946 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



cardium and skeletal muscle, since reducing the 

 oxygen content of the arterial blood produces a 

 rather large increase in coronary (fig. 14A) and in 

 skeletal muscle flow, whereas there is almost no change 

 in flow in either bed when arterial blood C0 2 content 

 is increased (12, 49). The fact that coronary flow is 

 influenced more by coronary artery Oo content than 

 tension (51) is not incompatible with the concept 

 that tissue O2 tension is the controlled variable. The 

 feedback loop in the heart must involve something 

 other than O2 tension, since intra-arterial injection of 

 cyanide causes as great an increase of coronary flow- 

 as does hypoxia (fig. 14Z?) (49). 



The increase in blood flow in the brain in response 

 to decreased arterial blood oxygen content is relatively 

 minor compared to that which follows an increase in 

 CO2 content (fig. 15) (44), suggesting that brain CO2 

 tension may be the controlled variable for this tissue. 



Elevation of arterial blood hydrogen ion concen- 

 tration decreases resistance to flow through cutaneous 

 (18, 25), renal (23), and skeletal muscle (18) vascular 

 beds. Depression of the hydrogen ion concentration 

 below normal is accompanied by increase of resistance 

 to flow in skin (18, 25) and kidney (23); however, in 

 skeletal muscle depressed hydrogen ion causes about 

 the same degree of decrease of resistance to flow as 



104 . 



Arterial Pressure 

 mm Hg 







123 



94 



Cerebral Flow 



cm*/ mm 

 



II 6 



4' 30" 8% 02 



100 



Arterial Pressure 



mm Hg 

 0- 



Cerebral Blood Flow 

 cm3 /mm 



5' 10% C0 2 90% 2 



fig. 15. Records of cerebral venous outflow and systemic 

 arterial pressure during a 4.5-min period of breathing 8% O2 

 (upper pair of curves) and in response to a 5-min period of breath- 

 ing 10% CO; in 90% O2 (lower pair of curves) in the dog. Brain 

 was perfused directly from the aorta. 



does an elevation of hydrogen ion concentration (18). 

 Effects of hydrogen ion concentration on myocardial 

 blood flow are reported to be the reverse of those 

 in skin and kidney (38). These findings suggest that 

 hydrogen ion might be one of the controlled variables 

 in autoregulation. 



Role of nervous system in autoregulation. Autoregulation 

 is prominent in denervated vascular beds. High 

 activity in the extrinsic nerves may even minimize or 

 prevent manifestation of autoregulation; for instance, 

 central reflex effects of hypoxia may overpower the 

 local dilatory effect in the anesthetized dog's inner- 

 vated skeletal muscle vascular bed (75) (see also 

 p. 943). Autoregulation in kidney is not abolished 

 by procaine anesthetization, adrenergic blocking 

 agents, or gamma-aminobutyric acid (m), suggest- 

 ing that the feedback loop contains no essential link 

 that responds pharmacologically as does nervous 

 tissue. 



The behavior of cerebral blood flow in response to 

 changes of perfusion pressure (see above) cannot be 

 stated conclusively to represent strict autoregulation, 

 since in these studies a reflex neural mechanism was 

 not excluded. However, no influence of extrinsic 

 autonomic constrictor nerves upon cerebral blood 

 flow has been demonstrated conclusively (45), and 

 therefore, it is unlikely that an autonomic reflex is 

 involved in the cerebral studies. 



Myogenic theory of autoregulation. Bayliss (3) proposed 

 from studies of dog's hind legs and isolated arteries, 

 that the arterial wall responds directly to a rise of 

 intraluminal pressure by an increase in its state of 

 contraction (or tone) sufficient to bring about a 

 reduction in the lumen of the vessel (and presumably 

 therefore, a decrease in the flow through the vessel). 

 This concept received support from Johnson (66) 

 who failed to find an appropriate correlation between 

 change in the O2 concentration of the venous blood 

 draining an isolated segment of gut and the occurrence 

 of a decreased resistance to flow as perfusion pressure 

 was lowered. Since he found, also, no correlation with 

 nerve activity, gut contraction, or presence of meta- 

 bolites, Johnson concluded that the autoregulatory 

 change of flow represented a myogenic response. 

 Waugh & Shanks ( 1 1 1 ) observed that hypothermia 

 (3-10 C), intrarenal infusion of chloral hydrate, or 

 high concentrations of procaine abolished auto- 

 regulation but that anoxic perfusion did not depress 

 the autoregulatory reaction; since nerve block also 

 did not interfere (see above) they concluded that 

 renal autoregulation is due to "•myogenic vaso- 

 motion." Folkow (27) also postulated a myogenic 



