Decrease In Peripheral Vascular Resistance Research Articles

Cardiovascular responses to experimental weight gain in humans: a feasibility study.

Obesity and hypertension share a well known association. However, the mechanisms underlying their relationship are not well understood. Our goal was to assess the feasibility of a longitudinal, interventional weight gain study with detailed cardiovascular measurements in humans. Sixteen healthy, normotensive, young, male volunteers (28 ± 7 years) were enrolled. Body composition, biochemical and cardiovascular data were obtained at baseline, and after an 8-week period of overfeeding (800-1000 kcal/day). Blood pressure (BP), cardiac output (CO) and peripheral vascular resistance (PVR) were determined, as were the minimum forearm vascular resistance (MFVR), forearm blood flow (FBF) response to mental stress and heart rate variability (HRV) parameters. Overfeeding resulted in a median weight gain of 5.6 kg [interquartile range (IQR) 4.6-6.4 kg; P < 0.001]. Seated systolic and diastolic BP were significantly increased by 10 ± 9 and 4 ± 6 mmHg, respectively, after weight gain ( P < 0.001 and P = 0.011, respectively). CO also increased and PVR decreased significantly as a result of weight gain ( P = 0.032 and P = 0.044, respectively). MFVR was also significantly decreased after weight gain ( P = 0.023). The FBF response to mental stress was blunted significantly ( P = 0.002), and sympathovagal balance and responsiveness to orthostatic challenge altered moderately after weight gain. Our overfeeding regimen resulted in moderate weight gain and significant increases in BP. An increase in CO is likely to be the dominant mechanism underlying the observed BP changes, with decreases in PVR partially compensating for these effects. Experimental weight gain, coupled with detailed cardiovascular phenotyping, is a feasible model to examine potential mechanisms underlying obesity-associated hypertension in young adults.

Patophysiological basis of folate cycle disorders and vitamin D deficiency in the development of syncope in childhood

There are many reports about the role of vitamins B6, B9, B12, and D in the development of cardiovascular diseases. However, most of them relate mainly to the adult population and are limited relative to grades in children with syncope. Understanding the role of these vitamins in the pathogenesis of syncope will help expand the range of therapeutic and preventive care for children. The purpose of the study was to analyse current scientific achievements regarding the role of the folate cycle and vitamin D in the genesis of syncope in childhood. The PubMed Medline and Scopus databases were used and the following search terms were used: “syncope” and “vitamin B”; “syncope” and “homocysteine”; “syncope” and “vitamin D”. The paper summarises the role of vitamin B12 deficiency in delayed myelination and nerve conduction, increased serum norepinephrine levels, and possible pathogenetic mechanisms for the development of noncardiogenic syncope. Scientific facts of the effect of vitamins B1, B6, and B9 on the functioning of the cardiovascular and nervous systems in children are described. The prevalence of vitamin D deficiency in 60-73% of children with vasovagal syncope and its relationship with the symptoms of the disease was established. Probable pathogenetic mechanisms of vitamin D deficiency in the development of syncope, namely a decrease in peripheral vascular resistance, a violation of neuronal conduction of the baroreflective mechanism, and heart muscle dysfunction, are analysed. The findings will allow doctors and researchers to better approach the diagnosis, prevention, and treatment of syncope in childhood and can serve as a basis for developing new strategies to manage the condition and improve medical practices

