FLOW OF BLOOD IN MESENTERIC VESSELS 



1447 



found that pilocarpine increased flow in the cat. 

 Bishton (16) made a similar observation in guinea 

 pigs when the pilocarpine was administered topically. 

 Schnitzlein (117) saw mucosal engorgement in the 

 rat under the influence of this drug. Lim et al. (94) 

 observed little effect of Pitressin in their perfused 

 preparation, but both Cutting et al. and Boenheim 

 (18) found a decrease in flow under the influence of 

 this hormonal preparation. Lim et al. found that 

 sodium nitrite and Cutting's group that erythrol 

 tetranitrate increased flow. Dolcini and co-workers 

 (40) observed an increase in the gastric mucosal 

 content of arterially administered India ink in the 

 rat given serotonin or 5-hydrox\ tryptophan. 



Salmon et al. (112) demonstrated that cooling the 

 dog stomach to 15 C reduced the blood flow to 30 to 

 40 per cent of control. Heating was shown by Cut- 

 ting's group to have the opposite effect. 



Richards et al. (1 10) found that a variety of emo- 

 tional states, anxiety, tension, resentment, all in- 

 creased flow in the human gastric mucosa as evi- 

 denced by the increase of heat uptake by the luminal 

 surface. Wolf & Wolff (138) made an extensive study 

 of color changes (i.e., blood volume changes) in a 

 human gastrostomy. There was an increase in redness 

 following administration of histamine, alcohol, beef 

 juice, acetylmethylcholine, exposure to local warm- 

 ing, during discussion of food and coincident with 

 evidence of hostility. Blanching occurred during 

 fear, sadness, discouragement, exposure to cold, and 

 after administration of epinephrine, ergotamine, or 

 Pitressin. 



Intestine 



It is generally agreed that stimulation of the 

 splanchnic nerves causes vasoconstriction in the 

 intestine. As early as 1899, Bayliss & Starling (11) 

 demonstrated that such stimulation decreased the 

 volume of intestinal segments. Burton-Opitz (27) 

 observed a reduction in mesenteric venous flow in 

 etherized dogs without a significant increase in portal 

 vein pressure, thus showing that mesenteric resistance 

 was increased. Deal & Green (38) measured flow in 

 the cranial mesenteric artery and the appropriate 

 pressures in dogs anesthetized with pentobarbital 

 in order to determine intestinal vascular resistance. 

 Although their control flows were abnormally low 

 (less than 0.1 ml 'min g of tissue), they found an 

 increase of 50 per cent in resistance during splanchnic 

 stimulation. Both Celander (34) and Kock (91) 

 determined venous outflow from jejunal loops in 



vagotomized cats under pentobarbital or chloralose- 

 urethan anesthesia and also found that splanchnic 

 stimulation reduced the flow. 



Bulbring & Burn (25) observed a reduction in 

 intestinal volume in plethvsmographic studies with 

 etherized, adrenalectomized dogs and cats during 

 stimulation. After administration of ergotoxine, the 

 same procedure produced an increase in volume. 

 Atropine did not block the dilation phase, and they 

 concluded that the splanchnic nerves contained some 

 noncholinergic vasodilator fibers as well as the vaso- 

 constrictor elements. Deal and Green also found that 

 the sympatholytic agent, Ilidar, sometimes reversed 

 the constrictor effect of splanchnic stimulation and 

 that atropine had no influence on the reversal. 

 Folkow et al. (47) in their studies on cats concluded 

 that the vasodilator fibers could not be adrenergic 

 either and hence that there were probably no splanch- 

 nic vasodilators. They thought that the vasodilation 

 seen during splanchnic stimulation after ergotamine 

 or Dibenamine was probably due to relaxation of the 

 intestinal smooth muscle. 



The primary effect of both epinephrine and nor- 

 epinephrine on the intestinal vasculature seems to 

 be the same as that of splanchnic stimulation. 

 Schwiegk (118) found epinephrine to decrease both 

 arterial and venous flow in dogs anesthetized with 

 chloralose. In cats, also anesthetized with chloralose, 

 Clark (35) found that epinephrine in all concentra- 

 tions reduced intestinal venous outflow. Folkow et 

 al. (47) observed vasoconstriction in the cat with 

 both epinephrine and norepinephrine, as also did 

 Kock (91). Grayson's group (61-64), using a calori- 

 metric method, demonstrated that both compounds 

 produced vasoconstriction in the mucosa and muscle 

 of human ileostomies and colostomies. Binit et al. 

 (15) observed an increase in the resistance of the 

 mesenteric arterial bed upon intra-arterial injection 

 of epinephrine in the dog under chloralose anesthesia. 

 Green and co-workers (38, 65) in their studies on 

 mesenteric artery flow in dogs anesthetized with 

 pentobarbital found that both compounds caused a 

 several hundred per cent increase in resistance. 

 Selkurt et al. (121) observed a reduced flow through 

 artificially perfused, denervated ileal segments under 

 the influence of both substances. Bohr et al. (19) 

 used the Zweifach preparation of the rat mesoap- 

 pendix to show that epinephrine and norepinephrine 

 were both constrictors whether administered intra- 

 venously or topically. Although these workers found 

 epinephrine the more potent compound, all the 

 other investigators (47, 65, 91) who compared the 



