendicular to the vessels.
The same research group futher analyzed the effects of SMF (≤587 mT) on tumor
microcirculation (Strieth et al. 2008). In vivo fluorescence microscopy was performed in
A-Mel-3 tumors growing in dorsal skinfold chamber preparations of hamsters. Shorttime exposure (≥150 mT) resulted in a significant reduction of v RBC and segmental blood
flow in tumor microvessels. At the maximum strength of 587 mT, a reversible reduction of
v RBC (40%) and of FVD (15%) was observed. Prolongation of the exposure time (1 minute
to 3 hours) resulted in reductions. Microvessel diameters and leukocyte–endothelial cell
interactions remained unaffected by SMF exposures. However, in contrast to tumor-free
striated muscle controls, exposure at the maximum flux density of 587 mT induced a
significant increase in platelet–endothelial cell adherence in a time-dependent manner
that was reversible after reducing the strength of the SMF. The authors assumed that
these reversible changes may have implications for functional measurements of tumor
microcirculation by MRI and new therapeutic strategies using strong SMFs. The same
research group futher evaluated the effects of an SMF (586 mT, for 3 hours) on tumor
angiogenesis and growth (Strelczyk et al. 2009). Analysis of microcirculatory parameters
revealed a significant reduction of FVD, vessel diameters, and RBC velocity in tumors
after SMF exposure compared with the control tumors. These changes reflect retarded
vessel maturation by antiangiogenesis. The increased edema after SMF exposure indicated an increased tumor microvessel leakiness possibly enhancing drug uptake. The
authors concluded that SMF therapy appears to be a promising new anticancer strategy, as an inhibitor of tumor growth and angiogenesis and as a potential sensitizer to
chemotherapy.
Ghibelli et al. (2006) examined whether exposure to the SMF of NMR (1 T) generated
by an NMR apparatus can affect apoptosis induced on reporter tumor cells of hematopoietic origin. The impressive result was the strong increase (by 1.8–2.5-fold) of
damage-induced apoptosis by NMR. This potentiation is due to cytosolic Ca 2+ overload consequent to NMR-promoted Ca 2+ influx, since it is prevented by intracellular
(BAPTA-AM) and extracellular (EGTA) Ca 2+ chelation or by inhibition of plasma membrane L-type Ca 2+ channels. A 3-day follow-up of treated cultures showed that NMR
decreases long-term cell survival, thus increasing the efficiency of cytocidal treatments.
Mononuclear white blood cells are not sensitized to apoptosis by NMR, showing that
NMR may increase the differential cytotoxicity of antitumor drugs on tumor versus
normal cells. The authors suggested that this strong, differential potentiating effect of
NMR on tumor cell apoptosis may have important implications, as in fact a possible
adjuvant for antitumor therapies.