Cardiovascular Diseases Associated with Pregnancy: An Overview

Valvular heart disease is the most common cardiac problem complicating pregnancy, and pregnancy in most women with heart disease has a favourable maternal and fetal outcome. With the exception of patients with Eisenmenger syndrome, pulmonary vascular obstructive disease, and Marfan syndrome with aortopathy, maternal death during pregnancy in women with heart disease is rare. However, pregnant women with heart disease do remain at risk for other complications including heart failure, arrhythmia, and stroke. Women with congenital heart disease now comprise the majority of pregnant women with heart disease seen at referral centres. The next largest group includes women with rheumatic heart disease. Peripartum cardiomyopathy, though infrequent, will be discussed in view of its unique relation to pregnancy. Two groups of conditions not discussed further are coronary artery disease which is infrequently encountered, and isolated mitral valve prolapse, which generally has an excellent outcome. Hormonally mediated increases in blood volume, red cell mass, and heart rate result in a major increase in cardiac output during pregnancy; cardiac output peaks during the second trimester, and remains constant until term. Gestational hormones, circulating prostaglandins, and the low resistance vascular bed in the placenta result in concomitant decreases in peripheral vascular resistance and blood pressure. During labour and delivery, pain and uterine contractions result in additional increases in cardiac output and blood pressure. Immediately following delivery, relief of caval compression and autotransfusion from the emptied and contracted uterus produce a further increase in cardiac output. Most haemodynamic changes of pregnancy resolve by two weeks postpartum.

Different cardiovascular and pulmonary phenotypes for single- and double-knock-out mice deficient in BMP9 and BMP10.

Aims BMP9 and BMP10 mutations were recently identified in patients with pulmonary arterial hypertension, but their specific roles in the pathogenesis of the disease are still unclear. We aimed to study the roles of BMP9 and BMP10 in cardiovascular homeostasis and pulmonary hypertension using transgenic mouse models deficient in Bmp9 and/or Bmp10.Methods and resultsSingle- and double-knockout mice for Bmp9 (constitutive) and/or Bmp10 (tamoxifen inducible) were generated. Single-knock-out (KO) mice developed no obvious age-dependent phenotype when compared with their wild-type littermates. However, combined deficiency in Bmp9 and Bmp10 led to vascular defects resulting in a decrease in peripheral vascular resistance and blood pressure and the progressive development of high-output heart failure and pulmonary hemosiderosis. RNAseq analysis of the lungs of the double-KO mice revealed differential expression of genes involved in inflammation and vascular homeostasis. We next challenged these mice to chronic hypoxia. After 3 weeks of hypoxic exposure, Bmp10-cKO mice showed an enlarged heart. However, although genetic deletion of Bmp9 in the single- and double-KO mice attenuated the muscularization of pulmonary arterioles induced by chronic hypoxia, we observed no differences in Bmp10-cKO mice. Consistent with these results, endothelin-1 levels were significantly reduced in Bmp9 deficient mice but not Bmp10-cKO mice. Furthermore, the effects of BMP9 on vasoconstriction were inhibited by bosentan, an endothelin receptor antagonist, in a chick chorioallantoic membrane assay.ConclusionsOur data show redundant roles for BMP9 and BMP10 in cardiovascular homeostasis under normoxic conditions (only combined deletion of both Bmp9 and Bmp10 was associated with severe defects) but highlight specific roles under chronic hypoxic conditions. We obtained evidence that BMP9 contributes to chronic hypoxia-induced pulmonary vascular remodelling, whereas BMP10 plays a role in hypoxia-induced cardiac remodelling in mice.

The influence of plant saponins on the elasticity parameters of the great arteries in patients with multifocal atherosclerosis

