Static magnetic field blood pressure buffering, baroreflex vs. vascular blood pressure control mechanism

Gmitrov, Juraj

doi:10.3109/09553000903419973

Cited by 9 publications

(11 citation statements)

References 58 publications

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“…phenylephrine blood pressure ramps (Fig. 4) [Gmitrov, 2010]. Carotid baroreceptor magnetic activation in healthy volunteers [Gmitrov, 1996] may anticipate a similar macro‐ and microcirculatory response.…”

Section: Discussionmentioning

confidence: 99%

“…In VER series (Fig. 5), control BRS measurement was taken at 15 min and compared with that after 30 min of VER infusion (20 µg/kg/min, 60–90 min) [Gmitrov, 2010].…”

Section: Methodsmentioning

confidence: 99%

“…To exclude the direct effect of sodium nitroprusside and phenylephrine on blood pressure, HR, and skin microcirculatory blood flow, the measurement of the hemodynamic parameters preceded BRS testing. Details of experimental protocol, BRS and MPPG techniques, can be found elsewhere [Okano et al, 1999; Gmitrov et al, 2002; Gmitrov, 2010, 2013].…”

Section: Methodsmentioning

confidence: 99%

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Static Magnetic Field Versus Systemic Calcium Channel Blockade Effect on Microcirculation: Possible Mechanisms and Clinical Implementation

Gmitrov

2020

Bioelectromagnetics

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The goal was to compare static magnetic field (SMF, generated by Nd 2-Fe 14-B magnets) vasodilator capacity with verapamil (VER, a potent, clinically verified Ca 2+ channel-blocking agent), aimed to assess SMF implementation in conditions with vascular ischemia. Skin microcirculatory blood flow measured by microphotoelectric plethysmogram was recorded in conscious rabbits after 40 min of 0.25 T SMF regional exposure to ear microvascular net (SMF-Vas, n = 20), or 0.35 T to carotid baroreceptors (SMF-Car, n = 14), and compared with that after 30 min VER intravenous infusion (20 µg/kg/min, n = 20). The principal finding is that SMF-Vas, SMF-Car, and VER significantly increased microcirculatory blood flow by 17.9 ± 9.58%, 22.6 ± 11.11%, and 30.5 ± 14.06% (mean ± SEM) respectively, and there was no significant difference between all three treatments (P = 0.986). Microvascular dilation was accompanied by significant decrease of blood pressure in VER and SMF-Car cases. The decrease of arterial baroreflex sensitivity in VER contrasted with its increase in SMF-Car, coupled with improved vessel sensitivity to nitric oxide (NO) dilatory effect. This suggests that SMF can have a strong vasodilator property tailored to address diabetic, mainly NO-deficient, neural, and myogenic microvascular dysfunction, especially employing both SMFs' vasodilation synergy.

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Section: Discussionmentioning

confidence: 99%

“…In VER series (Fig. 5), control BRS measurement was taken at 15 min and compared with that after 30 min of VER infusion (20 µg/kg/min, 60–90 min) [Gmitrov, 2010].…”

Section: Methodsmentioning

confidence: 99%

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Static Magnetic Field Versus Systemic Calcium Channel Blockade Effect on Microcirculation: Possible Mechanisms and Clinical Implementation

Gmitrov

2020

Bioelectromagnetics

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“…A lot of data from basic research and clinical trials show that the exogenous magnetic field has a significant impact on many biological systems, and moderate‐intensity SMF can affect many biological systems [Ghodbane et al, 2013]. In some studies, SMF has been reported to alleviate pain [Laszlo and Gyires, 2009], hypertension [Okano and Ohkubo, 2001], wound healing [Man et al, 1999], inflammation [Weinberger et al, 1996], and microvascular circulation [Gmitrov, 2010]. However, reports of the effect of moderate‐intensity SMF on blood glucose in animals is controversial, and the effect of moderate‐intensity SMF on blood glucose in diabetic animals is rare.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Moderate Intensity Static Magnetic Fields on Diabetic Mice

