CENTRAL CARDIOVASCULAR CONTROL 



■45 



reflex or other cardiovascular reflexes produced by 

 various drugs. The influence of the vagal aff'erent 

 impulse traffic on the cardiovascular efferent dis- 

 charge, and the physiologic significance of this 

 traffic, are quite unknown. 



d) Other receptors and afferent fibers. The ability of 

 sensory and nociceptive impulses to influence the 

 cardiovascular discharge is demonstrated by the 

 fact that stimulation of afferent nerves, as the sciatic, 

 brachial or trigeminal nerve, produces pressor or 

 depressor effects, depending on the parameters of 

 the stimuli, the depth and nature of narcosis, and 

 other related factors. These reflexes are, according to 

 some authors, at least partly relayed through the 

 medulla oblongata. Alexander (7) observed volleys of 

 impulses in the inferior cardiac nerves in response to 

 single shocks applied to the central end of the sciatic 

 nerve. Repetitive stimulation of the sciatic nerve 

 elicited a pressor reflex and a considerably increased 

 discharge in the inferior cardiac nerves. Transection 

 in the medulla oblongata just below the pressor area 

 (see p. 1 1 39) completeK' abolished the reflex cardio- 

 vascular discharge as well as the pressor reflex. 



e) Cardiovascular responses. The cardiovascular re- 

 sponse pattern a.s.sociated with different pressor and 

 depressor reflexes has been incompletely elucidated. 



The fall of arterial pressure attending activation 

 of the baroceptors, at all e\ents those in the carotid 

 sinus region, is due partly to bradycardia and partly 

 to peripheral vasodilatation. The principal factor 

 here is the vasodilatation, which is reported chiefly to 

 affect the visceral region ijut also occurs in muscles 

 and skin [Folkow el al. (8g), Frumin et al. (93), 

 Lindgren & Uvnas (153, 154)]- Since vasodilatation 

 is due to inhibition of vasoconstrictor tone, it is proba- 

 ble, though not experimentally verified, that vaso- 

 dilatation affects different vascular regions in inverse 

 proportion to their vasoconstrictor tone. 



Bcrnthal (31) is one of the few investigators who 

 has studied the reflex vasomotor reactions which at- 

 tend changes of the chemical milieu in a perfused 

 carotid sinus. Anoxia, cyanide, hypercapnia and lactic 

 acid caused pressor reactions with bradycardia and 

 reffex vasoconstriction in a foreleg. Since an increase 

 of the normal oxygen tension and a decrease of the 

 normal carbon dioxide tension in the perfusion fluid 

 resulted in vasodilatation, his findings accord with 

 the supposition of von Euler et al. (213) that the 

 chemoceptors are already activated at the oxygen 

 and carbon dioxide tensions which occur under phys- 

 iologic conditions. 



Although the pressor effect of anoxia is usually ac- 



companied by cardiac acceleration, there is very 

 little experimental evidence as to the heart rate re- 

 sponse to a chemoceptor stimulus. Heymans & 

 Bouckaert (118) reported that injection of nicotine 

 and cyanide into the carotid sinus produced pressor 

 responses with bradycardia. Bernthal et al. (32) ob- 

 served that chemoceptor reffexes capable of produc- 

 ing pressor reflexes caused not tachycardia, but 

 bradycardia. In these experiments the pressor re- 

 sponses were blocked by a compensation device. The 

 bradycardia, therefore, could not be ascribed to a 

 reflex produced by the arterial pressure rise. Neil 

 (166), believing results more applicable to systemic 

 anoxic conditions could be obtained with chemo- 

 ceptor impulses bombarding an anoxic medulla 

 rather than, as in experiments of Bernthal et al., an 

 adequately oxygenated medulla, found that such 

 systemic anoxia produced tachycardia and hyper- 

 tension. However, when both carotid sinuses wen 

 then perfused with adequately oxygenated blood, 

 the hyperpnea and hypertension were reduced but 

 the tachycardia persisted. It thus seems as if chemo- 

 ceptor reflexes produce an increase of vasoconstrictor 

 discharges but no cardiac acceleration. 



The reflex vasoconstriction due to excitation of 

 chemoceptors probably concerns all vascular fields, 

 although quantitative diflferences may exist. Bernthal 

 & Schwind (34) claim that excitation of chemoceptors 

 by anoxia cau.ses more marked vasoconstriction in 

 the limbs than in the intestines. Folkow & Uvnas 

 (90, 91) reported the chemoceptor-induced pressor 

 responses to occlusion of the common carotids to be 

 due to marked vasoconstriction in both the .skeletal 

 muscles and the splanchnic region. 



As to the cardiova.scular respon.se pattern asso- 

 ciated with depressor and pressor reflexes due to 

 afferent impulses in sensory nerves, satisfactory in- 

 formation is still lacking. 



/) Efferent pathways. The bradvcardia attending the 

 sinus depressor reflex has been shown to be due to 

 the comijined action of vagal activation and sympa- 

 thetic inhibition, vagal activity being most marked 

 immediately following sinus distention, while the 

 slowing due to sympathetic inhibition appeared slowly 

 and became the major restraining influence as the 

 vagal effect diminished [\V'ang & Borison (217)]. 

 There have been no similar investigations on the role 

 played by the vagal and sympathetic innervation of 

 the heart in pressor reflexes. 



All observations — both those made with modern 

 electrophysiologic techniques and those made with 

 more classical methods for determination of arterial 



