Modulatory effects of static magnetic fields on blood pressure in rabbits

Acute effects of locally applied static magnetic fields (SMF) on pharmacologically altered blood pressure (BP) in a central artery of the ear lobe of a conscious rabbit were evaluated. Hypotensive and vasodilator actions were induced by a Ca(2+) channel blocker, nicardipine (NIC). Hypertensive and vasoconstrictive actions were induced by a nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME). The hemodynamic changes in the artery exposed to SMF were measured continuously and analyzed by penetrating microphotoelectric plethysmography (MPPG). Concurrently, BP changes in a central artery contralateral to that of the exposed ear lobe were monitored. SMF intensity was 1 mT and the duration of exposure was 30 min. A total of 180 experimental trials were carried out in 34 healthy adult male rabbits weighing 2.6-3.8 kg. Six experimental procedures were chosen at random: (1) sham exposure without pharmacological treatment; (2) SMF exposure alone; (3) decreased BP induced by a single intravenous (iv) bolus injection of NIC (100 microM/kg) without SMF exposure; (4) decreased BP induced by injection of NIC with SMF exposure; (5) increased BP induced by a constant iv infusion of L-NAME (10 mM/kg/h) without SMF exposure; (6) increased BP induced by infusion of L-NAME with SMF exposure. The results demonstrated that SMF significantly reduced the vasodilatation with enhanced vasomotion and antagonized the reduction of BP via NIC-blocked Ca(2+) channels in vascular smooth muscle cells. In addition, SMF significantly attenuated the vasoconstriction and suppressed the elevation of BP via NOS inhibition in vascular endothelial cells and/or central nervous system neurons. These results suggest that these modulatory effects of SMF on BP might, in part, involve a feedback control system for alteration in NOS activity in conjunction with modulation of Ca(2+) dynamics.     

Effects of neck exposure to 5.5 mT static magnetic field on pharmacologically modulated blood pressure in conscious rabbits

Static magnetic fields (SMF) in the millitesla (mT) range have been reported to modulate microcirculatory hemodynamics and/or blood pressure (BP) under pharmacologically modified state in mammals. This study was designed to investigate the acute effects of local application of a SMF to neck or pelvic region under pharmacologically modulated BP; norepinephrine (NE)-induced hypertension as well as an L-type voltage-gated Ca(2+) channel blocker, nicardipine (NIC)-induced hypotension in conscious rabbits. Magnetic flux densities were up to 5.5 mT and the spatial magnetic gradient peaked in neck (carotid sinus baroreceptor) region at the level of approximately 0.06 mT/mm. The duration of exposure was 30 min (including 10 min of pretreatment) and the effects on BP were investigated up to 100 min postexposure. Baroreflex sensitivity (BRS) was estimated from invasive recordings of systolic BP and pulse interval. Neck exposure to 5.5 mT significantly attenuated the pharmacologically induced vasoconstriction or vasodilation, and subsequently suppressed the increase or decrease in BP compared with sham exposure. In contrast, pelvic exposure to 5.5 mT did not significantly antagonized NE-elevated BP or NIC-reduced BP. The neck exposure to 5.5 mT has a biphasic and restorative effect on vascular tone and BP acting to normalize the tone and BP. The neck exposure to 5.5 mT caused a significant increase in BRS in NE-elevated BP compared with sham exposure. The buffering effects of the SMF on increased hemodynamic variability under NE-induced high vascular tone and NIC-induced low vascular tone might be, in part, dependent on baroreflex pathways, which could modulate NE-mediated response in conjunction with Ca(2+) dynamics.     