Background. Among the goals of pathogenetic therapy in patients with multifocal atherosclerosis, not only control of the intensity of atherogenesis, but also the elastic properties of the arterial system is becoming increasingly important, which opens up additional ways to reduce overall and cardiovascular mortality in this category of patients.&#x0D; Aim. To evaluate effectiveness of medication Vazosponin (ZAO Vifitekh, Russia), which is a source of plant saponins in a dosage 400 mg per day, on the indicators of the elasticity of the great arteries.&#x0D; Materials and methods. The study included 100 patients with multifocal atherosclerosis: those who had had myocardial infarction or percutaneous coronary intervention during the previous 2 1 2 months and who had stenosing atherosclerosis of peripheral arteries brachiocephalic arteries and/or arteries of the lower extremities. The main group MG (n=50) consisted of patients who received combined hypolipidemic treatment: atorvastatin in dosage 40 mg/day + Vazosponin 400 mg/day along with baseline treatment. The control group (CG) included 50 patients who received only atorvastatin in dosage 40 mg/day along with baseline treatment. The observation period for each patient was 90 days with 3 control points (on the 1st, 10th and 90th days of therapy), in which were evaluated the elasticity indicators of the main arteries pulse wave velocity, linear blood flow velocity, total peripheral vascular resistance, actual specific vascular resistance.&#x0D; Results. There was a decrease in pulse wave velocity in both groups by the 90th day of the study, with a significant advantage in the group of patients who received Vazosponin: in the CG the indicator decreased by 7.3% (p0.05), in the MG by 19.3% (p0.05). The decrease in linear blood flow velocity was 14.3% (p0.05), in the CG the indicator decreased by 5.7% (p0.05). The dynamics of peripheral vascular resistance indicators showed an obvious advantage in the group of patients who received plant saponins: in the MG of patients, a decrease in total peripheral vascular resistance was detected by an average of 11.0% (p=0.006) and actual specific vascular resistance by 39.3% (p=0.0008), while in the CG by 4.5% and 5.0%, respectively.&#x0D; Conclusion. The addition of Vazosponin to the basic therapy of patients with multifocal atherosclerosis made it possible to achieve an additional increase in the elasticity of the arterial system, a significant decrease in peripheral vascular resistance, and the elimination of the escape effect of basic therapy. The data presented make it possible to consider the possibility of using preparations of plant saponins in combination therapy of patients with multifocal atherosclerosis who have instrumentally verified violations of the elastic properties of the arterial system.

Propofol Decreases the Augmentation Index of Central Arteries via a Delay in the Pulse Wave Reflection

Background Procedural sedation with propofol is widely used to reduce stress and suppress cardiovascular responses to anxiety and fear during medical and dental treatments. A well-known adverse event of propofol is a decrease in peripheral vascular resistance resulting in hypotension; however, the effects on intravascular pressure at the central arteries are unknown. Intravascular pressure is formed by the synthesis of reflected waves from the periphery with forward pulse waves produced during ejection, and the augmented pressure by the reflected waves is one of the determinants of the systolic blood pressure (BP) at the central arteries and is known to be related to cardiovascular events. We tested the hypotheses that propofol reduces the augmentation index (AIx) in the carotid artery and that the reduction is caused by a delay in the arrival time of the reflected wave (Tr). Methods Beat-by-beat finger BP and heart rate (HR) were continuously recorded in seven healthy young men (Age: 30 ± 2 years). Central BP, AIx, Tr of the carotid artery, and carotid-to-femoral pulse wave velocity (cfPWV) were measured using applanation tonometry during supine rest before (BL) and 20 min after the onset of continuous administration of propofol (PRO). This study was approved by the Institutional Review Board of Matsumoto Dental University. Results Systolic BP was lower in PRO than in BL (P < 0.001) in both peripheral and central arteries, while it was lower in the central artery than in the peripheral artery in PRO (80 ± 5 and 96 ± 6 mmHg, P < 0.001). HR in PRO remained unchanged from BL. AIx was decreased (−40.9 ± 10.3 vs −11.8 ± 11.3%, P < 0.001), and Tr was prolonged (199 ± 14 vs 173 ± 8 ms, P < 0.001) in PRO than in BL at the carotid artery. A negative correlation was found between AIx and Tr (r = −0.91, P < 0.001). Furthermore, Tr was negatively correlated with cfPWV (r = −0.72, P = 0.004), but not with the effective reflected length (P = 0.291). Conclusions Since propofol delayed the time when the reflected wave reached the large vessels, the interval between the peaks of the forward wave and the reflected wave widened, resulting in a decreased peak value of the augmented pressure. These results suggest that the carotid artery pressure is decreased by propofol-induced reduction in augmentation pressure, which is dependent on the delay in the arrival time of the reflected wave to the central arteries.

