Elastic properties and Windkessel function of the human aorta.
An understanding of the role of the aortic elastic properties indicates their relevance at several sites of cardiovascular function. Acting as an elastic buffering chamber behind the heart (the Windkessel function), the aorta and some of the proximal large vessels store about 50% of the left ventricular stroke volume during systole. In diastole, the elastic forces of the aortic wall forward this 50% of the volume to the peripheral circulation, thus creating a nearly continuous peripheral blood flow. This systolic-diastolic interplay represents the Windkessel function, which has an influence not only on the peripheral circulation but also on the heart, resulting in a reduction of left ventricular afterload and improvement in coronary blood flow and left ventricular relaxation. The elastic resistance (or stiffness), which the aorta sets against its systolic distention, increases with aging, with an increase in blood pressure, and with pathological changes such as atherosclerosis. This increased stiffness leads to an increase in systolic blood pressure and a decrease in diastolic blood pressure at any given mean pressure, an increase in systolic blood velocity, an increase in left ventricular afterload, and a decrease in subendocardial blood supply during diastole, and must be considered a major pathophysiological factor, for example, in systolic hypertension. The elastic properties of the aortic Windkessel can be assessed in vivo in humans in several ways, most easily by measuring the pulse wave velocity along the aorta. The higher this velocity, the higher the elastic resistance, that is, the stiffness. Other methods depend on assessment of the ratio between pulse pressure and aortic volume changes (delata P/delta V), which can be assessed noninvasively by ultrasonic or tomographic methods. All assessments of vessel stiffness have to take into account the direct effect of current blood pressure, and thus judgements about influences of interventions rely on an unchanged blood pressure. Alternatively, to derive the "intrinsic" stiffness of the aortic wall one has to correct for the effect of the blood pressure present. Recently reports about pharmacologic influences on the elastic properties of the aorta have emerged in the literature.(ABSTRACT TRUNCATED AT 400 WORDS)
Belz
G G
GG
Zentrum für Kardiovaskuläre Pharmakologie, Mainz-Wiesbaden, Germany.
D000375:Aging / Q000502:physiology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D001011:Aorta / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D004547:Elastic Tissue / Q000187:drug effects / Q000502:physiology; D004548:Elasticity; D006801:Humans; D009569:Nitric Oxide / Q000096:biosynthesis; D011379:Prognosis; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects; D016277:Ventricular Function, Left / Q000502:physiology
D000806:Angiotensin-Converting Enzyme Inhibitors; D009569:Nitric Oxide