Effect of 0.25 T static magnetic field on microcirculation in rabbits

We showed previously in rabbits that 0.2 and 0.35 T static magnetic field (SMF) modulated systemic hemodynamics by arterial baroreceptors. We now have measured the effect of 0.25 T SMF on microcirculation within cutaneous tissue of the rabbit ear lobe by the rabbit ear chamber (REC) method. Forty experimental runs (20 controls and 20 SMF) were carried out in eight different rabbits with an equal number of control and SMF experiments on each individual. Rabbits were sedated by pentobarbital sodium (5 mg/kg/h, i.v.) during the entire 80 min experiment. SMF was generated by four neodium-iron-boron alloy (Nd2-Fe14-B) magnets (15 x 25 x 30 mm, Neomax, PIP - Tokyo Co., Ltd., Tokyo, Japan), positioned around the REC on the observing stage of an optical microscope. The direct intravital microscopic observation of the rabbit's ear microvascular net, along with simultaneous blood flow measurement by microphotoelectric plethysmography (MPPG), were performed PRE (20 min, baseline), DURING (40 min), and POST (20 min) magnetic field exposure. The control experiments were performed under the same conditions and according to the same time course, but without magnetic field. Data were analyzed comparing MPPG values and percent change from baseline in the same series, and between corresponding sections of control and SMF runs. In contrast to control series (100+/-0.0%-90.0+/-5.4%-87.7+/-7.1%, PRE-EXPOSURE-POST), after magnetic field exposure we observed increased blood flow (100+/-0.0%-117.8+/-9.6%*-113.8+/-14.0%, *P<0.05) which gradually decreased after exposure cessation. We propose that long exposure of a high level nonuniform SMF probably modifies microcirculatory homeostasis through modulation of the local release of endothelial neurohumoral and paracrine factors that act directly on the smooth muscle of the vascular wall, presumably by affecting ion channels or second messenger systems.     

Geomagnetic field modulates artificial static magnetic field effect on arterial baroreflex and on microcirculation

Spreading evidence suggests that geomagnetic field (GMF) modulates artificial magnetic fields biological effect and associated with increased cardiovascular morbidity. To explore the underlying physiological mechanism we studied 350 mT static magnetic field (SMF) effect on arterial baroreflex-mediated skin microcirculatory response in conjunction with actual geomagnetic activity, reflected by K and K _p indices. Fourteen experiments were performed in rabbits sedated by pentobarbital infusion (5 mg/kg/h). Mean femoral artery blood pressure, heart rate, and the ear lobe skin microcirculatory blood flow, measured by microphotoelectric plethysmogram (MPPG), were simultaneously recorded before and after 40 min of NdFeB magnets local exposure to sinocarotid baroreceptors. Arterial baroreflex sensitivity (BRS) was estimated from heart rate/blood pressure response to intravenous bolus injections of nitroprusside and phenylephrine. We found a significant positive correlation between SMF-induced increase in BRS and increment in microvascular blood flow (ΔBRS with ΔMPPG, r=0.7, p<0.009) indicated the participation of the arterial baroreflex in the regulation of the microcirculation and its enhancement after SMF exposure. Geomagnetic disturbance, as opposed to SMF, decreased both microcirculation and BRS, and counteracted SMF-induced increment in microcirculatory blood flow (K-index with ΔMPPG; r _s=−0.55, p<0.041). GMF probably affected central baroreflex pathways, diminishing SMF direct stimulatory effect on sinocarotid baroreceptors and on baroreflex-mediated vasodilatatory response. The results herein may thus point to arterial baroreflex as a possible physiological mechanism for magnetic-field cardiovascular effect. It seems that geomagnetic disturbance modifies artificial magnetic fields biological effect and should be taken into consideration in the assessment of the final effect. An erratum to this article can be found at     

Effects of 25 mT static magnetic field on blood pressure in reserpine-induced hypotensive Wistar-Kyoto rats