Dexamethasone blunts postspinal hypotension in geriatric patients undergoing orthopedic surgery: a double blind, placebo-controlled study

BackgroundPost-spinal anesthesia (PSA) hypotension in elderly patients is challenging. Correction of PSA hypotension by fluids either colloids or crystalloids or by vasoconstrictors pose the risk of volume overload or compromising cardiac conditions. Dexamethasone is used to treat conditions manifested by decrease of peripheral vascular resistance. The research team was the first to test the hypothesis of its role in preventing or decreasing the incidence of PSA hypotension.MethodsOne hundred ten patients, aged 60 years or more were recruited to receive a single preoperative dose of dexamethasone 8 mg IVI in 100 ml normal saline (D group) (55 patients) 2 h preoperatively, and 55 patients were given placebo (C group) in a randomized, double-blind trial. Variations in blood pressure and heart rate in addition to the needs of ephedrine and/or atropine following spinal anesthesia (SA) were recorded. SA was achieved using subarachnoid injection of 3 ml hyperbaric bupivacaine 0.5%.ResultsDemographic data and the quality of sensory and motor block were comparable between groups. At 5th, 10th minutes post SA; systolic, diastolic and mean arterial pressures were statistically significant higher in D group. At 20th minutes post SA; the obtained blood pressure readings and heart rate changes didn’t show any statistically significance between groups. The need for ephedrine and side effects were statistically significant lower in D group than C group.ConclusionPost-spinal anesthesia hypotension, nausea, vomiting and shivering in elderly patients were less common after receiving a single preoperative dose of dexamethasone 8 mg IVI than control.Registration numberClinicalTrials.gov Identifier: NCT 03664037, Registered 17 September 2018 - Retrospectively registered, http://www.ClinicalTrial.gov

IL (Interleukin)-1 Receptor Antagonist Increases Ang (Angiotensin [1-7]) and Decreases Blood Pressure in Obese Individuals.

IL (Interleukin)-1 antagonism decreases blood pressure in obese individuals. The underlying mechanisms are unknown. Based on experimental data, we hypothesized an effect of IL-1 antagonism via modulation of the renin-angiotensin-aldosterone system. In this explorative study, we examined shorter- (2 days) and longer-term effects (4 weeks) of IL-1 antagonism (anakinra/Kineret) on renin-angiotensin system peptide profiles and on hemodynamic parameters assessed by noninvasive measurement in obese (body mass index ≥30 kg/m2) individuals from 2 interventional trials (a prospective interventional trial [n=73] and a placebo controlled-double blinded interventional trial [n=67]). A total of 140 patients were included. Systolic blood pressure decreased after short-term (absolute difference -5.2 mm Hg [95% CI, -8.5 to -1.8]; P=0.0006) and after longer-term treatment with anakinra (absolute difference -3.9 mm Hg [95% CI, -7.59 to -0.21]; P=0.04), with no change in blood pressure in the placebo group. Upon IL-1 antagonism, equilibrium levels of Ang II (angiotensin II), Ang I, aldosterone, and renin remained unchanged. In contrast, Ang (1-7) peptide levels increased after 4 weeks (between-group difference 16.35 pmol/L [95% CI, 1.22-30.17], P=0.03), as well as the Ang (1-7)/Ang II ratio (between-group difference 0.42 [95% CI, 0.17-0.67], P=0.02) in comparison to placebo. Consistently, the stroke systemic vascular resistance index significantly decreased in the anakinra group (between-group difference of -62.65 dyn/sec per cm-5 per m2 [95% CI, -116.94 to -18.36], P=0.008, consistent with a 25% decrease). IL-1 antagonism increased the vasodilatory Ang (1-7) peptide after 4 weeks of treatment in obese individuals, paralleled by a decrease in peripheral vascular resistance. These findings point to an IL-1 mediated blood pressure-lowering mechanism via modulation of Ang (1-7). Registration- URL: https://www.clinicaltrials.gov. Unique identifiers: NCT02227420 and NCT02672592.

