PHYSICAL EQUILIBRIA OF HEART AND VESSELS 



99 



by the theory of slight physiological importance. 

 The following considerations apply. 



a) The CCP might exist in vascular beds, but be 

 of so small a magnitude, say i or 2 mm Hg, as to be 

 of negligible importance in the circulation, where 

 driving pressures (and thus transmural pressures) 

 of 100 mm Hg or more are available to prevent the 

 closure of vessels. The closure of some of the blood 

 vessels of a vascular bed can be detected, in perfusing 

 a vascular bed with a driving pressure which is 

 steadily reduced. If closure takes place at a critically 

 low value of the "arterial" pressure (which cor- 

 responds to a certain value of transmural pressure 

 of the vessels which clo.se), that flow will become 

 zero even though the driving pressure has some 

 significant positive value. Ii flow does so cease, the 

 pressure drop up to the point of closure will disappear 

 (no flow equals no gradient), so the arterial pressure 

 will equal the transmural pressure of the closing 

 vessels, i.e., is equal to the CCP. 



h) In view of the fact that vascular beds have an 

 enormous number of channels in parallel through 

 which blood can flow from artery to vein, only if 

 all such parallel channels sufTer critical closure will 

 the flow actually reach zero. It is therefore remark- 

 able to find that in several different vascular beds, 

 e.g., the frog's leg (20), the rabbit's ear (14, 20), 

 the rabbit's hind limb (14, 20), the splanchnic vascular 

 bed of dogs (i), the human forearm (4), finger (29), 

 and the hind quarters of rats (11), such "zero-flow" 

 pressures exist, or to find other evidences that arterial 

 and venous systems are not connected (i, 10, 19). 



c) Evidently in these beds no parallel channels 

 lacking \asomotor tone, which would fail to close, 

 exist. In other vascular beds there may be critical 

 closure of certain vessels, but since other channels 

 remain open (having very low or no CCP), flow will 

 not fall to zero. However, a careful study of the 

 flow-pressure curves in such ca.ses should reveal an 

 abrupt decrease of flow, though not to zero, at a 

 critical level of perfusion pressure. Indeed, this has 

 been ob.served in the case of the perfused mesenteric 

 bed in the frog (Burton, unpublished data). 



d) In the determination of CCP the perfusion of a 

 vascular bed has to ise reduced, and this may, in 

 those cases where "reactive hyperemia" is a promi- 

 nent feature as in the \essels of skeletal muscle, lead 

 to a disappearance of the original tone, so no CCP 

 will be found. The same may apply to the perfusion 

 with a vasoactive agent, e.g., adrenaline, where 

 there are enzymes, e.g., amineoxidase and O-methyl 

 transferase, which rapidly destroy the agent. As the 



flow decreases, the enzymic destruction may catch 

 up with the supply, so closure never occurs. In cer- 

 tain circumstances this may be illustrated, in a 

 rabbit ear, by a periodic closure and opening up 

 of the vessels when perfused by adrenaline solutions 



(19)- 



e) In many cases in the literature where the exist- 

 ence of closure (or zero-flow pressure) has been 

 denied, the vascular beds under study were probably 

 completely dilated and the pressure was not lowered 

 enough to find the very low CCP that would be 

 expected (5 to 10 mm Hg) in this case. 



The proponents of the theory of critical closure 

 are thus in the fortunate position of being able to 

 explain the failure of many experimenters to find 

 evidence of closure when the pressure is lowered, 

 while citing many experimental positive evidences 

 of its occurrence. 



The possibility that the cessation of flow is due, 

 not to an active closure of vessels under tone, but 

 perhaps to obstruction of the lumen of vessels, was 

 early excluded (fig. 17). In the experiments the 

 flow-pressure curve was obtained by the "vertical 

 tube method." The constant pressure head perfusing 

 a rabbit's ear was cut off, so the ear was perfused 

 from the column of solution in a vertical tube at the 

 arterial cannula. As the flow proceeded at a steadily 

 diminishing rate, the curve of fall of level in the tube 

 allowed the rate of flow (from knowledge of the 

 cross-sectional area of the tube) at each of the driving 

 pressures to be calculated. With a pressor drug added 

 to the perfusate, the fall of level, and the flow ceased 

 altogether at the critical closing pressure. If at this 

 point (fig. 17) some fluid was removed from the 

 system, lowering the pressure below the critical point, 

 it subsequently rose as shown. The only explanation 

 seems to be that with the lowering of pressure more 

 vessels under tone reach the critical state and close, 

 forcing fluid retrogradely out of the artery as well 

 as out of the \enous side. 



As for the existence of a critical closing active 

 tension, this is generally accepted, for "spasm" of 

 vessels endowed with smooth muscle has often been 

 observed. In the view of the theoiy, "spasm" is 

 simply evidence that the critical closing pres.sure has 

 risen above the available blood pressure. The "criti- 

 cal" nature of such spasm is illustrated by figure 18, 

 where a srnall rise of perfusion pressure above the 

 critical value resulted in an abrupt opening to allow 

 quite a considerable flow. 



The theory of critical closure, and the experimental 

 evidence for its occurrence, have been unacceptable 



