ВРЕМЕННАЯ СТРУКТУРА ЭЛЕКТРОЛИТНОГО И МИКРОЭЛЕМЕНТНОГО ГОМЕОСТАЗА ПРИ СТРЕССЕ И ИШЕМИЧЕСКОЙ БОЛЕЗНИ СЕРДЦА

Four-hour urine and blood specimen were collected over a span of 48-120 hours from 70 healthy subjects, 40 patients with IHD, 15 intact rabbits, 20 rabbits under the action of stress. Each specimen was analyzed for electrolytes (sodium, potassium, phosphorus, chlorine, calcium, magnesium) and trace elements (iron, copper, zinc, chromium, cadmium, vanadium). Rhythm parameters have been estimated by dispersion analysis for nonsinusoidal rhythms and by nonlinear least squares method for sinusoidal rhythms. In healthy subjects in 91% cases of 593 rhythmological investigations urinary excretion electrolytes and trace elements statistically significant rhythms were observed. In healthy subjects and in intact rabbits electrolytes and trace elements rythms were circadian in 75-92% of cases. Acrophases of rhythms were mostly individual. In early stage of IHD and in rabbits under the action of stress electrolytes and trace elements rhythms were statistically non significant in 20-43% of cases. Among significant rhythms of infradian ones (45-60%) prevail. Mesors of sodium, chlorine, phosphorus, iron, copper, zinc, chromium and vanadium excretion rhythms were statically significantly higher than in healthy subjects. Mesors of calcium and magnesium were statically significantly lower than in healthy subjects. Amplitudes of chlorine, phosphorus, iron, copper, zinc were statistically significantly higher than in healthy subjects. Amplitudes of sodium/potassium, magnesium statistically significantly lower than in healthy subjects.Проведено клинико-экспериментальное исследование временной структуры электролитного и микроэлементного гомеостаза при стрессе и ишемической болезни сердца (ИБС). Обследованы 70 здоровых лиц, 40 больных ИБС. Исследование проводилось во все времена года при сохранении одинаковых условий сна и бодрствования, приёма пищи, поваренной соли и жидкости. Забор мочи осуществлялся в течение 72-120 ч с 4-часовыми интервалами. Определение 14 показателей (объём мочи, натрий, калий, коэффициент натрий/калий, хлор, кальций, магний, фосфор, железо, медь, цинк, хром, кадмий и ванадий) проводилось в 18-30 порциях мочи для каждого обследуемого. Экспериментальная работа выполнена на кроликах-самцах породы шиншилла. Первая серия проведена на интактных животных. Во второй серии воспроизводили стресс. У всех животных в течение двух суток с 4-часовыми интервалами забирали кровь, а также 4-часовые порции мочи. Для оценки параметров ритмов использованы нелинейный метод наименьших квадратов и метод оценки повторяемости фрагментов исследуемой кривой, основанный на дисперсионном анализе. Показано, что при ИБС и длительном стрессе в эксперименте показатели циркадианной организации водно-минерального гомеостаза трансформируются в непериодические колебания или формируется в основном инфрадианная ритмичность, изменяются величины некоторых мезоров и амплитуд

Editorial 1. To prevent a million heart attacks and strokes by 2022: Mission impossible

[No abstract available

Can functional food security decrease the epidemic of obesity and metabolic syndrome? A viewpoint

The world is still ignorant about the role of functional food security characterized by diversity and adequacy of nutrients that may have been beneficial and abundant in the Paleolithic diet 40,000 years ago because of food diversity. Therefore, the increased prevalence of metabolic syndrome and the resultant type 2 diabetes, hypertension and heart disease throughout the world, are closely linked to food security via westernized dietary patterns, physical inactivity, and rapid increase in the rate of obesity. There is substantial evidence that increased intake of functional foods can bring about a significant decline in the epidemic of obesity and metabolic syndrome, resulting in health promotion. We therefore propose that functional food security can maintain the normal physiology and metabolism of our bodies, resulting in prevention of diseases and improvement of world health. © 2016 Nova Science Publishers, Inc

Can functional food security decrease the epidemic of obesity and metabolic syndrome? A viewpoint

The world is still ignorant about the role of functional food security characterized by diversity and adequacy of nutrients that may have been beneficial and abundant in the Paleolithic diet 40,000 years ago because of food diversity. Therefore, the increased prevalence of metabolic syndrome and the resultant type 2 diabetes, hypertension and heart disease throughout the world, are closely linked to food security via westernized dietary patterns, physical inactivity, and rapid increase in the rate of obesity. There is substantial evidence that increased intake of functional foods can bring about a significant decline in the epidemic of obesity and metabolic syndrome, resulting in health promotion. We therefore propose that functional food security can maintain the normal physiology and metabolism of our bodies, resulting in prevention of diseases and improvement of world health. © 2016 Nova Science Publishers, Inc

Can climate, weather, cosmos, and environmental degradation predispose to cardiovascular and other diseases?