SAT-066 Effect Of Interleukin-1-receptor Antagonist On Hemodynamics And Renin-angiotensin-aldosterone System In Obese Individuals

Background: Interleukin (IL)-1 antagonism led to a decrease of systolic blood pressure (5mmHg) in obese individuals. The underlying mechanism is unknown. Based on experimental data in animals we hypothesised a blood-pressure lowering effect of IL-1-antagonism via modulation of the Renin-Angiotensin-Aldosterone System (RAAS). Methods: In this post-hoc explorative study, we examined short- (2 days) and long-term effects (4 weeks) of IL-1 antagonism (anakinra/Kineret®) on RAAS-peptide-profiles and on hemodynamic parameters assessed by a non-invasive measurement using HOTMAN® system in 128 obese (BMI > 30kg/m2) individuals with at least one feature of the metabolic syndrome from two previous interventional trials (CortIL trial a prospective interventional trial (n= 61) and TestIL trial, a placebo controlled-double blinded interventional trial (n=67)). Results: Upon IL-1 antagonism circulating levels of angiotensin II, angiotensin I, aldosterone and renin remained unchanged after short- and long-term treatment, respectively. In contrast, the vasodilatory angiotensin 1-7 peptide significantly increased after 4 weeks compared to placebo (in between group difference 16.35 pmol/L [1.22 to 30.17], p=0.028), without short-term effect on day 2. Non-invasive hemodynamic measurement revealed a decrease in the stroke systemic vascular resistance index (SSVRI) with an in between group difference of -62.65 dyn.sec.cm-5.m2 [95%CI -116.94 to -18.36], p=0.008 (consistent with a 25%-decrease) after 4 weeks of treatment compared to baseline. Conclusion: IL-1 antagonism in obese individuals with features of the metabolic syndrome led to an increase of the vasodilatory angiotensin 1-7 peptide and a decrease in peripheral vascular resistance, reflected by the SSVRI after 4 weeks of treatment. These findings point to a possible blood pressure lowering mechanism via modulation of the RAAS-system of IL-1 antagonism.

Mechanisms Underlying Obesity‐Related Hypertension: An Experimental Weight Gain Study in Humans

BackgroundThe association between body size and blood pressure (BP) is well recognised. However, not all overweight individuals have elevated BP suggesting that important adaptive mechanisms are present in some. Cardiac output (CO, a key determinant of BP, is elevated in young overweight individuals, but is not associated with the level of BP. However, peripheral vascular resistance (PVR) is associated with the level of BP in these individuals, suggesting that the ability to modulate PVR in response to increased CO is important.ObjectiveWe hypothesized that weight gain increases CO in healthy humans and that the ability of the peripheral vasculature to adapt to this increase determines BP. Therefore, we undertook an exploratory study of experimental weight gain in healthy young adults.MethodsSixteen healthy non‐obese males were recruited (mean±SD age 29±6 years). All participants were overfed approximately 1000kcal/day, alongside their normal diet, for 6–8 weeks, until a weight gain of 5kg was achieved and held stable for at least 1 week. Detailed anthropometric characteristics, BP, CO and PVR were assessed at baseline and at completion of the overfeeding intervention.ResultsOverfeeding resulted in a significant increase in body weight (6.11±3.08kg, P&lt;0.001), lean mass (3.61±3.40kg, P=0.001) and fat mass (2.64±2.89kg, P=0.002). The increases in systolic BP (2±9mmHg) and diastolic BP (2±6mmHg) were not significant (P&lt;0.2 for both) and the increase in heart rate was of borderline significance (5±10bpm, P=0.055). As hypothesised, there was a significant increase in cardiac output (0.81±1.35L/min, P=0.031), which was accompanied by a decrease in PVR (129±205dynes.sec.cm5, P=0.024). Dichotomising individuals on the basis of a systolic BP response to weight gain of ≥5mmHg (BP responders) revealed small differences vs non‐responders in the change in CO (+1.34±0.99L/min vs +0.4±1.50L/min) and PVR (−111±142 dynes.sec.cm5 vs −143±251 dynes.sec.cm5), although neither comparison was statistically significant.ConclusionsModest weight gain in healthy, non‐obese men is associated with an increase in both lean and fat tissue mass. A compensatory reduction in PVR in response to elevated cardiac output is likely to explain the lack of change in BP. Examining ‘responders’ versus ‘non responders’ in terms of BP change in response to weight gain is likely to provide useful insights into obesity‐associated hypertension in a larger trial.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Imaging sublingual microcirculatory perfusion in pediatric patients receiving procedural sedation with propofol: A pilot study.

