Anti-pressor effects of whole body exposure to static magnetic field on pharmacologically induced hypertension in conscious rabbits

Acute effects of whole body exposure to static magnetic field (SMF) on pharmacologically induced hypertension in a conscious rabbit were evaluated. Hypertensive and vasoconstrictive actions were induced by norepinephrine (NE) or a nonselective nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-l-arginine methyl ester (l-NAME). The hemodynamics in a central artery of the ear lobe was measured continuously and analyzed by penetrating microphotoelectric plethysmography (MPPG). Concurrently, blood pressure (BP) changes in a central artery, contralateral to that of the MPPG measured ear lobe, were monitored. Magnetic flux densities were 5.5 mT (Bmax), the magnetic gradient peaked in the throat at the level of approximately 0.09 mT/mm, and the duration of exposure was 30 min. The results demonstrated that under normal physiological conditions without treatment of pharmacological agents, there were no statistically significant differences in the hemodynamics and BP changes between the sham and the SMF exposure alone. Under pharmacologically induced hypertensive conditions, the whole body exposure to nonuniform SMF with peak magnetic gradient in the carotid sinus baroreceptor significantly attenuated the vasoconstriction and suppressed the elevation of BPs. These findings suggest that antipressor effects of the SMF on the hemodynamics under NE or l-NAME induced high vascular tone might be, in part, dependent on modulation of NE mediated response in conjunction with alteration in NOS activity, thereby modulating BPs.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Verapamil protective effect on natural and artificial magnetic field cardiovascular impact

Previously we found an opposite effect of artificial static magnetic field (SMF) and natural geomagnetic field (GMF) on arterial baroreceptors. A 0.35 T SMF increased baroreflex sensitivity (BRS), whereas GMF disturbance decreased BRS. Here, we investigated interrelated impacts on arterial baroreceptors of 0.35 T SMF, generated by Nd(2)-Fe(14)-B alloy magnets, GMF, and verapamil, a Ca(2+) channel blocking agent. We measured BRS in rabbits before and after local SMF exposure of sinocarotid baroreceptors or after simultaneous SMF and verapamil application, in conjunction with geomagnetic disturbance during actual experimental run (determined by K-index) and geomagnetic disturbance over the preceding 24 h of each experiment (A(k)-index). BRS was estimated from peak responses of mean arterial pressure (MAP) and heart rate, expressed as percentages of the resting values preceding each pair of pressure (phenylephrine) and depressor drug (nitroprusside) injections. Prior to verapamil and/or SMF application we found a significant positive correlation of K-index with MAP (t = 2.39, P =.021, n = 44), but negative with BRS (t = -4.60, P =.0003, n = 44), and found a negative correlation of A(k)-index with BRS (t = -2.7, P = 0.01, n = 44). SMF induced an increase in BRS (0.79 +/- 0.1 vs. 1.15 +/- 0.1 bpm%/mmHg%, initial value vs. SMF exposure, P <.0002, n = 26). Verapamil infusion blocked the SMF and GMF effect on BRS, indicating Ca(2+) channels as a possible site of both fields' impact. SMF and GMF probably affect baroreceptor sensory transduction, modulating baroreceptor membranes' Ca(2+) channel permeability.     

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.     

Acute exposure to a moderate strength static magnetic field reduces edema formation in rats

External application of static magnetic fields (SMF), used specifically for the treatment of inflammatory conditions such as soft tissue injuries, has recently become popular as a complementary and/or alternative therapy with minimal investigation into efficacy or mechanism. Localized inflammation was induced via injection of inflammatory agents lambda-carrageenan (CA) or histamine into rat hindpaws, alone or in conjunction with pharmacological agents, resulting in a spatially and temporally defined inflammatory reaction. Application of a 10- or 70-mT, but not a 400-mT, SMF for 15 or 30 min immediately following histamine-induced edema resulted in a significant, 20-50% reduction in edema formation. In addition, a 2-h, 70-mT field application to CA-induced edema also resulted in significant (33-37%) edema reduction. Field application before injection or at the time of maximal edema did not influence edema formation or resolution, respectively. Together, these results suggest the existence of a therapeutic threshold of SMF strength (below 400 mT) and a temporal dependence of efficacy. Administration of pharmacological agents directed at nitric oxide signaling and L-type Ca(2+) channel dynamics in conjunction with SMF treatment and histamine-induced edema revealed that the potential mechanism of SMF action may be via modulation of vascular tone through effects on L-type Ca(2+) channels in vascular smooth muscle cells.     

