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HANDBOOK OF PHVSIOLc K ,Y 



CIRCULATION II 



occurred when the arteriole narrowed. Clark & Clark 

 (27) had previously made a similar observation in 

 Amphibia, and also had observed that the contraction 

 of small vessels on which no adventitial cells de- 

 veloped was the same as those in which adventitial 

 cells were present. These observations seemed to rule 

 out any possibility that the adventitial or Rouget cell 

 was responsible for contraction. Sandison also noticed 

 that, as newly formed vessels changed from capillary 

 to arterial forms, the adventitial cells disappeared and 

 circular smooth muscle cells took their place. It was 

 shown later by Clark & Clark (33) that adventitial 

 cells actually differentiated into smooth muscle cells 

 as new capillaries developed into arterioles. 



A year later Sandison (106) stated that it was clear 

 from continuous microscopic observation of minute 

 vessels that contraction and relaxation of smooth 

 muscle cells of arteries and arterioles were responsible 

 for alterations in blood flow through capillaries, and 

 that neither Rouget cells nor endothelial cells played 

 any part in contraction of vessels. 



In the same year, Clark & Clark (29), after observing 

 capillaries of normal ear tissue through a trans- 

 parent chamber, stated that if any capillary contrac- 

 tility did occur it was too negligible to have any influ- 

 ence on the circulation. In subsequent papers Clark & 

 Clark (33, 34) summarized the accepted ideas regard- 

 ing capillary and endothelial contractility as follows: 

 a) Studies on mammalian vessels in transparent cham- 

 bers, where details of the cellular structures could be 

 clearly seen in unanesthetized animals, gave no evi- 

 dence for any contractile power of either endothelial 

 or adventitial cells. This view was supported by other 

 investigators (61, 101, 102). b) The real factors re- 

 sponsible for the control of circulation in the minute 

 vessels of the mammal are smooth muscle cells on 

 arteries, arteriovenous anastomoses, and large veins 

 (105). c) No contractile activity is seen in mammalian 

 capillary endothelium (29, 31, 33, 86), although 

 definite active spontaneous contractions occur in the 

 capillary endothelium of Amphibia (28, 142, 143). 

 They point out that the experimental evidence for 

 contractility of mammalian capillaries was based, in 

 some instances, on studies of nontransparent regions in 

 which the structure of the wall of the minute vessels 

 and their true diameters could not be seen. Therefore, 

 conclusions as to whether they were contracted or 

 dilated could only be inferred from the number of red 

 cells present in them. Also, belief in contraction of 

 mammalian capillaries was often based on observa- 

 tions of amphibian vessels in which contractions had 



been seen to occur with and without extra-enclothelial 

 cells. 



In spite of overwhelming contrary evidence, some 

 investigators still held for a time to their belief in 

 capillary contractility. It seems unnecessary to review 

 the disagreements in the face of the general accept- 

 ance at the present time of the opinions originally ex- 

 pressed by Sandison (106) and extended by Clark & 

 Clark (29). If one accepts the definition of a capillary 

 as a nonmuscular endothelial tube between the ar- 

 terial and venular systems, one may state unequiv- 

 ocally that mammalian capillaries are noncontractile. 



Nicoll & Webb (88) stated that observations on 

 capillaries in the bat wing showed that no perivascu- 

 lar cells, such as Rouget cells, existed in the region of 

 these vessels. The smooth muscle cells, at the tran- 

 sitional points from the terminal arteriole to the 

 capillary, end rather abruptly. Beyond the termina- 

 tion of smooth muscle cells within the walls no change 

 in the diameter of the capillaries, due to activity of 

 perivascular cells, has been observed. 



The question of the role played by the endothelial 

 cell in caliber changes in capillaries is more unsettled. 

 To cite some of the recent descriptions of endothelial 

 cell activity, Nicoll & Webb (88) reported modifica- 

 tions in capillary diameter that may result from elas- 

 tic recoil of the endothelial wall due to pressure varia- 

 tions either inside or outside the vessel. The caliber 

 change is due neither to active contraction of the 

 endothelium nor to intracellular swelling. Later, 

 Webb & Nicoll (130) pointed out that loss or gain of 

 fluid through the walls of endothelial cells may result 

 in apparent changes in their size. Also, since capil- 

 laries are distensible, they may show deformation 

 under variable conditions (89). These responses are 

 usually slow in their development and give no indica- 

 tion of active participation by the endothelial cells. 

 Chambers & Zweifach (2 1 ) believe that slow spon- 

 taneous endothelial responses for the most part repre- 

 sent accommodation to changes in pressure; that 

 endothelial cells possess a cellular tone which gives a 

 degree of elasticity to the capillary wall. Lutz el al. 

 (82) found that endothelium did not respond to me- 

 chanical stimulation. 



Folkow (44) summarizes current opinion in stating 

 that "slow swellings of the capillary endothelium are 

 sometimes observed, but are more probably to be 

 looked upon as passive osmotic effects or deformations 

 due to passive luminal changes, caused by variations 

 in intravascular pressure." 