ObjectiveProcedural sedation with propofol is widely used in the pediatric population. A well‐known side effect of propofol is a decrease in peripheral vascular resistance resulting in hypotension, but little is known about the effects on microcirculation in humans. We aimed to evaluate the effects of propofol on the sublingual microcirculatory perfusion by continuous video imaging in pediatric patients undergoing procedural sedation.MethodsPatients admitted to the Pediatric Intensive Care Unit for procedural sedation were recruited. Oral microcirculation was measured employing a continuous monitoring strategy with incident dark‐field illumination imaging. Measurements were obtained before and 3 minutes after propofol induction. Total and perfused vessel densities, proportion of perfused vessels, microvascular flow index, blood vessel diameter (Øbv), and systemic hemodynamics were analyzed.ResultsContinuous measurements were achieved in seven patients. Three minutes after propofol induction mean arterial pressure decreased (P = 0.028) and total and perfused vessel densities increased by 12% (P = 0.018) and 16% (P = 0.018), respectively. MFI was unaltered and mean Øbv increased but not significantly.ConclusionsPropofol induction induces a reduction in mean arterial pressure and a rise in sublingual microvascular perfusion. The observed effects of propofol on the sublingual microcirculation may be due to a decrease in microvascular resistance.

Vasopressin: the level of evidence is growing

Distributive shock, especially septic shock, is the most common type of shock in the critically ill patients (1). Distributive shock is characterized by a decrease in peripheral vascular resistance and vasodilation resulting in arterial hypotension. To prevent organ dysfunction, fluid resuscitation and vasopressor infusion are required.

Rehabilitation training in artificially heated environment.

Sauna has become a popular club house facility where the dweller enjoys relaxation. Some exercise groups like yoga and Qigong practitioners, are making use of the heated environment to achieve quicker and better results of trainings. Sauna therapy is producing a thermal stress through hyperthermia. The cardiovascular system readily responds by increasing the heart rate which can become double the resting stage within minutes and cardiac output may have a 70% increase. The body’s surface response to heat leads to a 40% of decrease in peripheral vascular resistance, thus allowing rapid peripheral blood flow which is responsible for greater heat dispersal directly from the skin. The chained physiological reactions of increased cardiac and pulmonary outputs, while blood pressure drops suggest that Sauna could be good for chronic diseases. When active stretching are executed simultaneously with controlled breathing in a smooth synchronized chain of activities under the individual’s free will, a harmonized state of mind reaching the level of meditation follows. Sauna room environment initiates a physiological stat equivalent to moderate exercises. Qigong practice is typical anaerobic training. Both Sauna and Qigong lead to a tranquility of the mind. The unique nature of practicing Qigong in a heated environment is therefore clear. A small pilot study on Qigong practice within the Sauna room showed a higher increase in heart rate which amounted to 30%–40% above the pre-exercise level. The blood pressure checked after Qigong, on the contrary, remained stable or even slightly decreased.

ранняя диагностика нарушений регуляции гемодинамики в ортостазе

The article deals with the informative content of spectral analysis of heart rate variability in the assessment of the regulatory impacts on the systemic hemodynamics during orthostatic test. It was observed that the patients who suffer from neurogenic syncope already at a young age had had a decrease in low frequency oscillations, as well as a decrease in peripheral vascular resistance during the test. It allows us to make a conclusion about the sympathetic vasomotor regulation dysfunction, even before the symptoms of orthostatic hypotension were evident. The decrease in the tonic vagal effect which follows from the depression of high-frequency oscillations, makes for increasing the chronotropic function of the heart and keeps a relative sympathetic predominance in order to maintain adequate level of blood pressure

Changes in Cerebral Blood Flow in the Postischemic Period.