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.     

Real-time measurement of cytosolic free calcium concentration in HL-60 cells during static magnetic field exposure and activation by ATP

Calcium ions are involved in a number of important signal transduction pathways in cells. Cytosolic calcium concentration ([Ca(2+)](c)) can be affected by the activation of Ca(2+) channels through the action of ligands such as ATP. The response of [Ca(2+)](c) to ligands may be affected by external factors like magnetic fields. The purpose of this study was to determine if exposure to a static magnetic field (SMF) for 800 s altered the [Ca(2+)](c) response to ATP in undifferentiated HL-60 cells. We sham exposed or field exposed fura-2 loaded HL-60 cells to a SMF of 1, 10, and 100 mT. Cells were activated with ATP 300 s into the exposure. The level of [Ca(2+)](c) was followed before, during, and after field or sham exposure with a ratiometric fluorescence spectroscopy system. It was found that high concentrations of ATP resulted in greater [Ca(2+)](c) responses, but faster recovery to near basal levels. The application of 1, 10, or 100 mT SMF did not affect the [Ca(2+)](c) response to ATP. Future work could examine the effect of a longer SMF exposure on the [Ca(2+)](c) response to ATP. Longer exposures might provide sufficient time for morphological changes in the plasma membrane to occur.     

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.     

Artificial static and geomagnetic field interrelated impact on cardiovascular regulation

Spreading evidence suggests that environmental and artificial magnetic fields have a significant impact on cardiovascular system. The modulation of cardiovascular regulatory mechanisms may play a key role in observed effects. The objective was to study interrelated impacts of artificial static magnetic field (SMF) and natural geomagnetic field (GMF) on arterial baroreceptors. We studied baroreflex sensitivity (BRS) in conscious rabbits before and after 40 min of sham (n = 20) or application of Nd2-Fe14-B alloy magnets (n = 26) to the sinocarotid baroreceptor region in conjunction with GMF disturbance during the actual experiment, determined by K- and A(k)-indexes from a local geomagnetic observatory. SMF at the position of baroreceptors was 0.35 T. BRS was estimated from peak responses of mean arterial pressure (MAP) and heart rate expressed as percentages of the resting values preceding each pair of pressure (phenylephrine) and depressor drug (nitroprusside) injections. We observed a significant increase in BRS for the nitroprusside depressor test (0.78 +/- 0.1 vs. 1.15 +/- 0.14 bpm/mmHg%, initial value vs. SMF exposure, P <.0002) and a tendency for phenylephrine pressor test to increase in BRS. Prior to SMF exposure, a significant positive correlation was found between actual K index values and MAP (t = 2.33, P =.025, n = 46) and a negative correlation of the K index with BRS (t = -3.6, P =.001, n = 46). After SMF exposure we observed attenuation of the geomagnetic disturbance induced a decrease in BRS. Clinical trials should be performed to support these results, but there is a strong expectation that 0.35 T SMF local exposure to sinocarotid baroreceptors will be effective in cardiovascular conditions with arterial hypertension and decreased BRS, due to a favorable SMF effect on the arterial baroreflex. Magnets to the sinocarotid triangle along with modification of the pharmacotherapy for hypertension should be especially effective on days with intense geomagnetic disturbance, in moderating sympathetic activation and baroreceptor dysfunction.     

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.     

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.     

Effect of static magnetic fields on survival of leukaemia-prone AKR mice

Summary The influence of a life-long exposure to static magnetic fields (SMF) on the lifespan of female AKR mice which develop spontaneous lymphoblastic leukaemia was investigated. Exposure all day long to a circular SMF, 4.6 mT maximal intensity or 2 h a day, 5 consecutive days a week to a uniform SMF of 400 mT did not modify the lifespan of mice. Exposure 2 h a day, 5 consecutive days a week to a uniform SMF of 600 or 800 mT modified the lifespan: about 50% of the population had a longer survival than the controls. Mice exposed 30 min a day 5 consecutive days a week to a non-uniform SMF presented the same trend.     

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.     

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