Qin

Fang²,

et al. 2020

Bioelectromagnetics

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The purpose of this study was to investigate the effects of moderate-intensity static magnetic field (SMF) on diabetic mice. We studied the effects of SMF on blood glucose of normal mice by starch tolerance and glucose tolerance tests. Then, we evaluated the effects of SMF on blood glucose of diabetic mice by establishing alloxan-induced type 1 diabetic mice and high-fat diet + streptozotocin (STZ)-induced type 2 diabetic mice. The results showed that different magnetic field intensities and blank control did not affect the blood glucose of normal mice. After starch and glucose administration, different magnetic fields could improve the glucose tolerance of normal mice, and this was obvious in the 600 mT group. In the experiment of type 1 diabetic mice induced by alloxan, the results showed that different magnetic field intensities could improve the starch tolerance of mice, and that in the 400 mT group was obvious. In the experiment of type 2 diabetic mice induced by a high-fat diet + STZ, the 400 mT group could reduce food intake and water consumption in the later period. The 600 mT group could improve the starch tolerance of mice. The 400 and 600 mT groups could reduce fasting blood glucose. At the same time, total cholesterol and triglyceride decreased in different magnetic field intensities, and the 600 mT group could significantly increase the serum insulin content of mice. In summary, the results of this study suggest that SMF has a protective role in diabetic mice.

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“…NO is a highly reactive signaling molecule with basic role in an array of fundamental intracellular processes leading to vasorelaxation, inhibition of platelet aggregation, suppression of vascular smooth muscle cell proliferation, cardiovascular remodeling and atherosclerosis [2,3]. NO is permanently secreted by endothelial cells opposing vasoconstrictor effect of tonic sympathetic drive [4], contributes to arterial baroreflex and vascular blood pressure buffering mechanisms [5], and participates in fine regulation of microcirculatory blood flow adjusted to actual metabolic demands. Therefore in insulin resistant states NO deficit is coupled with severe vasodilatory dysfunction, generating a major cardiovascular risk even before the manifestation of hyperglycemia.…”

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confidence: 99%

Insulin Resistance Modification is a Game Changer for Type 2 Diabetes Treatment Strategy

Gmitrov¹

2018

Int J Diabetes Clin Res

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Insulin resistance, appearing years before diabetes main diagnostic sign, hyperglycemia, stands in the origin of type 2 diabetes (T2DM), generated by complex impairment of a spectrum biochemical processes the most important of which is the failure of phosphatidylinositol 3-kinase enzymatic chain responsible for glucose uptake and endothelial nitric oxide (NO) synthase activation. Therefore in conditions with insulin resistance the impairment of glucose uptake is strongly coupled with NO deficit and severe vasodilatory dysfunction. However T2DM conventional treatment even worsens diabetes fundamental pathophysiological mechanisms reflected by aggravated obesity and insulin resistance. These may generate vasodilatory dysfunction, arterial hypertension and dyslipidemia, diminishing intensive glycemic control mainly microvascular benefit. Glucocentric model of T2DM management should be replaced by approach focused primarily to impede insulin resistance rather then manage its cardiometabolic consequences. Antidiabetics should be selected to achieve hypoglycemic goals without increase of body weight and with ability to decrease insulin resistance, the key triggering factor of global vascular impairment and T2DM cardiovascular mortality.

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Static magnetic field blood pressure buffering, baroreflex vs. vascular blood pressure control mechanism

Cited by 9 publications

References 58 publications

Static Magnetic Field Versus Systemic Calcium Channel Blockade Effect on Microcirculation: Possible Mechanisms and Clinical Implementation

Static Magnetic Field Versus Systemic Calcium Channel Blockade Effect on Microcirculation: Possible Mechanisms and Clinical Implementation

Protective Effects of Moderate Intensity Static Magnetic Fields on Diabetic Mice

Insulin Resistance Modification is a Game Changer for Type 2 Diabetes Treatment Strategy

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