Abstract
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.
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