We investigated the interrelated antihypotensive effects of static magnetic fields (SMF) and plasma catecholamine levels in reserpine-induced hypotensive Wistar-Kyoto rats. Seven-week-old male rats were exposed to two different ranges of SMF intensities, 3.0-10 mT (Bmax) or 7.5-25 mT (Bmax) for 12 weeks. Six experimental groups of 10 animals each were examined: (1) no exposure with intraperitoneal (ip) saline injection (sham exposed control); (2) 10 mT SMF exposure with ip saline injection (10 mT); (3) 25 mT SMF exposure with ip saline injection (25 mT); (4) no exposure with ip reserpine injection (RES); (5) 10 mT SMF exposure with ip reserpine injection (10 mT + RES); (6) 25 mT SMF exposure with ip reserpine injection (25 mT + RES). Reserpine (5 mg/kg) was administered three times a week for 12 weeks, and 18 h after each injection, arterial blood pressure (BP), heart rate, skin blood flow, plasma nitric oxide metabolites, plasma catecholamine levels, and behavioral parameters of a functional observational battery (FOB) were monitored. The action of reserpine significantly decreased BP, reduced plasma norepinephrine (NE), increased the FOB hunched posture score and decreased the number of rearing events in the RES group, compared with the respective age-matched control group. Exposure to 25 mT, but not 10 mT, for 2-12 weeks significantly prevented the reserpine-induced decrease of BP in the 25 mT + RES group compared with the respective RES group. Moreover, exposure to 25 mT for 5 weeks partially suppressed the reserpine-induced NE reduction, but did not bring about a complete reversal of reserpine effects. NE levels for the 25 mT + RES group for 5 weeks were significantly higher compared with the RES group, but still lower compared with the control group. In addition, the FOB hunched posture score for the 25 mT + RES group was significantly lower and the number of rearing events was higher compared with the RES group, but these behavioral parameters did not revert to control levels. There were no significant differences in any of the physiological or behavioral parameters measured between the 10 mT + RES and RES groups, nor between the two different SMF groups and the control group. These results indicate that 25 mT SMF with spatial gradients significantly suppressed the reserpine-induced hypotension and bradykinesia. The antihypotensive effects of SMF on the reserpine-treated group might be at least partially related to the inhibition of NE depletion.     

Effects of 12 mT static magnetic field on sympathetic agonist-induced hypertension in Wistar rats

We investigated the combined effects of a moderate-intensity static magnetic field (SMF) and two different sympathetic agonists, an alpha(1)-adrenoceptor agonist, phenylephrine and a beta(1)-adrenoceptor agonist, dobutamine, which induced hypertension and different hemodynamics in Wistar rats. Five-week-old male rats were continuously exposed to the SMF intensity of 12 mT (B(max)) with the peak spatial gradient of 3 mT/mm for 10 weeks. A loop-shaped flexible rubber magnet was adjusted to fit snugly around the neck region of a rat (diameter-adjustable to an animal size). Sham exposure was performed using a dummy magnet. Six experimental groups of six animals each were examined: (1) sham exposure with intraperitoneal (ip) saline injection (control); (2) SMF exposure with ip saline injection (SMF); (3) sham exposure with ip phenylephrine (1.0 microg/g) injection (PE); (4) SMF exposure with ip phenylephrine injection (SMF + PE); (5) sham exposure with ip dobutamine (4.0 microg/g) injection (DOB); (6) SMF exposure with ip dobutamine injection (SMF + DOB). Fifteen minutes after the injection of each agent, the first set of parameters, arterial blood pressure (BP) and heart rate (HR), the second set of parameters, skin blood flow (SBF) and skin blood velocity (SBV), or the third set of parameters, the number of rearing (exploratory behavior) responses and body weight was monitored. Each agent was administered three times a week for 10 weeks, and each set of parameters was monitored on different days, once a week. The dose of phenylephrine significantly increased BP and decreased HR, SBF, SBV, and the number of rearing responses in the PE group compared with those in the respective age-matched control group. The dose of dobutamine significantly increased BP and HR, increased SBF, SBV, and the number of rearing responses in the DOB group compared with those in the control group. Continuous neck exposure to the SMF alone for up to 10 weeks induced no significant changes in any of the measured cardiovascular and behavioral parameters. The SMF exposure for at least 2 weeks (1) significantly depressed phenylephrine effects on BP, SBF, SBV, and rearing activity (SMF + PE group vs. PE group); (2) significantly depressed dobutamine effects on BP, SBF, and SBV, and suppressed dobutamine-induced increase in the rearing activity (SMF + DOB group vs. DOB group). These results suggest that continuous neck exposure to 12 mT SMF for at least 2 weeks may depress or suppress sympathetic agonists-induced hypertension, hemodynamics, and behavioral changes by modulating sympathetic nerve activity.     

