CENTRAL CARDIOVASCULAR CONTROL 



I 149 



hypothalamic vasoconstrictor-vasodilator pathway 

 that Uviias and his associates traced from the hypo- 

 thalamus, throusjh the mesencephalon and medulla 

 oblongata, down towards spinal le\els. It seems plau- 

 sible to assume that this and other such functional 

 vasomotor units are directly projected to the spinal 

 vasomotor neurons whereby they should have greater 

 possibilities for inediating distinct vasomotor response 

 patterns of supramedullary origin. 



Cerebral Cortex 



The earlier view that the suprabulbar integrati\e 

 control of the autonomic nervous system, including 

 that controlling the cardiovascular system, was lo- 

 calized solely in subcortical structures, chiefly the 

 hypothalamus, has gradually been superseded by the 

 opinion that it has an extensive representation in the 

 cerebral cortex. Experimental and clinical data sug- 

 gest that the cardiovascular medullospinal mecha- 

 nisms can be influenced from different regions of the 

 cerebral cortex, especially the motor area, the orbital 

 surface of the frontal lobe, the rhinencephalon and the 

 temporal lobe. 



Unfortunately these data throw little or no light on 

 the mechanisms through which the cortical control 

 acts. This is partly because only arterial pressure re- 

 actions — pressor or depressor responses — generally 

 have been followed, but sometimes cardiac respon.ses 

 — acceleration or retardation — also have been re- 

 corded. Moreover, the responses are greatly influenced 

 by various experimental conditions — as for instance 

 the intensity and frequency of stimulation, the type 

 and depth of anesthesia, and the species of animal. 

 Thus, it is not surprising that the experimental find- 

 ings afford a somewhat kaleidoscopic picture. In 

 virtually no case has an electrophysiologic technique 

 been employed in the study of cortical cardiovascular 

 control. 



MOTOR CORTEX. Hoff and Green (107, 126) ob.served 

 pressor responses and cardiac acceleration on stimu- 

 lation of the gyrus poreus and the gyrus sigmoideus 

 in the cat, and on stimulation of the cortex adjacent 

 to the superior precentral sulcus as well as scattered 

 points in the trunk and arm areas in monkeys. De- 

 pressor responses with or without bradycardia were 

 elicited from various precentrally localized points. 

 They observed a reduction of the renal volume and 

 usually an increase, although sometimes a decrease, 

 of the leg volume. Since these peripheral vasomotor 

 reactions were independent of the changes in arterial 



pressure, the results show that a peripheral redistribu- 

 tion of the blood flow may be initiated from the cere- 

 bral cortex. Similar observations were reported by 

 Lund (157). 



Hoff and co-workers (127) observed that bilateral 

 electrical stimulation of foci in the anterior sigmoid 

 gyrus produced, in acute experiments on cats, transient 

 elevations of arterial pressure of 80 to 100 mm Hg 

 together with pronounced renal cortical ischemia. 

 Stimulation of the brain through the intact cranium, 

 in chronic experiments lasting i to 6 weeks, caused 

 pathologic changes in the kidneys, presenting the 

 picture of lower nephron nephrosis, presumably due 

 to anoxia caused by the repeated arteriolar constric- 

 tion. Pronounced arterial pressure rises were observed 

 by Wall & Davis (215) and Kessler (141 j in dogs anes- 

 thetized with diallyl barbituric acid on stimulation 

 in the sensorimotor cortex. In man and subhuman 

 primates Kennard (139) observed that lesions in the 

 prcmotor cortex result in alterations of skin temper- 

 ature and color on the contralateral side of the body. 

 Ablation of the prefrontal cortex of Brodmann's areas 

 4 and 6 in monkeys has been observed to result in a 

 consistent decrease of the skin temperature on the 

 contralateral side. 



FRONT.^L LOBES. The frontal lobes have attracted con- 

 siderable interest in recent years since they have been 

 found probably to exert an inhibitory influence on 

 autonoinic functions. Total or partial removal of the 

 frontal lobes in cats and monkeys has been followed 

 by signs of excessive sympathetic activity, e.g. cardiac 

 acceleration, increased release of epinephrine and 

 augmented cutaneous vasoconstrictor reflexes [Ken- 

 nard (140), Livingston et al. (156)]. A depressor path- 

 way has in fact been traced continuously from just 

 behind the frontal pole of the hemisphere as far cau- 

 dally as the rostral end of the diencephalon and has 

 been regarded as a corticofugal inhibitory pathway 

 [Rabat et al. (136)]. 



Electrical stimulation of the orbital surface has 

 been reported to produce both pressor and depressor 

 reactions [Bailey & Sweet (24), Livingston et al. (54, 

 155, 156), Sachs et al. (186)]. The experiments were 

 performed on cats, dogs, monkeys and humans. Strom 

 (197) reported that electrical stimulation of structures 

 in the frontal lobe and the anterior hypothalamus 

 could produce cutaneous vasoconstriction as the sole 

 response. A marked poststimulatory inhibition of the 

 cutaneous vasoconstrictor tone was observed. In the 

 cat the cutaneous vasomotor responses were mainly 

 localized to the pads. 



