The normal artery has both the function of conduit and buffering
The arterial system has two functions:
(1) to transport blood from the left ventricle to the capillaries of organs and tissues in the whole body according to the needs, that is, the function of conduit;
(2) buffer the heart beat and maintain the continuity of capillary blood flow, that is, buffer function. The average pressure from the aorta to the peripheral artery (such as the radial artery) only decreased by about 1mmhg, while the average pressure from the above mentioned muscular artery to the starting point of the resistance arteriole only slightly increased; the pulsating blood flow usually only exists in the larger artery with an internal diameter of > 200 u03bc m, which will not affect the arteriole and the capillaries at the farther end; because the pulsating blood flow does not exist in the resistance artery, the systemic vascular system beat The energy loss caused by the artery is very small, and only about 10% of the energy loss is caused by the steady propulsion blood flow in the artery, arteriole, capillary and vein. Another function of the arterial system is that the mean systolic pressure is only 3-4mmhg higher than that of the whole cardiac cycle, while the mean diastolic pressure is 2-3mmhg lower.
Another function of the cardiovascular system is to align vascular activity (reflexes) with cardiac activity (aortic valve closure). In an ideal state, the reflected wave would not increase the systolic pressure, but only the diastolic pressure, which would increase the perfusion of the microvascular bed. Therefore, the heart and blood vessels usually work together to achieve the best effect. This is further confirmed by the fact that the minimum impedance coefficient of the ascending aorta is consistent with the frequency distribution of the maximum ejection wave of the left ventricle.
Aging of arteries mainly involves the great arteries
Most of the researches on aging focus on the factors affecting vascular endothelium and intima, but ignore the load-bearing middle layer of the great arteries. Therefore, aging can not be separated from the role of disease, nor can damage be distinguished from repair or Reconstruction role. I suggest that the classic idea of using physical terms to compare arteries to passive elastic pipes is the same with aging changes. We should mainly focus on the elasticity of the middle layer of arteries. With the increase of age, there will be two kinds of physical changes in the elastic artery: dilatation and rigidity of the wall of the tube. The most obvious change is in the proximal part of the aorta and its main branches (brachiocephalic trunk, carotid artery and subclavian artery), and the change of aging will first affect the compliance (elasticity) of the wall of the tube.
In young people, beating of the heart causes dilation of the proximal elastic artery and the aorta by about 10%, while the muscular artery dilates by only 2% - 3%. From the point of view of arterial component fatigue, this difference in dilation degree can explain the difference in aging changes between the proximal and distal arteries. Fatigue principle refers to the change of crystal structure caused by material deformation, and the possibility of fracture can be predicted according to the degree and times of deformation. When the expansion is 10%, the natural rubber can break after 9 u00d7 108 times expansion (the heart rate is 60 times / min, equivalent to 30 years). As people age, rupture of the aortic elastic layer can be seen, which can be attributed to arterial dilation (by elongation, followed by rupture of the load-bearing component) and stiffness (by the transfer of pressure to the stiffer collagen component of the arterial wall). If the expansion is 5%, the rubber will break after more than 3 u00d7 108 expansions at the same heart rate, which is equivalent to a life span of more than 100 years. Histological studies have found that the middle elastin of the proximal artery is severely damaged (see Fig. 1), while the distal muscular artery rarely shows aging changes. Therefore, the main characteristics of arterial aging are structural destruction, rigidity and dilation of the proximal aorta, which is called Senile Arteriosclerosis.
Effect of aging on arterial function
Aging only causes the expansion of the proximal elastic artery, which has no effect on the function of the artery system, but has a significant progressive effect on the buffering function, and ultimately damages the heart, microcirculation, especially the microcirculation of the brain and kidney. With the increase of age, the arterial stiffness showed the increase of pulse wave velocity, especially in the aorta, and the change of muscular artery (such as upper extremity artery) was the least.
Active pulse wave velocity (PWV) is the velocity of pulse wave conduction along the arterial wall. It can be measured noninvasively by the time delay and pulse conduction distance from the bottom of the pressure wave to the femoral artery. It is 5m / s at the age of 20 and 12m / s at the age of 80 (see Figure 2). According to the classical Moens Korteweg formula, PWV depends on the square root of the elastic modulus, so it indicates that the elastic modulus of the aorta has increased more than 4 times. It is worth noting that the influence of aging on arterial function has been underestimated due to over dependence on brachial artery cuff sphygmomanometer and systolic pressure measured by it.
With the increase of age, the increase of aortic stiffness leads to the increase of systolic and diastolic pressure, the left ventricular hypertrophy and the further increase of oxygen demand. The decrease of diastolic pressure and the decrease of diastolic period can lead to the decrease of coronary blood supply. When the diastolic left ventricular pressure increases, the coronary blood supply further decreases. Therefore, the progress of the impairment of coronary blood supply ability is not dependent on coronary stenosis, and any degree of atherosclerosis can aggravate it. The increase of coronary blood flow demand and the decrease of blood flow perfusion are the most likely causes of myocardial ischemia. Any degree of myocardial ischemia can further damage the left ventricular diastolic function, prolong the ejection time of the heart, and reduce the diastolic coronary perfusion.