Spatial gradient effects of 120 mT static magnetic field on endothelial tubular formation in vitro

This study investigated the spatial magnetic gradient effects of static magnetic fields (SMF) on endothelial tubular formation by applying the maximum spatial gradient to a target site of culture wells for cell growth. The respective maximum values of magnetic flux density (B(max)), magnetic flux gradient (G(max)) and the magnetic force product of the magnetic flux density and its gradient (a parameter of magnetic force) were 120 mT, 28 mT/mm and 1428 mT(2)/mm. The effects of gradient SMF on tubular formation were compared with those of uniform SMF that has no spatial gradients on the entire bottom area of culture wells. Five experimental groups of 25 samples each were examined: (1) sham exposure (control); (2) peak gradient exposure in the peripheral part; (3) peak gradient exposure in the central part; (4) uniform exposure to 20 mT; (5) uniform exposure to 120 mT. The SMF or sham exposure was carried out for 10 days. Photomicrographs of tubular cells, immunostained with an anti-platelet-endothelial cell adhesion molecule-1 (PECAM-1 [CD31]) antibody as a pan-endothelial marker, were analyzed after the 10-day culture. Gradient SMF in the peripheral or central part was found to significantly promote tubular formation in terms of the area density and length of tubules in each peak gradient/force part of the wells, compared with the sham exposure. In contrast, uniform SMF did not induce any significant change in the tubular formation. These findings suggest that tubule formation can be promoted by applying the peak gradient/force to a target site of culture wells.     

The Influence of a gradient static magnetic field on an unstirred Belousov-Zhabotinsky reaction

It is believed that static magnetic fields (SMF) cannot affect the pattern formation of the Belousov-Zhabotinsky (BZ) reaction, which has been frequently studied as a simplified experimental model of a nonequilibrium open system, because SMF produces no induced current and the magnetic force of SMF far below 1 T is too low to expect the effects on electrons in the BZ reaction. In the present study, we examined whether the velocity of chemical waves in the unstirred BZ reaction can be affected by a moderate-intensity SMF exposure depending on the spatial magnetic gradient. The SMF was generated by a parallel pair of attracting rectangular NdFeB magnets positioned opposite each other. The respective maximum values of magnetic flux density (B(max)), magnetic flux gradient (G(max)), and the magnetic force product of the magnetic flux density its gradient (a magnetic force parameter) were 206 mT, 37 mT/mm, and 3,000 mT(2)/mm. The ferroin-catalyzed BZ medium was exposed to the SMF for up to 16 min at 25 degrees C. The experiments demonstrated that the wave velocity was significantly accelerated primarily by the magnetic gradient. The propagation of the fastest wave front indicated a sigmoid increase along the peak magnetic gradient line, but not along the peak magnetic force product line. The underlying mechanisms of the SMF effects on the anomalous wave propagation could be attributed primarily to the increased concentration gradient of the paramagnetic iron ion complexes at the chemical wave fronts induced by the magnetic gradient.     

Static magnetic field effect on the arterial baroreflex-mediated control of microcirculation: implications for cardiovascular effects due to environmental magnetic fields

Increasing evidence suggests that time-varying and static magnetic fields in the environment might affect the cardiovascular system. To explore the underlying physiology, the effect of static magnetic fields (SMFs) on the carotid baroreflex control of microcirculation was studied. Twenty-four hemodynamic monitorings were performed in rabbits sedated by pentobarbital infusion (5 mg/kg/h) during experiments that lasted 120 min. Mean femoral artery blood pressure, heart rate, and ear lobe skin microcirculatory blood flow, measured by microphotoelectric plethysmogram (MPPG), were simultaneously recorded before and after a 40 min exposure of the sinocarotid baroreceptors to Nd₂–Fe₁₄–B alloy magnets (n = 14) or sham magnets (n = 10, control series). The local SMF field was 350 mT, at the baroreceptors’ site. Arterial baroreflex sensitivity (BRS) was estimated from heart rate/blood pressure response to intravenous bolus injections of nitroprusside and phenylephrine. A significant positive correlation was found between the SMF-induced increase in BRS (ΔBRS = BRS_afterSMF − BRS_priorSMF) and the increment in microvascular blood flow (ΔMPPG = MPPG_afterSMF − MPPG_priorSMF) (r = 0.66, p < 0.009). The SMF probably modulated the arterial baroreflex-mediated microcirculatory control. This could represent one possible mechanism how environmental magnetic fields act on the cardiovascular system, and a method how to complexly adjust macro- and microcirculation with potential clinical implementation.     

