HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



contain some obliquely oriented smooth muscle 

 cells which are apparently inserted on elastic fibers 

 (4). Their action and function are difficult to assess. 

 It is the current opinion that they exert tension on the 

 elastic fibers and thus afi"ect both the caliber and 

 distensibility of the aorta in silu (4, 6, 68). 



In the so-called muscular arteries, such as the 

 carotids, brachials, radials, iliacs, femorals, mesen- 

 teries, etc., elastic and collagenous fibers are found 

 chiefly in the intima and adventitia; the media, 

 which comprises two-thirds of the wall's thickness, 

 is composed almost entirely of smooth muscle fibers 

 arranged concentrically or, as some histologists say, 

 spirally (68). The muscle fibers are under a plastic 

 as well as contractile tonus. The former determines 

 the viscous characteristics of the wall; the latter resists 

 the tendency of internal pressures to distend the 

 arteries. Physically, the muscle elements are arranged 

 in parallel with the elastic and collagenous fibers; 

 they participate in resisting distention by internal 

 pressures and replace the action of collagenous ele- 

 ments in stiff"ening the walls under high internal pres- 

 sures (4, 68). The autonomous state of contractile 

 tonus is increased by mechanical and chemical agents, 

 as well as through excitation by vasoconstrictor 

 nerves. Hilton (34) has recently presented evidence 

 that muscular arteries, such as the femoral, may dilate 

 secondarily to a primary dilatation of arterioles, as a 

 result of the centripetal spread of a wave of inhibition 

 within the arterial walls. 



It was formerly believed that the contractile tonus 

 of the smooth muscle fibers alters the distensibility 

 of the muscular arteries and perhaps also adapts 

 their capacity to the volume of circulating blood, but 

 exerts no significant eff"ect on resistance to flow. 

 During the past two decades evidence has accrued 

 that changes in the diameter of long arteries may 

 affect regional resistance materially. The claim that 

 vascular contraction acts as an accessory mechanism 

 in the propulsion of blood is based on tenuous evidence 

 only; smooth muscles contract much too slowly to 

 follow the pace set by the heart. 



Artninles 



The arterioles constitute the terminal branches of 

 the distributing system and are the primary stopcocks 

 that regulate capillary flow. Their walls are relatively 

 thick compared to their lumens. The abundant 

 circularly arranged muscular elements are under an 

 autonomous state of contraction (tonus) which can 

 be augmented or inhibited by chemical agents or 



by the action of vasomotor nerves. Vasoconstrictor 

 fibers are generally routed over sympathetic path- 

 ways. It is in fact probable that so-called sympathetic 

 dilators to the coronary arteries are misnamed; they 

 seem to cause dilatation through release of metabolites 

 [Gregg (24)]. Vasoconstrictor nerves have been 

 demonstrated for vessels of all organs, but the in- 

 tensity of vasomotion induced is less marked in vessels 

 of the lungs, brain, and heart. Because of these differ- 

 ences in vasomotor reactivity, increased discharges 

 from the medullary vasomotor center can induce 

 large changes in splanchnic and renal resistances, 

 thereby mechanically diverting more blood to vital 

 organs, such as the brain and heart. This hemody- 

 namic concept is not new. For example, L. Hill (33) 

 stated in 1900, "It is by means of the great splanchnic 

 area that the blood supply of the brain is controlled. 

 . . .We have in the vasomotor center a protective 

 mechanism by which blood can be drawn at need 

 from the abdomen and supplied to the brain." [See 

 also Folkow (16-18).] 



Neurogenic vasodilatation is generally induced 

 through inhibition of vasoconstrictor activity which, 

 however, still leaves arterioles under a state of auton- 

 omous contraction. In the heart, abdominal organs, 

 and skeletal muscles, this residual tonus can also be 

 inhibited by action of sympathetic vasodilator nerves, 

 thus causing additional dilatation. In vessels of the 

 head, pelvic organs, and genitals, excitation of para- 

 sympathetic nerves induces extreme dilatation. The 

 interpretation of Gesell (21) that such vasodilatation 

 is not due to direct nervous action but through re- 

 lease of vasodilator metabolites has recently received 

 considerable support (18, 65). In the skin, vasodilata- 

 tion may occur through operation of axon reflexes, 

 and in mucous membranes by action of posterior 

 root dilators (18, 65). 



Through reflex control of vasomotion, shifts of 

 blood from viscera to the skin and vice versa may 

 take place, as for example during exercise and diges- 

 tion as well as in hemorrhage and shock (32, 49, 72). 



Control of Capillary Blood Flow 



The capillary walls consist of a single layer of 

 endothelial cells mounted on a basement membrane. 

 The thin walls adapt the capillaries admirably for 

 interchange of substances between the blood and 

 tissue spaces. According to older views (8), a "cement 

 substance" between cells is produced by them and 

 can be modified by such agents as the Ca:K ratio 

 and hormones. Advances in methodologies, including 



