PHYSIOLOGY OF AORTA AND MAJOR ARTERIES 



8o 3 



stretch curve (fig. 1). Hence for any given stretch two 

 different tension-length curves must be considered, 

 one for the extension and the other for the elastic 

 recoil. The difference between the two comprises a 

 hysteresis loop. The amount of hysteresis is always 

 greatest with the first stretch done after a prolonged 

 rest period. If this first stretch is followed by repetitive 

 stretches of the same size, the hysteresis is progressively 

 reduced until it becomes relatively constant. The 

 number of successive stretches required to achieve 

 this stable loop varies among vessels, for two or three 

 stretches will suffice with the aorta, but more may be 

 needed with a muscular artery. In the gradual re- 

 duction of hysteresis, the stretch-release curve 

 remains almost or completely constant, its values 

 being set by the peak load used (96). It is the exten- 

 sion curve which shows progressively larger length 

 values at any given tension value. Hysteresis is present 

 in some metals, too, although its amount is relatively 

 small as compared to that seen with vascular tissues. 



The presence of hysteresis is often taken to indicate 

 simplv a viscous retardation of the extension of elastic 

 elements, and handled in formulas as though it were 

 simple viscosity (48). This would mean that the size 

 of the loop is an index to the frictional energy dis- 

 sipation, which, in turn, would be directly related 

 to the rate of the imposed stretch. Hysteresis of the 

 vessel wall is not so easily formulated. We can sum- 

 marize its main features by saying that at least three 

 factors seem involved. 



/) While a viscous retardation is present, it can be 

 demonstrated for the aorta only at very rapid rates 

 of stretch (96). A rate dependency has not been seen 

 for the stretch-release curve. The muscular arteries 

 have more rate-dependent hysteresis than does the 

 aorta. 



2) When a stretched length is held constant for a 

 period of time, some internal elongation of elements 

 still continues, so that the tension falls. This decline 

 is called stress relaxation. Or if a tension value is 

 maintained, the length will continue to increase 

 slowly, which process is known as "creep." The 

 amount of creep is a function of time, but the relation 

 is not easily formulated in quantitative terms. 



Muscle physiologists have frequently referred to 

 this slow continued elongation under stress as plasticity 

 (13, 93). This use of the term "plastic" is not very 

 appropriate. With metals, when an applied increasing 

 stress reaches a certain critical value, the material 

 becomes deformed. The length change accompanying 

 this deformation may show the properties of viscosity, 

 but the term plastic does not denote the presence or 



absence of such viscosity. Once deformed, the material 

 does not return to the original length upon removal 

 of the stress, but retains the increased length. The 

 choice of the word plasticity for the slow elongation 

 of muscle lay with the belief that any reversibility 

 could be brought about only by an active muscle 

 contraction. However, the process which underlies 

 stress relaxation is spontaneously and completely 

 reversible, if enough time is allowed, whether the 

 muscle is alive or dead (101). Muscle contraction 

 may, of course, hasten the return to the original 

 length. Stress relaxation involves a complicated type 

 of internal viscosity which is so arranged that the 

 driving force for length return lies with some parallel 

 elastic unit which is under stretch. 



Just as with rate-dependent viscosity, the stress- 

 relaxation component is but a minor part of hysteresis 

 as seen in the aorta (96). Its influence is more evident 

 the longer the vessel is kept at a peak load, or the 

 longer the vessel remains under no load, so that creep 

 recovery, or the reversible phase of stress relaxation, 

 can continue. 



3) When, with successive stretches, a final "stable 

 hysteresis loop" is obtained, neither the values from 

 the stretch phase nor those from the release phase 

 show any dependency upon the rate of stretch, and a 

 dependence upon time cannot be easily described. 

 For want of a better term for the remaining factor, 

 which seems to dictate the greatest part of the hyster- 

 esis behavior, I have called it simply an architectural 

 rearrangement. The change is certainly dependent 

 upon the amount of stress and involves a reversible 

 change in length. While there must be some time 

 dimension to this internal rearrangement, the change 

 presumably is very rapid. It may be at a molecular 

 level or at a tissue fiber level. 



What should be firmly emphasized is that a tissue 

 probably has a great many different viscous elements 

 with different time constants. When we refer to such 

 a tissue as being visco-elastic, it does not mean that 

 all the different viscosities can be lumped to give a 

 single viscosity, with an easily definable rate de- 

 pendency. 



In view of the complexities that influence a tension- 

 length curve, it is possible that we should think of the 

 firming of the aortic wall, upon removal from the 

 body, in terms quite different from that of a muscle 

 contraction. The vessel is held in situ under con- 

 siderable longitudinal restraint (104, 107). When a 

 segment is cut, elastic elements held lengthwise under 

 stretch should recoil and make the wall thicker. When, 

 with a circular stretch, no attempt is made to restore 