Exposure to a moderate intensity static magnetic field enhances the hypotensive effect of a calcium channel blocker in spontaneously hypertensive rats

We investigated the combined effects of a moderate intensity static magnetic field (SMF) and an L-type voltage-gated Ca(2+) channel blocker, nicardipine in stroke-resistant spontaneously hypertensive rats during the development of hypertension. Five-week-old male rats were exposed to SMF intensity up to 180 mT (B(max)) with a peak spatial gradient of 133 mT/mm for 14 weeks. Four experimental groups of 14 animals each were examined: (1) sham exposure with intraperitoneal (ip) saline injection (control); (2) SMF exposure with ip saline injection (SMF); (3) sham exposure with ip nicardipine injection (NIC); (4) SMF exposure with ip nicardipine injection (SMF + NIC). A disc-shaped permanent magnet or a dummy magnet was implanted in the vicinity adjacent to the left carotid sinus baroreceptor region in the neck of each rat. Nicardipine (2 mg/kg ip) was administered three times a week for 14 weeks, and then 15 min after each injection, arterial blood pressure (BP), heart rate (HR), baroreflex sensitivity (BRS), skin blood flow (SBF), skin blood velocity (SBV), plasma nitric oxide (NO) metabolites (NO(x) = NO(2) (-) + NO(3) (-)), plasma catecholamine levels and behavioral parameters of a functional observational battery were monitored. The action of nicardipine significantly decreased BP, and increased HR, SBF, SBV, plasma epinephrine and norepinephrine in the NIC group compared with the control respective age-matched group without changing plasma NO(x) levels. Neck exposure to SMF alone for 5-8 weeks significantly suppressed or retarded the development of hypertension together with increased BRS in SMF group. Furthermore, the exposure to SMF for 1-8 weeks significantly promoted the nicardipine-induced BP decrease in the SMF + NIC group compared with the respective NIC group. Moreover, the SMF induced a significant increase in plasma NO(x) in the nicardipine-induced hypotension. There were no significant differences in any of the physiological or behavioral parameters measured between the SMF + NIC and the NIC groups, nor between the SMF and the control groups. These results suggest that the SMF may enhance nicardipine-induced hypotension by more effectively antagonizing the Ca(2+) influx through the Ca(2+) channels compared with the NIC treatment alone. Furthermore, the enhanced antihypertensive effects of the SMF on the nicardipine-treated group appear to be partially related to the increased NO(x). Theoretical considerations suggest that the applied SMF (B(max) 40 mT, 0 Hz) can be converted into a changing magnetic field (B(max) 30-40 mT, 5.7-6.5 Hz or 7.5-8.3 Hz) in the baroreceptor region by means of the carotid artery pulsation. Therefore, we propose that the moderate intensity changing magnetic field, i.e., the magnetic field modulated by the pulse rate, may influence the activity of baroreceptor and baroreflex function.     

Decreased plasma levels of nitric oxide metabolites, angiotensin II, and aldosterone in spontaneously hypertensive rats exposed to 5 mT static magnetic field