Experiments on Wistar rats showed that blood flow in the cortex and subcortical brain structures was not completely restored within 21 days after transient ischemia caused by bilateral carotid artery occlusion with controlled hypotension. After 7 days of reinfusion, the end-diastolic blood flow velocity increases with simultaneous decrease in pulsation index, which indicates the decrease in peripheral vascular resistance. During the following 14 days, peripheral blood resistance increases, as was seen from the increased peak systolic blood flow velocity, mean blood flow velocity over the heart cycle, and pulsation index. These changes are likely a delayed manifestation of ischemic reperfusion injury to brain microvessels (no-reflow phenomenon) and are determined by changes in blood rheologiy and pial vessel lumen.

HEMODYNAMIC MECHANISMS OF CLINICAL EFFECTS OF CYCLIC STAY OF A HUMAN IN NORMOBARIC HYPOXIC ENVIRONMENT

Purpose: in order to assess the adaptive hemodynamic responses formed in humans during cyclic stay (daily, for 2 hours, 15 sessions in total) in normobaric hypoxic gaseous environment with oxygen content in nitrogen of 15% (NHGE-15). Materials and methods: a study has been conducted with participation of 12 male test subjects aged 25-52. In course of cyclic stay in NHGE-15, systemic and cerebral blood flow parameters were evaluated in the test subjects. Results: in response to stay in NHGE, at the initial stage of the testing procedure, the test subjects showed hyperkinetic systematic circulation reactions: cardiac acceleration, increase in systemic blood pressure and cardiac output, with decrease in peripheral vascular resistance. At the same time, an increase in blood flow to cerebral vessels and hypersthenia in major cerebral vessels were revealed. Further stay in NHGE-15 was accompanied by a statistically significant reduction in severity of the above responses reflecting a gradual decrease in «stressfulness» of hypoxic effect due to formation in the body of primary adaptational structural and functional alterations in oxygen transport systems, regulatory and plastic processes. The fact of systemic and regional hemodynamics parameter optimizing was also revealed, recorded under normal conditions of gaseous environment, in course of the cyclic hypoxic impact. Summary: hypoxic exposure on the human body leads to centralization of the circulatory system, aimed at the maintenance of oxygen supply of vital organs. The result of hypoxic training is to reduce the severity of the reaction by increasing the reliability of functioning of the system of hemodynamics and its regulatory mechanisms.

Arterial hypertension and sport. Related aspects to certification for physical activity and contraindications to sports practice in hypertensive child and adolescent.

The control of blood pressure during exercise is a complex process as it involves increases in stroke volume and heart rate, changes in peripheral vascular resistance and in sympathetic tone; it is related to the type of exercise practiced as its intensity and duration, ratio of lean mass/fat mass, depending on the sex. We distinguish two main types of exercise, aerobic or dynamic and isometric or static. The first is a type of exercise that involves an increase in cardiac output associated with rapid increases in heart rate and systolic BP (with a minimum decrease in diastolic BP) but with a significant decrease in peripheral vascular resistance. The isometric exercise, or static, involves a sharp increase in both systolic and diastolic blood pressure, a modest increase in heart rate with a range stable or slightly reduced but no decrease in peripheral vascular resistance. In Figure ​Figure11 are shown the modifications and interactions between the various parameters [1]. Figure 1 Cardiovascular response to physical exercise Legend: (A) Response to dynamic exercise gradually to the increase in workload to the maximum oxygen consumption; (B) Response to static exercise (handgrip at 30% of maximum voluntary contraction); VO2 (ml/min/kg); ... From these premises it emerges therefore the need to start young people suffering for arterial hypertension to play a type of sport that is suitable for the individual cardiovascular status. In Italy, compared to the US, to practice a sport activity is required medical certification that involves a civil and criminal liability on the part of the physician certification and which is regulated by specific decrees, in particular the latest amendments to the Balduzzi Decree [2]. In the case of healthy children, or apparently healthy, it is scheduled to perform at least once a 12-lead ECG at rest and blood pressure measurement (as specifically stated on the label of certification then signed at the bottom by a doctor). In the case of children and adolescents with arterial hypertension, both for primary and secondary hypertension, you need to pay more attention and care, both in relation to cardiovascular stresses that this entails as previously exposed, both in relation to the importance of implementing the changes in lifestyle who are always the first step, no drugs, which will contribute to the maintenance of blood pressure in the normal range. For what concerns instead the practice of competitive sports activities, please refer to specialists in Sports Medicine, which is reserved for the certification.

