Actions of PMF

Vasodilatation can be caused by Ca₂⁺ that as a consequence causes relaxation of vascular musculature, mainly in preacapillary sphincters. The role of parasympathetic part activation can be considered as well. On the basis of the enhanced metabolic activity in the exposed area (endothelial cells including) higher production of EDRF can be considered as well as increased prostacycline production. Finally, mastocyte activation and M and N receptors block can contribute to this effect.

Analgesic action can be explained by proved enhanced endorphines production as well as by anti-inflammatory and anti-oedematous activity and by spasmolytical action, e.g. in paravertebral muscles. It does not seem to be plausible that as in animals destruction of nerve endings and nerve fibres damages occurs. This should cause skin sensoric disturbances that have never been seen with the only exception in professionals. However, here this effect onset after 1-2 years of the employment.

Anti-inflammantory action - theoretical rationale was proposed by J. Jerabek (1989,1990) based on the above described observations.

Fig.1. Proposed anti-inflammantory activity of PMF

Weak electric currents (magnetic fields also) are able to amplify phagocytic activity of PMNLs together with enhanced superoxide anion production (luminometry, INT test). This process is probably followed by induction of superoxide dismutase (SOD) bound to endothelium. Induced SOD reduces superoxide anion and H₂O₂ is created. As superoxide anion inhibits catalase activity, H₂O₂ is not decomposed and is able to destroy oxidatively the most potent phagocytosis activators, -leukotriens.
This proposed mechanism can explain controversial findings that magnetic fields can effectively influence both sterile and microbially induced inflammations. In cases of microbially induced inflammations enhanced phagocytosis is responsible for fast inflammation suppression in the exposed area. On the other hand this phenomenon explains temporary impairment of rheumatic patients within the first exposure period, when enhanced concentration of superoxide anion amplifies inflammatory signs. After these events SOD induction must be considered together with leukotriens destruction and this can explain the subsequent improvement.
In the Fig. 2 Rheumatoid Arthritis (RA) is described as an example of chronic inflammation.

Fig.2. Rheumatoid Arthritis as an example of chronic inflammation

Arrow 1 indicates the proposed inhibitory action on macrophages. Experimental results by Hurych et al. (unpublished preliminary report) showed that in experimental silicosis induced by quartz dust instillated into the lungs suppression of inflammatory signs was observed if the animals were exposed to alternating sinusoidal magnetic fields with B=10.5mT, exposure duration 2 hours daily. This effect was confirmed by histological and biochemical tests, but in bronchoalveoloar lavages 8-10 times more cells then controls (unexposed rats) were obtained, majority of them were macrophages. We suppose that macrophages migrated to the locus of quartz dust inhaled, however their activity and adherence capacity diminished.
Arrow 2 signifies T-lymphocytes. It was shown that IL-1 receptors expression was subdued under the influence of magnetic fields. Arrow 3 underlines that if T-lymphocytes were exposed without any stimulus, no changes in killer activity were observed. However, if the cells were exposed to a magnetic field acted after stimulation by IL-2, their killer activity was significantly suppressed. Arrow 4 shows the above described influence on PMNLs. Arrow 5 shows anti-aggregation activity of magnetic fields with all the sequelae. Arrows 6 and 7 show to the antibody production changes induced by magnetic fields.

From epidemiological studies interesting results were described. In workers in aluminium plants reversal of the ratio T4/T8 in lymphocytes in favour of suppressors was found. This result was interpreted by authors as alarming in healthy persons, but for persons suffering from chronic inflammation it should be regarded as positive.

Ivanova et al. (1977) explained anti-inflammatory activity of magnetic fields by changes of microcirculatory relations, coagulation suppression and phagocytosis activation. In addition they considered the direct influence on the plasma membrane of the cells. In cases of microbial agents it was proved that their sensitivity to antibiotics (ATBs) in vitro, as well as in vivo, corresponded to magnetic field strenght, gradient, exposure duration and numbers of exposures.

Myorelaxation - spasmolytic activity in skeletal muscles is very often described. In cases of paravertebral contractions we can consider the effect of magnetic fields as mainly analgesic . In addition perfusion improvement is of importance in washing away acid metabolites causing muscle irritation. Moreover higher lectate dehydrogenase (LDH) activity was confirmed. Ca₂⁺ efflux is important as well as the role of the central nervous system (CNS).

Healing acceleration was proved not only in bones but also in soft tissues. This can be explained by Oberlay's hypothesis. He proposed that a non-specific stimulus on the cytoplasma membrane activates a chain of biochemical reactions resulting in changed cAMP/cGMP ratio. This event is initiated by induction of NAD(P)H-OX binding to the cytoplasma membrane that represents a source of superoxide anion. Moreover by means of these receptors cellular respiration is activated, respiratory chains are another source of superoxide anions. Cellular respiration is activated through changed cytoplasma membrane permeability for H⁺, i.e. increased proton influx causes a reduction of intracellular pH and respiration is activated.
In pseudoarthroses osteoclast activation is proposed as the healing agent. Evidence for this idea is the apparent worsening of X-ray picture in patients. We regularly observed that one month after magnetotherapy dilatation and diffusion of the fracture line commenced. This could only be explained by osteoclastic activation. Further healing progress is aided through increased fibronectine production by these cells, with subsequent acceleration of connective tissue synthesis. Another positive phenomenon is inflammation suppression and improved macro- and microcirculation.

Anti-oedematous activity - magnetic field effectiveness in controlling oedema progression appears to be connected with the above described mechanisms.

In the Fig. 3 and Fig. 4 the general mechanisms of magnetotherapy are described.

Fig.3. Local action of PMF

Fig.4. Systemic action of PMF

It seems that the only negative feature of properly performed magnetotherapy is possible induction of hypotension. For experimentally observed damage the following biochemical processes might be responsible:
1) An increase in superoxide anion, leading to oxidation of -SH groups of enzymes, mainly of glyceraldehyde-3-PDH.
2) An intracellular pH decrease, leading to conversion of xanthine-DH to xanthine-OX.
3) Initiation of adenosine triphosphate (ATP) catabolism through phosphate removal from ATP by oxidised glyceraldehyde-3-PDH.

Further ATP, and ADP catabolism, together with an improvement in perfusion and the presence of xanthine-OX results in a strong and a sudden superoxide anion synthesis source, which can only be partially detoxified by SOD with its existing activation level. In consequence peroxidation of lipid structures and -SH groups of proteins, enzymes included, occurs, with all the negative consequences for cellular metabolism. See Fig. 5.

Fig.5. Possible lipid peroxidation pathways from PMF

On the other hand, this same mechanism can also be partially responsible for positive results in malignant tumour therapy. It is known that in the majority of malignant cells antioxidant enzyme activity is at very low levels or even absent. So every enhancement of radical flux acts on these cells as a strong toxin. Not surprisingly, exposures that do not cause damage in healthy cells caused serious damage in tumour cells and potentiated the action of certain types of cytostatic agents.
Based on the fact above it necessarily follows that one should consider doses which can be roughly estimated from the following formula:

Dose = dB/dt x Bmax x Exp x f
where
dB/dt = change of magnetic flux density [T/s] Bmax = peak value of magnetic flux density [T] f = repeating frequency of the applied field [Hz] Exp = exposure duration in hours [h]

For safe use of PMF therapy daily exposure duration should not exceed 60 minutes with magnetic flux density Bmax up to 50 mT. Obviously, counter-indications for magnetotherapy must be respected.

The excerpt from the book MAGNETOTHERAPY, author Jiri Jerabek, M.D.,Ph.D., 1993. Also published in London 1996, as a part of First World Congress in Magnetotherapy.