Previously, we found that whole body exposure to static magnetic fields (SMF) at 10 mT (B(max)) and 25 mT (B(max)) for 2-9 weeks suppressed and delayed blood pressure (BP) elevation in young, stroke resistant, spontaneously hypertensive rats (SHR). In this study, we investigated the interrelated antipressor effects of lower field strengths and nitric oxide (NO) metabolites (NO(x) = NO(2)(-) + NO(3)(-)) in SHR. Seven-week-old male rats were exposed to two different ranges of SMF intensity, 0.3-1.0 mT or 1.5-5.0 mT, for 12 weeks. Three experimental groups of 20 animals each were examined: (1) no exposure with intraperitoneal (ip) saline injection (sham-exposed control); (2) 1 mT SMF exposure with ip saline injection (1 mT); (3) 5 mT SMF exposure with ip saline injection (5 mT). Arterial BP, heart rate (HR), skin blood flow (SBF), plasma NO metabolites (NO(x)), and plasma catecholamine levels were monitored. SMF at 5 mT, but not 1 mT, significantly suppressed and retarded the early stage development of hypertension for several weeks, compared with the age matched, unexposed (sham exposed) control. Exposure to 5 mT resulted in reduced plasma NO(x) concentrations together with lower levels of angiotensin II and aldosterone in SHR. These results suggest that SMF may suppress and delay BP elevation via the NO pathways and hormonal regulatory systems.     

Biphasic effects of static magnetic fields on cutaneous microcirculation in rabbits

The biphasic effects of locally applied static magnetic fields (SMF) on the cutaneous microcirculation within a rabbit ear chamber (REC) were evaluated under conscious conditions. The microcirculatory vasomotion within a REC was measured continuously and analyzed multilaterally by microphotoelectric plethysmography, a real-time image analyzer and an image shearing monitor. SMF intensities at the REC were controlled at 1 mT and the duration of exposure was 10 min. Seventy-eight experimental trials were carried out on 22 healthy adult rabbits weighing 2.6-3.5 kg. Five experimental groups were chosen at random: 1) no pharmacological treatment or SMF exposure, 2) increased vascular tone induced by noradrenaline infusion without SMF exposure, 3) increased vascular tone induced by noradrenaline infusion with SMF exposure, 4) decreased vascular tone induced by acetylcholine infusion without SMF exposure, 5) decreased vascular tone induced by acetylcholine infusion with SMF exposure. The results demonstrated that SMF significantly enhanced vasodilatation, with increased vasomotion under noradrenaline-induced high vascular tone as well as vasoconstriction with reduced vasomotion under acetylcholine-induced low vascular tone. This suggests, therefore, that SMF can modulate vascular tone due to biphasic modification of vasomotion in the cutaneous tissue.     

Static magnetic field effect on microcirculation,direct versus baroreflex-mediated approach

We compared in conscious rabbits, sedated using pentobarbital intravenous (i.v.) infusion (5 mg kg^{? 1} h^{? 1}), the effect of a static magnetic field (SMF), generated by Nd₂–Fe₁₄–B magnets, on microcirculation during its 40 min local exposure to the microvascular network in cutaneous tissue [20 sham exposure and 20 SMF (0.25 T) exposure runs] or to sinocarotid baroreceptors [14 sham exposure and 14 SMF (0.35 T) exposure runs]. Mean femoral artery blood pressure (BP), heart rate (HR), arterial baroreflex sensitivity (BRS), assessed from HR and BP responses to i.v. bolus of nitroprusside and phenylephrine, and microcirculatory blood flow, using microphotoelectric plethysmography (MPPG), were simultaneously monitored. SMF significantly increased microcirculation on a 17.8% in microvascular and on a 23.3% in baroreceptor exposure series. In baroreceptor exposure series, SMF significantly decreased BP, increased heart rate variability, BRS and sodium nitroprusside (NO-donor) i.v. bolus microcirculatory vasodilatory effect. These suggest augmentation of the arterial baroreflex capacity support NO-dependent vasodilation, by increased sensitivity of vessels to NO, to be a new physiological mechanism of BP buffering and microcirculatory control. A significant positive correlation was also found between increase in BRS and in MPPG (r = 0.66, p < 0.009), indicating baroreflex participation in the regulation of the microcirculation and its enhancement after SMF exposure. Both direct and baroreflex-mediated approaches demonstrate SMF significant vasodilatory effect with potential clinical implication in macro- and microcirculatory disorders.     

