In vasoconstriction, the blood vessels constrict. This narrows the vessel cross-section and the blood pressure changes. Smooth vascular musculature is responsible for vasoconstriction and, if necessary, induces vasodilation as well as relaxation and expansion of the vessels. The state of tension of the vascular muscles is mediated by various substances, such as vasoconstriction, for example, by so-called vasoconstrictors.
A reflex vasoconstriction distinguishes the Euler-Liljestrand mechanism. This natural body process occurs in a hypoxia, so in a Sauerstoffminderversorgungen of the tissue on. Both global and local oxygen deprivation can trigger the Euler-Liljestrand reflex, causing hypoxic pulmonary vasoconstriction or hypoxic pulmonary vascular response. The reflex increases the airway resistance locally.
Vaso-constriction in the context of the Euler-Liljestrand mechanism exclusively affects the pulmonary circulation. In all other vessels of the body, hypoxia causes vasodilation. As the pulmonary circulation contracts, all other vessels dilate to allow more oxygen-carrying blood to pass through.
The flow of blood through the lungs is local. The same applies to the degree of lung ventilation. The lung tissue is locally ventilated and perfused differently. Due to physical relationships, such as gravity, the blood flow in the basal portions is higher, so that the basal lungs have a better blood circulation. In addition, because the basal lung areas are less dilated, ventilation in these areas is also at a higher level. The apical lung components are therefore less well perfused and ventilated in direct comparison to the basal areas.
Especially the blood circulation decreases from basal to apical extremely. Although the ventilation also decreases, in comparison to the perfusion, the ventilation decrease in the direction of the apical but much lower. The ventilation perfusion quotient indicates the ratio of lung ventilation to lung perfusion and thus cardiac output. Due to the local differences of basal and apical parts, an apical ventilation-perfusion ratio is greater than one. By contrast, the basal ventilation-perfusion quotient is less than one. The optimal ventilation-perfusion ratio is once again one. This ratio is not achieved by the local differences. The oxygen uptake of the blood therefore does not correspond to the absolute optimum.
Of course, differences in perfusion and ventilation in each pulmonary area tend to deplete blood fractions, such as the intrapulmonary right-left shunt. To resolve this relationship, the Euler-Liljestrand mechanism reduces the affected shunts.
The reflex adjusts the perfusion of the lungs in the relevant areas to the ventilation, thus improving the ventilation perfusion quotient. The Euler-Liljestrand reflex achieves this goal with contraction of the vascular musculature in the pulmonary circulation, as mediated by oxygen deprivation.
For example, in ventilation disorders associated with pneumonia, vasoconstriction by the Euler-Liljestrand mechanism redistributes blood. In this case, poorly ventilated sections are less perfused than better ventilated areas. This effect is relevant in case of doubt to maintain the oxygen supply in individual tissues and results in a redistribution of the blood.
The Euler-Liljestrand mechanism is a natural reflex, but in certain contexts also has negative consequences for human health. This applies, for example, to the development of pulmonary hypertension in the context of chronic obstructive bronchitis or bronchial asthma. The Euler-Liljestrand reflex is significantly involved in the development of this pathological increase in vascular resistance and blood pressure in the pulmonary circulation. The reflex-mediated vasoconstriction increases the afterload of the right heart and simultaneously causes a ventricular pressure load. The heart reacts with compensation. As a result, there is a concentric hypertrophy in the right ventricle. This tissue enlargement of the right ventricle can result in right heart failure. The right heart does not have enough pump power to pump enough blood back into the bloodstream.
Another disease phenomenon associated with the Euler-Liljestrand mechanism is pulmonary edema of altitude sickness. Mountain climbers suffering from altitude sickness move at altitudes of more than 2000 meters above sea level. The disease is a disorder of adaptation of the organism, which causes functional disorders of the body. Particularly at risk are athletes who make speeding up the climb and have not acclimated enough. The first symptoms of altitude sickness include retinopathy, in which the blood vessels of the retina emerge and thus cause a progressive decrease in vision.
The pulmonary edema occurs only in acute altitude sickness and is caused by the hypoxic vasoconstriction, which has the Euler-Liljestrand-reflex result. Elevation of perfusion pressure results in altitude elevation edema when exerted at high altitudes, as fluid from the vessels of the lungs more often passes into the alveolar space. Elevated altitude edema is associated with acute mortal danger and should be clarified and treated immediately in case of doubt. High-altitude mountaineers ideally switch back to retinopathy and continue their descent or stay at least at the current altitude for acclimatization to prevent the development of pulmonary edema.Tags: