CENTRAL CARDIOVASCULAR CONTROL 



II53 



BLOOO PRESSURE 140 



BLOOD FLOW SmNNED 

 RIGHT HIND LIMB 



CUTANEOUS 

 BLOOD FLO* 

 RIGHT EAR 



SIGNAL 



TIME 60 StC 



FIG. 12. Concomitant vasodilator responses in muscles of 

 right hind leg {upper record), and vasoconstrictor responses in 

 skin of right ear (lower record) during stimulation of right half 

 of medulla. Dog with spinal cord ligated at L5. Voltage: 1.25 v. 

 Duration of each stimulation, 15 sec. Vasodilator responses in 

 right leg disappear but cutaneous vasoconstrictor responses in 

 ear persist and cause pressor response after atropine. [From 

 Lindgren & Uvnas (,152).) 



region of the decussatio dorsalis tegmenti. Stimulatory 

 exploration revealed that supracollicular and collicu- 

 lar stimulation produced bilateral \asodilator re- 

 sponses in the skeletal muscles, while inf'racoUicular 

 stimulation resulted only in ipsilateral responses. 

 The same was the case with vasoconstrictor responses 



in the skin. From this observation, Lindgren con- 

 cluded that the mesencephalon constitutes the lowest 

 integrating level for the vasodilator tract. Following 

 supracollicular decerebration, vasodilator responses 

 persisted on stimulation after a sufficient length of 

 time had elapsed for degeneration of the severed 

 neurons. This persistence of vasodilator responses 

 inust mean that fresh neurons originated from the 

 collicular area. 



Hypothalamus 



Intrahypothalamic stimulation produces vasodila- 

 tation in the skeletal muscles of both the cat and the 

 dog [Eliasson et al. (75, 76)], in the cat frequently ac- 

 companied by vasoconstriction in the skin of the paw 

 and in the intestines. In the dog, on the other hand, 

 it elicited a more or less selective activation of the 

 sympathetic \asodilator outflow. Neither acceleration 

 of the heart nor other signs of sympathetic activity 

 were observed to occur. The vasodilatation produced 

 in the muscles could amount to five or si.x times the 

 basal value; it could be made maximal (fig. 13) and 

 could arise without any significant changes in the 

 arterial pressure, evidently because compensatory 

 vasoconstriction simultaneously occurred elsewhere. 

 \'asodilatation elicited by hypothalamic stimulation 

 was invariably bilateral. 



In the experiments of Uvnas et al. sympathetic vaso- 

 dilator discharges could l)e evoked only h\ stimulation 

 within a fairly limited area of the hypothalamus ex- 

 tending along the mid-line. This finding contrasts with 

 the diffuse distribution of pressor and depressor points 

 throughout the hypothalamus, notably the lateral 

 part, reported by earlier workers. 



Since the sympathetic vasodilator outflow can also 

 be activated by intrahypothalamic stimulation in 

 chronic decorticate animals [Eliasson et al. (77)], 

 the cell bodies of these vasodilator neurons are located 

 in the hypothalamus where a vasodilator path origi- 

 nates. This path in its hypothalamic course ran from 

 3 mm rostral to the anterior commissure between the 

 internal capsule and the mid-line, extending caudad 

 along the mid-line in a somewhat dorsocaudolateral 

 direction, reaching the ventromedial border of the 

 ventrothalamic nuclei. During its posthypothalamic 

 course it ascends steeply towards the tectal region 

 where it reaches a position in the collicular area about 

 3 mm beneath the dorsal surface of the brain stein and 

 3 to 5 mm lateral to the mid-line. 