Combined effect of X‐ray radiation and static magnetic fields on reactive oxygen species in rat lymphocytes in vitro

The aim of this study was to investigate the effect of static magnetic fields (SMF) on reactive oxygen species induced by X‐ray radiation. The experiments were performed on lymphocytes from male albino Wistar rats. After exposure to 3 Gy X‐ray radiation (with a dose rate of 560 mGy/min) the measurement of intracellular reactive oxygen species in lymphocytes, using a fluorescent probe, was done before exposure to the SMF, and after 15 min, 1 and 2 h of exposure to the SMF or a corresponding incubation time. For SMF exposure, 0 mT (50 µT magnetic field induction opposite to the geomagnetic field) and 5 mT fields were chosen. The trend of SMF effects for 0 mT was always opposite that of 5 mT. The first one decreased the rate of fluorescence change, while the latter one increased it. Bioelectromagnetics 34:333–336, 2013. © 2012 Wiley Periodicals, Inc.     

Effects of 120 mT static magnetic field on TGF-beta1-inhibited endothelial tubular formation in vitro

We designed this study to examine the effects of static magnetic fields (SMF; 120 mT [B(max)] and a maximum spatial magnetic flux gradient of 21 mT/mm) on inhibited tubular formation when treated with human transforming growth factor (TGF)-beta1 at a relatively high concentration (5 ng/ml). Three experimental groups of 25 samples each were examined: (1) sham exposure alone (control); (2) sham-exposure with TGF-beta1; (3) SMF exposure with TGF-beta1. The SMF or sham exposure was carried out for 10 days. Photomicrographs of tubular cells, immunostained with an anti-platelet-endothelial cell adhesion molecule-1 (PECAM-1 [CD31]) antibody as a pan-endothelial marker, were analyzed after the 10-day culture. SMF was found to significantly reverse the inhibition of TGF-beta1 on tubular formation in terms of the area density and length of tubules (arteriogenesis) in the peripheral part of the wells, compared with the TGF-beta1 treatment alone. These findings suggest that one of the possible exogenous factors for arteriogenesis might involve 'magnetic force' (the product of the magnetic flux density, the magnetic gradient, and the volume susceptibility of the cells) because values are much larger in the peripheral part than in the central part.     

Changes in Saccharomyces cerevisiae development induced by magnetic fields

Saccharomyces cerevisiae cultures exposed to 110 mT and 220 mT steady magnetic fields (SMF) were studied to observe eventual induced growth alterations and changes in metabolic activity. Cell mass (biomass) growth was evaluated by light spectrometry, and metabolic alterations were estimated on the basis of the CO2 pressure produced and by the culture media pH changes, measured at the beginning and the end of the observation. The yeast strain DAUFPE-1012, cultivated in a nonaerated liquid agar Sabouraud glucose medium, was exposed to SMF generated by NdFeBr magnets. Results showed alterations induced by 220 mT SMF as an increment in cell proliferation (1.84%) and an increased CO2 production (36.1%) as compared to control groups. Furthermore, the initial-to-final pH difference in 220 mT SMF exposed cultures was higher than the 110 mT SMF and the control values. The whole acidification and the rise in CO2 production observed after 220 mT SMF exposure did not correspond to the biomass growth values, as compared to the other cultures, and was apparently provoked by a enhancement in the cellular metabolic rate. This technique becomes very promising for future biotechnological applications in fermentative processes.     

Exposure to an inhomogeneous static magnetic field increases thermal pain threshold in healthy human volunteers

In the present experiment, the effect of a single 30 min inhomogeneous static magnetic field (SMF) exposure on thermal pain threshold (TPT) was examined in 15 young healthy human volunteers. The SMF had a maximum peak‐to‐peak amplitude of 330 mT with a maximum gradient of 13.2 T/m. In either of two experimental sessions (SMF or SHAM), four blocks of 12 TPT trials were carried out under SMF or SHAM exposure on all fingertips of the dominant hand, excluding the thumb. TPT and visual analog scale (VAS) data were recorded at 0, 15, and 30 min exposure time, and 30 min following exposure. SMF treatment resulted in a statistically significant increase in TPT during the entire exposure duration and diminished within‐block thermal habituation, leaving pain perception unchanged. These results indicate that SMF‐induced peripheral neuronal or circulatory mechanisms may be involved in the observed TPT increase by setting the pain fibre adaptation potential to higher levels. Bioelectromagnetics 32:131–139, 2011. © 2010 Wiley‐Liss, Inc.     