Autonomic Dysfunction, Sympathetic Hyperactivity and the Development of End-Organ Damage in Hypertension: Multiple Benefits of Exercise Training

Autonomic dysfunction is closely related to the development of hypertension, which is characterized by increased sympathetic activity, decreased vagal tonus and baroreflex dys - function. The hypertension-induced maladaptive changes progressively lead to heart failure, myocardial infarction and stroke. Hypertrophic remodeling of brain arterioles, chemoreceptors activation, blood-brain barrier abnormalities, oxidative stress and pro-inflammatory cytokines production in autonomic brain areas increase neuronal activity and sympathetic outflow. These responses, together with increased baroreflex dysfunction-induced pressure variability, renin- angiotensin system hyperactivation and capillary rarefaction, increase blood pressure levels and act as a positive feedback mechanism to perpetuate hypertension and development of end- organ damage. Exercise training, a non-pharmacological tool, has been used as an adjuvant therapy to treat hypertension. Our recent data showed that moderate aerobic training in adult SHR completely normalizes oxidative stress and inflammation in autonomic brain areas in - volved in cardiovascular control and promptly corrects baroreflex dysfunction and increases cardiac vagal activity. The early (2-weeks) training-induced beneficial responses improve auto - nomic control even in the persistence of hypertension, since a partial reduction of pressure lev- els was observed after 8 weeks of exercise training, which was related to reversion of arteriolar hypertrophic remodeling and consequent decrease of peripheral vascular resistance.

Physiology of the normal heart

The mechanical events of the cardiac cycle provide the circulation with normal cardiac output and blood pressure. This requires an appropriate venous return, regulation of outflow resistance, a normal myocardial contractile state and heart rate control, together with an adequate supply of oxygenated blood via the coronary circulation. Other neural influences contribute to cardiac regulation, including natriuretic peptides and the renin–angiotensin system. The atria and ventricles are richly supplied with adrenergic nerves that may augment cardiac function, particularly with increased cardiac output during exercise. Inhibitory vagal fibres are largely confined to the sinus and atrioventricular nodes. Exercise causes increased sympathetic outflow, with a decrease in peripheral vascular resistance, and increased cardiac output, heart rate, systolic blood pressure and venous return. Regular rhythmic exercise has a training effect, which enhances cardiac performance. This is important for the maintenance of many aspects of cardiovascular health.

Arterial hypertension and brain damage. New targets of therapy

Objective: to assess the feasibility of ARBs to reduce hypoperfusion of the brain that develops in patients with arterial hypertension of 1-2 degrees. Material and methods. A study of changes in the ultrasonic Doppler index (RI resistivity index and pulsatility index PI) and the structure of neurological symptoms in patients with arterial hypertension of 1-2 degrees (n=86) due to 53-week olmesartan medoxomil reception (Cardosal®). Results. Patients with arterial hypertension of 1-2 degrees have diagnosed diffuse neurological symptoms and mild cognitive impairment. Doppler ultrasound revealed an increase in peripheral resistance index in the internal carotid and middle cerebral arteries, compared with patients without hypertension. Through 53 weeks therapy of olmesartan medoxomil (Cardosal®) observed a statistically significant decrease in peripheral vascular resistance (p