PHYSIOLOGY OF AORTA AND MAJOR ARTERIES 



807 



under minimal load. Isolated aortic rings will, when 

 unloaded, respond to immersion in epinephrine, for 

 example, by a shortening of both their diameter and 

 length, to produce a pressure rise of some 3 to 5 mm 

 Hg. But if these contracted rings are subjected to 

 stretch, the decreased diameter is lost rather early 

 (fig. 1A), so that by the time loads equivalent to the 

 usual working pressures are reached, the contracted 

 and relaxed rings show identical extensibility curves. 

 With stretch release, the diameter does not return 

 to the contracted size. Either the muscle loses its 

 contraction early in the stretch, or the other parts of 

 the net have contributed more than usual to the total 

 extension. Even in muscular organs, such as the 

 bladder (102), the effect of contraction on the ex- 

 tensibility curve is small, and the contraction itself 

 seems not to be eliminated by the imposed stretch 

 (97, 1 18). The extensibility of a muscular organ is not 

 very different in the contracted or relaxed state (6, 



'3)- 



What is more disquieting is that if an aortic ring 



is first subjected to a load equivalent to a pressure in 

 the usual physiological range, immersion in epi- 

 nephrine will no longer produce a discernible diameter 

 or pressure change. It is hard to accept this finding 

 as rational. Yet neither viable isolated specimens nor 

 a temporarily occluded aorta in situ (5) has been 

 shown to have a more powerful muscle action. This 

 is not to say that a contraction in muscular arteries, 

 where the ratio of wall muscle to internal diameter is 

 greater, could not influence the diameter at the 

 higher pressure levels. 



Attempts have been made to record the effects of 

 muscle contraction in the intact aorta while it is 

 being pulsed by the heart. Most of these I have 

 learned of through conversations, since there is 

 reluctance toward publication of negative findings. 

 In the literature are the older experiments of Wiggers 

 & Wegria (138) in which an aortagraph was placed 

 around the thoracic aorta of a dog. After an intra- 

 venous injection of epinephrine or elicitation of a 

 strong pressor reflex, there was a recorded decrease 

 in diameter (the actual values not being given) at a 

 time when the aortic pressure was not changing. For 

 many years these results stood unchallenged and yet 

 unsupported. More recently, Patel and co-workers 

 (88) found a change in both diameter and wall 

 stiffness in the main pulmonary artery with muscle 

 contraction, a change persisting through several 

 normal pulsations. The pulmonary pressure is, of 

 course, much lower than that of the aorta and the 

 wall architecture is not the same. Then Peterson and 



co-workers (91) showed a change in diameter and an 

 increased stiffness, with arterial pressure unaltered, 

 when the femoral artery or carotid artery was painted 

 with norepinephrine. Opposite results were obtained 

 with acetylcholine. The authors claim a similar 

 directional change, but furnish no supporting figures, 

 for the aorta. These results, and particularly the 

 claim for the aorta, must be amplified and confirmed. 



Diameter and extensibility changes in the aorta of 

 living animals following the use of constrictor or 

 dilator drugs have been recorded (78) which do not 

 appear to fit with the stretch data obtained with 

 isolated rings. Since the arterial pressure also changed, 

 and since the physiological distensibility curve for 

 the intact aorta, quite aside from any muscle action, 

 remains to be formulated, an attempt to interpret 

 these changes on the basis of muscle contraction 

 would be premature. 



We are not yet in a position, then, to answer the 

 long-debated question as to whether muscle con- 

 traction should increase or decrease the wall ex- 

 tensibility. The effects of such contraction on the 

 stretch curves shown by isolated vessels are difficult 

 to phrase in terms of generalities. With an unloaded 

 vessel, contraction is not followed by relaxation. 

 Instead, over a period of time, the wall gradually 

 becomes stiffer, as though the fibers had been reset 

 to the shorter length. Whether the contraction had 

 any essential role in this resetting, aside from the 

 first reduction in length, remains uncertain. De- 

 pending upon the amount of this resetting, a small 

 stretch, starting from zero tension, will reflect this 

 initial stiffness of the wall. With more stretch, the 

 distensibility suddenly increases, so that the stretch 

 curves of the once contracted and the relaxed ring 

 are now parallel. At higher loads the two curves 

 merge. If one assays distensibility, it must always be 

 with respect to the amount of load used. Thus, if the 

 stretch is sufficient to cause the shift toward the 

 increased distensibility, one would conclude that the 

 muscle contraction had rendered the wall more 

 extensible. If the assay were on the basis of the very 

 first part of the stretch curve only, one would reach 

 the opposite conclusion of a lessened extensibility. 

 Whether the effects shown by an unloaded tissue 

 have any pertinence to what might happen at physio- 

 logical pressure levels remains to be shown. If, for 

 some reason, the muscle in the living aorta were more 

 powerful, or if the imposed stretch were made quite 

 small, we might anticipate a decreased wall dis- 

 tensibility. Even so, any interpretation of the effect 

 of muscle contraction would have to be phrased in 



