Architecture of Small Arteries during Vasoconstriction

Abstract

The cytoarchitectural changes which take place in the walls of small arteries (about 1 mm. O.D.) during vasoconstriction and vasodilation have been studied. Vessels were fixed while in their functional state by immersion in liquid isopentane at -170 C. and prepared for microscopic examination by freeze substitution. The walls of control vessels were thin in relation to the diameter of lumina (WT:L 1:30), indicating that they are more distended than they appear in routinely fixed sections. Vessels dilated with ACH had even thinner walls (WT:L 1:40). Vasoconstriction, induced by local application of epinephrine, increased the wall thickness and reduced the size of the lumen (WT:L 1:2) but in no case was the lumen obliterated in arteries of this size. Although an increase in the WT:L ratio is commonly employed as evidence of vascular hypertrophy, normal vessels which are fixed and sectioned while in a functional state of vasoconstriction may exhibit similar gross characteristics. Constricted vessels are characterized by progressive deformation of the internal elastic lamina, crowding of endothelial cells, and distortion of smooth muscle cells and their nuclei, particularly in the region immediately adjacent to the lumen. During intense vasoconstriction, the wall tension appears to be supported only by the outer layers of the vessel.

Critical closure reexamined.

“…To apply this to real blood vessels, Burton 3 and his students demonstrated that closure was actually produced by a concertina folding of the internal elastica and bulging of the endothelial cells into the lumen as the vessel circumference becomes severely reduced (cf. also VanCitters et al 4 ). Verification of the closure phenomenon was carried out in frog and rabbit preparations with the demonstration that higher closing pressures were exhibited as active vascular tone increased.…”

“…In the hypothetical arteriole analyzed in Figure 3, circular muscle fibers would have to contract by 60% to achieve closure at zero pressure, and even further to produce closure at positive pressures. In the real arteriole directly analyzed by VanCitters et al 4 (their Fig. 2) there was a 68% shortening of the midwall circumference and a 60% shortening of the outermost muscular elements in the constricted state.…”

“…Assuming that only passive forces are present in a dilated blood vessel, Wiederhielm 10 has provided data for the passive elastic behavior of a small muscular artery as a function of relative increase in vascular dimensions, relating wall tension to the midcircumference of the wall (c m ) with the aid of the relationship 100 c m = W a /W t , (3) which assumes that the decrease in wall thickness (W t ) as the vessel distends does not alter the cross-sectional area of the wall (W a ). For any wall tension, the corresponding pressure in the lumen of the vessel may be calculated by application of the Laplacian relationship in the form P = T27TW./1.35 c n (4) in which the constant of 1.35 yields pressure values in mm Hg when tension is expressed in g/cm 2 . By this method, the Wiederhielm data have been used to describe the passive properties of a dilated muscular artery which, at zero pressure, has a radius of 100 fj.m, a wall thickness of 20 /xm, and a length of 1 cm, yielding the "dilated" pressure-tension plot in Figure 1.…”

“…When vessel distention stretches the constricted vessel beyond 100% of its dilated unstressed circumfer- ence, the Wiederhielm passive tension value for that circumference was added to the active tension. The sum of the active and passive tensions for each circumference was then related to the corresponding intravascular pressure by application of Equation 4. The "constricted" curve of Figure 1 shows the result of these calculations.…”

Movement of Norepinephrine through the Media of Rabbit Aorta

“…Because the calculated value of the diffusion coefficient is very sensitive to the value assigned to the thickness of the preparations (15), we restricted the data used for calculation of the diffusion coefficient to preparations providing 10 ± 1 medial sections. During exposure of the vessel to NE in vivo there is an increase in medial thickness (19). In our studies, the change of thickness was minimal, because of the short time of exposure to S H-NE (maximal contraction of aortas is reached between 5 and 10 minutes) and because the strip once mounted on the tissue holder contracted under isometric conditions.…”