STUDY OF THE COMPOSITION OF LYMPH AND LYMPH NODES OF YOUNG AND OLD RATS UNDER THE INFLUENCE OF A NEW PHYTOCOMPOSITION

Cтарение - это процесс снижения функциональных резервов всех тканей и систем организма, связанных с воспалительными процессами и образованием тромбов, с последующим замещением их соединительной тканью. Достижения медицины увеличивают продолжительность жизни, что приводит к демографической ситуации, так как количество пожилых людей в обществе увеличивается. С возрастом наблюдаются изменения с исчезновением и нарушением регуляторного эффекта, наблюдаются значительные адаптационные изменения - повышенная чувствительность сердца и сосудов к гуморальным факторам и медиаторам в случае нервных окончаний, а также ослабление синтеза медиаторов. Возрастные изменения структуры микрососудистой сети способствуют снижению скорости кровотока в различных отделах головного мозга, нарушению диффузии кислорода из крови в ткани, нарушению реактивности церебральных артериол на неблагоприятные экзогенные и эндогенные факторы. Заболевания, встречающиеся у многих пожилых людей - стенокардия, гипертония, сахарный диабет, атеросклероз - усиливают возрастные патологические изменения системы кровообращения. Эти изменения приводят к снижению интенсивности капиллярного обмена Одна из причин старения - изменение микроциркуляторной системы. С возрастом происходит значительное уменьшение почечного кровотока, что напрямую связано с уменьшением микроваскуляризации. Aging is the process of reducing the functional reserves of all tissues and body systems associated with inflammatory processes and the formation of blood clots, followed by their replacement with connective tissue. Advances in medicine are increasing life expectancy, which leads to demographic situations as the number of elderly people in society increases. With age, changes are observed with the disappearance and disruption of the regulatory effect, significant adaptive changes are observed - increased sensitivity of the heart and blood vessels to humoral factors and mediators in the case of nerve endings, as well as a weakening of the synthesis of mediators. Age-related changes in the structure of the microvascular network contribute to a decrease in blood flow velocity in various parts of the brain, impaired diffusion of oxygen from the blood into the tissue, impaired reactivity of cerebral arterioles to unfavorable exogenous and endogenous factors. Diseases that occur in many elderly people - angina pectoris, hypertension, diabetes mellitus, atherosclerosis - increase age-related pathological changes in the circulatory system. These changes lead to a decrease in the intensity of capillary exchange. One of the causes of aging is a change in the microcirculatory system. With age, there is a significant decrease in renal blood flow, which is directly related to a decrease in microvascularization.

The coronary circulation in exercise training

Exercise training (EX) induces increases in coronary transport capacity through adaptations in the coronary microcirculation including increased arteriolar diameters and/or densities and changes in the vasomotor reactivity of coronary resistance arteries. In large animals, EX increases capillary exchange capacity through angiogenesis of new capillaries at a rate matched to EX-induced cardiac hypertrophy so that capillary density remains normal. However, after EX coronary capillary exchange area is greater (i.e., capillary permeability surface area product is greater) at any given blood flow because of altered coronary vascular resistance and matching of exchange surface area and blood flow distribution. The improved coronary capillary blood flow distribution appears to be the result of structural changes in the coronary tree and alterations in vasoreactivity of coronary resistance arteries. EX also alters vasomotor reactivity of conduit coronary arteries in that after EX, α-adrenergic receptor responsiveness is blunted. Of interest, α- and β-adrenergic tone appears to be maintained in the coronary microcirculation in the presence of lower circulating catecholamine levels because of increased receptor responsiveness to adrenergic stimulation. EX also alters other vasomotor control processes of coronary resistance vessels. For example, coronary arterioles exhibit increased myogenic tone after EX, likely because of a calcium-dependent PKC signaling-mediated alteration in voltage-gated calcium channel activity in response to stretch. Conversely, EX augments endothelium-dependent vasodilation throughout the coronary arteriolar network and in the conduit arteries in coronary artery disease (CAD). The enhanced endothelium-dependent dilation appears to result from increased nitric oxide bioavailability because of changes in nitric oxide synthase expression/activity and decreased oxidant stress. EX also decreases extravascular compressive forces in the myocardium at rest and at comparable levels of exercise, mainly because of decreases in heart rate and duration of systole. EX does not stimulate growth of coronary collateral vessels in the normal heart. However, if exercise produces ischemia, which would be absent or minimal under resting conditions, there is evidence that collateral growth can be enhanced. While there is evidence that EX can decrease the progression of atherosclerotic lesions or even induce the regression of atherosclerotic lesions in humans, the evidence of this is not strong due to the fact that most prospective trials conducted to date have included other lifestyle changes and treatment strategies by necessity. The literature from large animal models of CAD also presents a cloudy picture concerning whether EX can induce the regression of or slow the progression of atherosclerotic lesions. Thus, while evidence from research using humans with CAD and animal models of CAD indicates that EX increases endothelium-dependent dilation throughout the coronary vascular tree, evidence that EX reverses or slows the progression of lesion development in CAD is not conclusive at this time. This suggests that the beneficial effects of EX in CAD may not be the result of direct effects on the coronary artery wall. If this suggestion is true, it is important to determine the mechanisms involved in these beneficial effects.

Control of Edema in Hypertensive Subjects Treated With Calcium Antagonist (Nifedipine) or Angiotensin-Converting Enzyme Inhibitors With Pycnogenol

The presence of edema in different phases and stages of essential hypertension may be due to antihypertensive treatment. Some drugs may cause edema by inducing vasodilatation, increasing the capillary exchange surface and capillary filtration. Pycnogenol has an important anti-edema effect in diabetic microangiopathy and chronic venous insufficiency. This 8-week study evaluated capillary filtration in 2 comparable treatment groups with hypertension treated with a calcium antagonist (nifedipine) or angiotensin-converting enzyme inhibitor to define its efficacy in preventing edema caused by antihypertensives. A significant decrease in filtration was observed in the Pycnogenol groups. Pycnogenol controls this type of edema, it helps to prevent and limit long-term damage in the microcirculation in hypertensive patients, and allows the dose of anti-hypertensive drugs to be reduced in most patients.

Arteriovenous Pairing: a Determinant of Capillary Exchange

Venuloarteriolar signaling helps mediate microvascular function and dysfunction. Mediators produced at venular sites of inflammation appear to constrict arterioles and increase capillary permeability. In contrast, venules beneficially dilate arterioles to enhance capillary flow according to metabolic demand. These mechanisms are altered with cardiovascular risk factors, contributing to microvascular complications.