The internal environment of our body systems interacts with environment in the biosphere and cosmos; the earth rotates around its axis, and around the sun in the cosmos, all living species, including humans, animals and plants, are exposed to storms induced by solar activity, geomagnetic activity, cosmic ray activity and gravitational activity. Magnetic storms may be responsible for changes in climate weather in the biosphere and cosmos as well as on earth which may influence physiology and metabolisms as well as physio-pathogenesis of diseases. Cosmology is the science dealing with knowledge about origin and development of universe, including biology related to the cosmos. Therefore, it is pertinent to call cosmo-biology, when dealing with effects of the cosmos on biological functions. Mental and spiritual health, and also possibly physical and social health, may be under the influence of solar activity, geomagnetic activity and cosmic ray activity that have major effects on space weather and climate in the cosmos. Environmental degradation may disturb magnetic activity in the cosmos, leading to changes in climate with increase in environmental temperatures causing longer summer heat waves that increase mortality, particularly among vulnerable populations such as elderly and poor people, residents of urban heat islands, and people with mental illness. Higher temperatures also increase ozone levels, compromising lung function and exacerbating asthma which may worsen due to earlier and longer pollen seasons, elevating exposure to allergens and increasing allergic sensitization and asthma episodes. Higher temperatures may result in larger and longer forest fires, reducing downwind air quality and increasing hospitalizations for respiratory and cardiovascular conditions like heart attack and sudden death. Increases in temperatures above 40°C may also predispose to heart attack. © 2018, Nova Science Publishers, Inc.. All rights reserved

Brain-heart interactions and circadian rhythms in chronic heart failure (Homage to Dr. Franz Halberg on the 2nd anniversary of his death on 9th June 2013)

Background. Professor Franz Halberg contributed greatly to our understanding of the importance of chronobiology in prevention, intervention, and treatment of CVD: hence this article of remembrance. Clinical and biochemical manifestations of chronic heart failure (HF) may be due to interactions of the brain and the heart. Circadian rhythms may be lost via neuro-humoral adaptations, such as activation of the renin-angiotensinaldosterone and sympathetic nervous systems in the brain, heart, and peripheral vessels in a milieu of melatonin deficiency. Methods. Internet and database searches and discussion with colleagues. Results. Experimental and clinical evidence indicates that chronic HF may be associated with autonomic imbalance with increased sympathetic nerve activity and a withdrawal of parasympathetic activity, with the target of involvement being the heart. Brain-heart interactions may result from an increased systemic and cerebral angiotensin II signaling since plasma angiotensin II is increased in humans and animals with chronic HF. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites causing increased contractility of the heart, as an adaptation, during chronic HF. Angiotensin II signaling is enhanced in different brain sites such as the paraventricular nucleus (PVN), rostral ventrolateral medulla (RVLM) and area postrema (AP) via neuregulin-brain natriuretic peptide release from these sites which influences the function of cardiomyocytes and the heart. We propose that blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the PVN. Experimental studies indicate that administration of an angiotensin receptor blocker by injection into the AP activates the sympathoinhibitory baroreflex indicating that receptor blockers act by increasing parasympathetic activity which has a beneficial effect on cardiomyocyte function. Angiotensin II also elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings in chronic HF resulting in an increase in sympathetic nerve activity. A rise in circulating angiotensin II during chronic HF may increase the sympatho-excitatory chemoreflex and inhibit the sympatho-inhibitory baroreflex resulting in cardiomyocyte dysfunction and worsening of HF. Conclusion. Brain-heart interactions and damage to the circadian system with increased circulating angiotensin II signaling may directly act on the brain via the subfornical organ and the AP to increase sympathetic outflow and worsening of neuro-humoral adaptations leading to chronic HF. © 2015 Nova Science Publishers, Inc