Aging can cause vicious circulation (i.e. left ventricular hypertrophy), and it is easy to induce myocardial ischemia and angina pectoris. Even when there is no hemodynamic coronary stenosis or even coronary stenosis, and when the heart rate increases, it is easy to have diastolic dysfunction. Among them, left ventricular diastolic failure is the most common in the elderly.
It affects the microcirculation of the brain and kidney. The resistance of microcirculation vessels to blood flow is the greatest, and the pulsation blood flow becomes stable blood flow in the capillaries by reflecting the pulsation from the larger arteries. However, in the organs with large resting blood flow (especially the brain and kidney), the more the average arterial pressure of the larger artery decreases, the deeper the pulsation goes into the capillaries. Recent studies have shown that, independent of the values of traditional brachial artery systolic and diastolic pressures, arterial stiffness (active pulse wave velocity, enhancement index, pulse pressure and its increase) is not only closely related to the outcome of cardiovascular disease, but also closely related to the changes of cerebral and renal microvasculature, including cerebral white matter ischemia and renal proteinuria. Similarly, treatment to reduce the adverse effects of arterial stiffness can reverse or delay brain and kidney damage. There is also evidence that arterial stiffness is associated with inflammation, and inflammation is more pronounced in women, characterized by a greater degree of atherosclerosis than atherosclerosis. The aging changes of microcirculation secondary to aortic stiffness are related to the progressive decline of brain and renal function, and are serious enough to cause vascular inflammation, accompanied by the rise of C-reactive protein and other cardiac markers. It is possible to prevent, delay or even reduce the microvascular damage by the treatment of reducing arterial stiffness and wave reflection.
Cerebrovascular hypertension and increased blood flow pulsation associated with aging and arterial stiffness can cause arteriolar lesions, resulting in brain damage and dementia. The causes of brain lesions in the elderly are high pulsatile pressure of microcirculation and high blood flow, and the damage of the whole body is similar to this. So why does cerebral artery and microvascular pulsation increase in the elderly with aortic stiffness? Because the aorta and the elastic artery are very stiff, they cannot buffer the blood flow pulsation produced by the heart, so they are bound to expand to the microvascular bed, and preferentially enter the vasodilation and high blood flow perfusion organs - brain and kidney. Therefore, the pressure of weak blood vessels and the fluctuation of blood flow aggravate the energy loss, which can increase the micro hemorrhage and infarction of brain.
Renal arterioles and glomeruli are exposed to high pulsatile microvascular pressure and tension just like cerebral arteries, but the evidence of renal microvascular pulsation injury is not sufficient at present, we believe it is only temporary.
Prevention of arterial aging and adverse orientation
The pathological basis of arterial aging is the same as the aging process that determines the inherent objects, which is the result of repeated strain. The key factor of arterial aging is the fatigue and rupture of aortic elastin layer. The prevention and treatment should focus on how to reduce the extent and times of arterial extension. The application of u03b2 receptor blocker can reduce the times of extension, but the increase of central systolic pressure may lead to the increase of the extent of extension. Moreover, in bradycardia, the cardiac ejection time and systolic incident wave increase lead to the increase of the total reflected wave, which leads to the obvious potential adverse effect of u03b2 receptor blocker treatment, especially when there is microcirculation damage, but u03b2 receptor blocker treatment can delay the progressive expansion of ascending aorta in patients with Marfan syndrome. Regular aerobic exercise for a period of time is also a better way to reduce the cumulative number of stretches on heart injury. Although the heart rate increases during exercise, it usually stays at a lower level during a longer interval. Exercise can improve the endothelial function of the muscular artery and reduce the amplitude of the reflected wave returning to the heart. At present, the above principles have been used in blood pressure control, diabetes, heart failure and renal insufficiency patients. That is to say, through regular exercise and the application of drugs (ACEI, ARB, CCB and nitrates) to dilate the smooth muscle of large and small arteries in the whole body, the early wave reflex can be reduced, and the low-frequency components, apparent phase velocity, central artery pressure and blood flow pulsation of aortic impedance can be reduced. Moreover, the measurement of the central aortic pressure provides an effective help for monitoring and controlling the peripheral wave reflection, reducing the stiffness of the great arteries, maintaining the appropriate mean arterial pressure, and realizing the perfusion of the heart, brain, kidney and other important organs.
Modern research has confirmed that, with the increase of age, although the human aortic pulse experienced the same changes as the radial pulse, the current evaluation of arterial aging usually only based on the evaluation of blood pressure value and ignored the analysis of waveform. Throughout the 20th century, peoples biases on diastolic blood pressure misled clinicians comprehensive understanding of the risk of cardiovascular aging. The new technology of pulse wave analysis has expanded peoples initial understanding of pathology and physiology, and gained more attention in the study of human artery aging and its complications. (Lu Changlin, Gao runlin)
Source: Xinhuanet editor in charge: Geng Yiwen ufe63 nj6040