FLOW OF BLOOD IN MESENTERIC VESSELS 



1449 



triphosphate in the investigations of Selkurt et al. 

 (121) and of Binit et al. (15), and by topically applied 

 procaine in Grayson's research (61) on human mu- 

 cosal blood flow. Grayson also observed that cooling 

 a limb caused dilation in the colostomy mucosa 

 whereas heating the body produced constriction, the 

 direction of the changes being opposite to those in 

 the skin. Trapold (132) found that several ganglionic 

 blocking agents caused a small decrease in resistance 

 to flow in the mesenteric artery bed, although this 

 must be interpreted in light of the fact that his control 

 flows were abnormally low. 



Sidky & Bean (12, 126) used their isolated in- 

 testinal segment preparation to investigate the effects 

 of variations in the concentration of the respiratory- 

 gases in the perfusion fluid. They found that hyper- 

 capnia and hypoxia resulted in an increase in blood 

 flow; hypocapnia resulted in vasoconstriction. Brick- 

 ner et al. (22) determined the total mesenteric flow 

 less that through the spleen in dogs breathing gas 

 mixtures containing various percentages of C0 2 . 

 With less than 5 per cent C0 2 , the circulatory changes 

 were minor; at levels of 5 to 16 per cent, there was a 

 significant decrease in mesenteric resistance. 



Intestinal blood flow is profoundly influenced by 

 motor activity. Anrep et al. (4) perfused loops of dog 

 intestine and observed a decrease in venous outflow 

 during muscular contractions. Sidky & Bean (127) 

 in their studies of artificially perfused intestinal seg- 

 ments found that early in a contraction arterial inflow 

 decreased and venous outflow increased, with venous 

 pressure sometimes exceeding arterial pressure. If 

 the contractions were rhythmic and of short dura- 

 tion, they could augment the flow. If the duration of 

 a contraction was longer, the flow through the seg- 

 ment would decrease as a consequence of the fall in 

 arterial inflow. As expected, these effects were more 

 pronounced the stronger the contractions. 



Lawson & Chumley (93) showed that increases in 

 intraluminal pressure to values below 30 mm Hg 

 caused a temporary decrease in blood flow followed 

 by recovery to control values. At higher pressures 

 only a partial recovery' was noted. Recovery was not 

 observed in segments placed in plaster casts or treated 

 with procaine, and denervation was without in- 

 fluence. They concluded that the stretching of the 

 gut wall initiated a vasodilation mediated through 

 intrinsic nerve networks. 



Selkurt et al. (121) have investigated the relation 

 between blood flow through an artificially perfused 

 denervated ileal segment and the arterial-venous 

 pressure difference. They found the relationship to 



be slightly curvilinear, convex toward the pressure 

 axis, with a positive intercept on that axis of about 

 15 mm Hg. Since, as already pointed out, their 

 observed flows at normal arterial-venous pressure 

 differences were quite low, some caution must be 

 exercised in applying their results to the normal 

 situation. However, Johnson et al. (84) found a 

 similar intestinal pressure-flow relationship in the 

 totally perfused dog, although with higher flows for 

 any given pressure. 



Selkurt & Johnson (122) and Johnson (85) ob- 

 served that the effect of increasing intestinal venous 

 pressure was to produce a rise in vascular resistance 

 in the mesenteric bed. They concluded that the re- 

 sistance changes were not dependent on nervous 

 mechanisms but suggested that the elevation of 

 venous pressure induced a myogenic response in the 

 resistance vessels. 



Johnson (86) also investigated the influence on 

 flow resistance of partial occlusion of an intestinal 

 artery. In 70 per cent of the cases the resistance de- 

 creased with arterial pressure reduction. He con- 

 cluded that this autoregulation of intestinal blood 

 flow was not clue to a local reflex but rather was the 

 consequence of a myogenic response of the vascular 

 smooth muscle. 



Occlusion of the mesenteric artery also has an 

 effect on the systemic circulation, causing a rise in 

 arterial blood pressure. Sarnoff & Yamada (115) 

 observed large increases in blood pressure in the cat 

 and concluded that this effect was dependent upon 

 reflexes initiated by receptors in the abdominal 

 organs, particularly in the pancreas. In this species, 

 they considered such reflexes more important than 

 those originating in the carotid sinus and aortic 

 arch. Boyer & Scher (20) observed smaller pressure 

 changes in the same animal and concluded that 

 there was no evidence for the presence of baroceptors 

 in the mesenteric artery, and that the rise in systemic 

 arterial pressure was due only to mechanical diver- 

 sion of the blood away from the abdominal viscera. 

 Heymans et al. (79) performed similar studies with 

 the dog and decided that the general blood pressure 

 rise was a purely hemodynamic effect due to the 

 exclusion of an important arterial vascular area and 

 did not indicate the existence of abdominal baro- 

 ceptors. Selkurt & Rothe (123) performed similar 

 studies in both dogs and cats. The results with cats 

 agreed with the findings of Sarnoff and Yamada. 

 Those obtained from dogs led the authors to con- 

 clude, in agreement with Heymans, that splanchnic 

 baroceptor activity in that species is slight. 