Brain-heart interactions and circadian rhythms in chronic heart failure (homage to Dr. Franz Halberg on the 2nd anniversary of his death on 9th june 2013)

Background. Professor Franz Halberg contributed greatly to our understanding of the importance of chronobiology in prevention, intervention, and treatment of CVD: hence this article of remembrance. Clinical and biochemical manifestations of chronic heart failure (HF) may be due to interactions of the brain and the heart. Circadian rhythms may be lost via neuro-humoral adaptations, such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems in the brain, heart, and peripheral vessels in a milieu of melatonin deficiency. Methods. Internet and database searches and discussion with colleagues. Results. Experimental and clinical evidence indicates that chronic HF may be associated with autonomic imbalance with increased sympathetic nerve activity and a withdrawal of parasympathetic activity, with the target of involvement being the heart. Brain-heart interactions may result from an increased systemic and cerebral angiotensin II signaling since plasma angiotensin II is increased in humans and animals with chronic HF. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites causing increased contractility of the heart, as an adaptation, during chronic HF. Angiotensin II signaling is enhanced in different brain sites such as the paraventricular nucleus (PVN), rostral ventrolateral medulla (RVLM) and area postrema (AP) via neuregulin-brain natriuretic peptide release from these sites which influences the function of cardiomyocytes and the heart. We propose that blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the PVN. Experimental studies indicate that administration of an angiotensin receptor blocker by injection into the AP activates the sympatho-inhibitory baroreflex indicating that receptor blockers act by increasing parasympathetic activity which has a beneficial effect on cardiomyocyte function. Angiotensin II also elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings in chronic HF resulting in an increase in sympathetic nerve activity. A rise in circulating angiotensin II during chronic HF may increase the sympatho-excitatory chemoreflex and inhibit the sympatho-inhibitory baroreflex resulting in cardiomyocyte dysfunction and worsening of HF. Conclusion. Brain-heart interactions and damage to the circadian system with increased circulating angiotensin II signaling may directly act on the brain via the subfornical organ and the AP to increase sympathetic outflow and worsening of neurohumoral adaptations leading to chronic HF. © 2016 Nova Science Publishers, Inc

Brain-heart interactions and circadian rhythms in chronic heart failure (homage to Dr. Franz Halberg on the 2nd anniversary of his death on 9th june 2013)

Background. Professor Franz Halberg contributed greatly to our understanding of the importance of chronobiology in prevention, intervention, and treatment of CVD: hence this article of remembrance. Clinical and biochemical manifestations of chronic heart failure (HF) may be due to interactions of the brain and the heart. Circadian rhythms may be lost via neuro-humoral adaptations, such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems in the brain, heart, and peripheral vessels in a milieu of melatonin deficiency. Methods. Internet and database searches and discussion with colleagues. Results. Experimental and clinical evidence indicates that chronic HF may be associated with autonomic imbalance with increased sympathetic nerve activity and a withdrawal of parasympathetic activity, with the target of involvement being the heart. Brain-heart interactions may result from an increased systemic and cerebral angiotensin II signaling since plasma angiotensin II is increased in humans and animals with chronic HF. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites causing increased contractility of the heart, as an adaptation, during chronic HF. Angiotensin II signaling is enhanced in different brain sites such as the paraventricular nucleus (PVN), rostral ventrolateral medulla (RVLM) and area postrema (AP) via neuregulin-brain natriuretic peptide release from these sites which influences the function of cardiomyocytes and the heart. We propose that blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the PVN. Experimental studies indicate that administration of an angiotensin receptor blocker by injection into the AP activates the sympatho-inhibitory baroreflex indicating that receptor blockers act by increasing parasympathetic activity which has a beneficial effect on cardiomyocyte function. Angiotensin II also elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings in chronic HF resulting in an increase in sympathetic nerve activity. A rise in circulating angiotensin II during chronic HF may increase the sympatho-excitatory chemoreflex and inhibit the sympatho-inhibitory baroreflex resulting in cardiomyocyte dysfunction and worsening of HF. Conclusion. Brain-heart interactions and damage to the circadian system with increased circulating angiotensin II signaling may directly act on the brain via the subfornical organ and the AP to increase sympathetic outflow and worsening of neurohumoral adaptations leading to chronic HF. © 2016 Nova Science Publishers, Inc