The effect of 100 mT SMF on activation of the hsp70 promoter in a heat shock/luciferase reporter system

Human exposure to magnetic fields, increased through use of new technologies like magnetic resonance imaging (MRI), has prompted investigations into possible effects of static magnetic fields (SMFs) on cellular processes. However, controversy still remains between many studies, which likely results from a lack of uniformity across experimental parameters, including the length of magnetic field exposure, the strength of the magnetic field, and the cell type or organism under investigation. The purpose of this research was to monitor effects of SMF exposure using real‐time luminescence photometry. The study investigated the potential interaction of a 100 mT SMF on a heat shock protein (hsp70)/luciferase reporter construct in stably transfected NIH3T3 cells. Changes in heat shock promoter activation following 100 mT SMF exposure were analyzed and detected as bioluminescence in real‐time. Two heat parameters were considered in combination with sham‐ and 100 mT‐exposed experiments: no heat or 1,800 s heat. As expected, there was a significant increase in bioluminescence in response to 1,800 s of heat alone. However, no significant difference in average hsp70 promoter activation between sham and 100 mT experiments was observed for no heat or 1,800 s heat experiments. Therefore, a 100 mT SMF was shown to have no effect on the activation of the heat shock protein promoter during SMF exposure or when SMF exposure was combined with a heat insult. J. Cell. Biochem. 108: 956–962, 2009. © 2009 Wiley‐Liss, Inc.     

Reactive oxygen species (ROS) production in human peripheral blood neutrophils exposed in vitro to static magnetic field

The aim of this study was to determine the effect of gradient static magnetic field (SMF) on reactive oxygen species (ROS) production in human neutrophils in peripheral blood in vitro. Blood samples collected from healthy individuals were incubated in an inhomogeneous SMF (in a south or north pole of the field) for 15, 30 or 45 minutes. The maximum value of induction (B _max) amounted to ≈ 60 mT. To determine the strength of the ROS production, dihydrorhodamine (123DHR) as fluorophore and phorbol 12-myristate 13-acetate (PMA) as respiratory burst stimulator were used. 123DHR oxidation by ROS was measured by flow cytometry. The exposure of blood samples to SMF induced statistically significant changes in ROS production in unstimulated and PMA-stimulated neutrophils. The observed effects were highly correlated with the exposure time and depended on the orientation of the field. Although intracellular mechanisms underlying such interactions are not thoroughly understood, it could be presumed that SMF affects ROS metabolic oscillations and their formation and inactivation. This study emphasizes the importance of proper adjustment of exposure time to SMF for any potential therapeutic applications.     

SNAIL NEURON BIOELECTRIC ACTIVITY INDUCED UNDER STATIC OR SINUSOIDAL MAGNETIC FIELDS REPRODUCES MAMMAL NEURON RESPONSES UNDER TRANSCRANIAL MAGNETIC STIMULATION

We have applied static (SMF) or alternating magnetic fields (AMF) to snail (Helix aspersa) single-unit neurons, in the range of those applied in magnetic stimulation (MS)/transcranial magnetic stimulation (TMS). From the experiments we have performed during the past 10 years, we have collected a blind selection of neurons and their responses to either SMF or AMF. Blind selection means that we do not know the nature of neurons. We do not know whether they are sensitive, motor, secretory, pacemaker, or inter-neurons. We have seen that the behavior of single-unit neurons under SMF/AMF exposure (SMF range: 3 mT–0.7 T; AMF range: 1–15 mT) fits well with the electrophysiologic activity described for mammals and human whole brain under MS/TMS (pulsed magnetic field range: 0.3 mT–2.4 T). The neuron experiments shown here have been aleatorily selected from a collection of about 200 neurons studied. Our results could explain some of the effects described induced in mammal neurons under MS/TMS for clinical purposes.