CENTRAL CARDIOVASCULAR CONTROL II5I 



corticospinal pathways serve chiefly to facilitate auto- 

 nomic response patterns elicited at spinal and periph- 

 eral levels. However, available data do not eluci- 

 date the efferent pathways by which the vasomotor 

 reactions produced from the cortex are mediated. 

 Yet considering the knowledge we pcssess of the 

 central representation of the sympathetic vasodilator 

 outflow, it is probable that most, and perhaps virtually 

 all, of the observed vasomotor responses have been 

 produced via variations in vasoconstrictor tone. Of 

 the observations that have been reported, an analysis 

 of the peripheral vascular reaction pattern has been 

 made only by Lund (157) and Green & Hofif (107). 

 These authors stimulated the motor cortex in cats 

 and observed an increase of the leg volume, pointing 

 to vasodilatation there which inay have been pro- 

 duced by sympathetic vasodilator activity. 



Cerebellum 



Occa.sional early reports suggest that the cerebellum 

 in some way or other influences the central vasomotor 

 control [.see Wiggers (223, 224)], but its significance 

 in vascular regulation is not yet clear. 



According to Moruzzi (165), stimulation in the 

 vermis cerebelli may inhibit both pressor and de- 

 pressor reflexes elicited by stimulation of afferent 

 nerves, such as the sciatic, superior laryngeal and 

 central end of the vagus. Spontaneous vasomotor 

 waves of central origin are also inhibited. Moruzzi 

 further demonstrated that pressor reflexes elicited by 

 occlusion of the common carotids or by intracarotid 

 injections of cyanide were inhibited by stimulation 

 of vermian structures with intensities yielding strong 

 inhibition of the decerebrate rigidity. In his view, the 

 inhibition is due to a central effect on bulbopontine 

 centers. 



CENTRAL REPRESENTATION OF SYMPATHETIC 

 VASODILATOR NERVES 



In recent years Swedish investigators lia\'e been able 

 to activate sympathetic vasodilator nerves to the 

 skeletal muscles in dogs, cats and foxes by intra- 

 cerebral stimulation. This outflow has been shown to 

 have a widespread intracerebral representation. The 

 corticospinal course of a sympathetic xasodilator 

 tract (iig. 10) has Ijeen traced from its cortical origin 

 down to spinal levels Ijy Lindgren et al. (150). The 

 vasodilator responses to intracerebral stimulation were 

 completely abolished by small doses of atropine and 



CORTEX CEREBRI 



CAPSULA INTERNA 



■ \^A^_/J HYPOTHALAMUS 



ESENCEPHALON 



EDULLA OBLONGATA 



EOULLA SPINALIS 



TRUNCUS SYMPATICUS 



NERVUS SPINALIS 



MUSCULUS 



FIG. 10. Schematic drawing showing the central and pe- 

 ripheral course of the sympathetic vasodilator pathways. [From 

 Lindgren (149).] 



were augmented by physostigmine (figs. 11, 12). To 

 show that these effects were due to a peripheral action 

 and not to an action on ganglia or intracerebral syn- 

 apses, cross-perfusion experiments were performed in 

 which it was shown that these drugs blocked and aug- 

 mented, respectively, the vasodilator responses in the 

 muscles peripherally. It is thus safe to conclude that 

 these vasodilator responses are due to activation of 

 cholinergic syinpathetic vasodilator nerves. 



