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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



and man (251). Electrophysiologic studies (139, 141) 

 indicate that Pacinian corpuscles in the skin and 

 mesenteries are sensitive to pressure changes. The 

 spontaneous outflow of impulses in large afferent 

 fibers in the splanchnic nerve seem to derive in the 

 main from the Pacinian corpuscles. Gammon & 

 Bronk (139), recording impulses from the peripheral 

 end of the splanchnic nerve and its branches in cats, 

 found group discharges synchronous with systolic ar- 

 terial pressure peaks. During constant perfusion a 

 sustained discharge was observed. Sarnoff & Yamada 

 (259) have suggested that Pacinian corpuscles may 

 mediate the changes in arterial pressure noted during 

 manipulation of the splanchnic vessels, but recent 

 work (40) indicates that extrasplanchnic baroreceptors 

 are involved and that mesenteric pressure receptors do 

 not contribute significantly, at least in species other 

 than the cat. Nevertheless, afferent impulses originat- 

 ing in these areas may be implicated in local and 

 central reflex arcs of importance to hepatic circulatory 

 adjustments. 



Impulses passing from the splanchnic bed by all 

 these afferent routes evidently pass directly to the 

 central venous system. Central representation of 

 afferent fibers from the abdomen has been explored 

 by a variety of methods. Bain et al. (18) found that 

 stimulation of the central end of the divided splanch- 

 nic causes pupillary dilatation that is due to inhibi- 

 tion of the oculomotor nucleus and not to change in 

 blood pressure, release of adrenaline, or activity of 

 somatic afferent fibers, since it occurs after transection 

 of the spinal cord between the fifth and sixth thoracic 

 roots. Using this method as a means of detecting 

 splanchnic afferent impulses they found that splanch- 

 nic afferents enter the cord from the sympathetic 

 chain via the rami and the dorsal roots. No synaptic 

 junctions seem to occur in the dorsal roots or in the 

 lateral sympathetic ganglia which resemble those for 

 sympathetic afferents in the sympathetic ganglia. 

 According to Downman (113), stimulation of these 

 fibers, in both cats and dogs, evokes detectable changes 

 in cerebral action potentials within the trunk areas of 

 somatic sensory representation, viz, contralateral 

 area I and both contralateral and ipsilateral area II. 

 The distribution and latency of the responses elicited 

 by centripetal stimulation of the splanchnic nerve do 

 not differ from those elicited by stimulation of a body- 

 wall nerve. Amassian (9) reported similar cortical 

 representation of visceral afferent impulses in the 

 rabbit, monkey, dog, and cat with maximal primary 

 cortical responses in the trunk region of contralateral 

 areas I and II, with ipsilateral representation in area 



II for the cat alone. The lack of correlation between 

 the number of receptors and the intensity of responses 

 suggests that splanchnic afferent projection may be 

 but partially derived from Pacinian bodies. In addi- 

 tion, the projection to somatovisceral areas in the 

 cortex raises additional doubt whether Pacinian 

 corpuscles are primarily concerned in vascular read- 

 justments rather than visceral sensation. The path- 

 ways through the cord have been mapped out to some 

 extent by Aidar et al. (2) who found that action 

 potentials were detectable in the cat to levels as high 

 as the thalamus. Faster impulses course through the 

 ipsilateral fasciculus and nucleus gracilis, internal 

 arcuate fibers, and contralateral medial lemniscus to 

 reach the thalamus. Slower impulses ascend in the 

 lateral spinothalamic tracts. These findings have been 

 confirmed by Gardner et al. (140) in studies of cortical 

 projections of fast visceral afferent impulses in the 

 cat and monkey. Since section of the dorsal funiculi 

 does not always abolish cortical potentials evoked by 

 stimulation of the splanchnic nerve they suggest that 

 additional pathways are followed. The anatomical 

 basis for reflex regulation of the hepatic and splanch- 

 nic circulation is clearly evident in these studies. The 

 status of a controlling "vasomotor center" for the 

 splanchnic bed is most obscure and it cannot be said 

 with certainty that discrete splanchnic vasomotor 

 representation is detectable within the cortex. Never- 

 theless, the cortical representation of visceral sensory 

 and motor functions that may involve vascular smooth 

 muscle seems to imply, on the one hand, a measure of 

 influence upon splanchnic vascular changes by cortical 

 activity directly, or, on the other, a reflection of 

 visceral circulatory adjustments in cortical function. 



Reflex responses almost certainly occur within the 

 splanchnic and hepatic vasculature, although they 

 are extremely difficult to characterize. Axon reflexes, 

 involving afferent nerves like those responsible for the 

 vasodilation of the "flare" in the skin during the 

 "triple response," are not demonstrable (80). The 

 phenomenon of "autoregulation" of hepatic blood 

 flow is possibly an exception but, as noted above, a 

 local stretch-and-response myogenic balance may be 

 responsible (180). Expansion of the portal venous 

 chamber may also elicit what Yamada & Burton 

 (313) have referred to as a "veni-vasomotor reflex" 

 characterized by arteriolar vasoconstriction proximal 

 to the site of venous distention. Mesenteric arteriolar 

 constriction observed during an elevation in portal 

 venous pressure (268) may be explained on this basis 

 but, here again, retrograde elevation of pressure to the 

 level of the arterioles with the slowing of flow cannot 



