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HVNDBOOK OF HHVSIOLOGY 



NEUROPHYSIOLOGY III 



though the arterial pressure at head level had fallen 

 to very low values. The explanation for this phenom- 

 enon lay in the internal jugular pressure which, 

 influenced by the same hydrostatic forces, had fallen 

 well below atmospheric levels, exerting a siphon-like 

 effect. 



Cerebral I 'oscular Resistant t 



L'nder normal circumstances of maintained arterial 

 pressure and normally low venous pressure, the regu- 

 lation of the cerebral circulation resides entirely 

 within the brain itself through the operation of a 

 variety of factors, all of which affect the resistance to 

 the flow of blood. The first of these factors is intra- 

 cranial pressure, an increase in which has been 

 shown to produce a parallel increase in resistance 

 ( ",; i, causing, at intracranial pressures above 500 mm 

 of water, a moderate to severe restriction in cerebral 

 circulation. 



The viscosity of the blood is another factor which 

 affects its resistance to flow, although in only two 

 conditions -polycythemia vera and anemia — is the 

 viscositv altered sufficiently to produce marked 

 effect*. In the former, a blood flow of less than half the 

 normal values has been observed (48), while in 

 severe anemia the cerebral circulation is significantly 

 increased (40, 82). To what extent changes in local 

 carbon dioxide and oxygen tension brought about by 

 the altered hemoglobin content of the blood operate 

 in association with the viscosity changes in these 

 condition* has not been investigated. 



By far the most important single factor, however, 

 is the narrowing or dilatation of cerebral vessels, 

 especially the arterioles; a number of variables 

 operate to alter \ ascular dimensions, including neuro- 

 genic, humoral and organic factors. 



\ 1 urogi nil I ontrol 



There is an intrinsic nervous supply to the arteries 

 and arterioles of the brain (81). This appears to 

 originate from the carotid and vertebral plexus, .1 

 network oi nerve fibers and ganglia which accompany 

 these vessels as thc\ enter the skull. The carotid 

 plexus i* supplied b\ libers from the superior cervical 

 .■■lion and also by a bundle which emerges from 

 the cranium along with the facial nerve, continuing 

 through the greater superficial petrosal. A number of 

 studies in lower animals has demonstrated thai stimu- 

 lation of the cervical sympathetic 1 hain usually pro- 

 dua ii tii hi in the brain, v\ bile stimulation 



of the greater superficial petrosal or facial nerve pro- 



duces vasodilatation (27, 76, 81, 96). It has been 

 found, however, that section of both of these supplies 

 does not cause degeneration of the intracerebral 

 vascular nerves, an observation which led to the 

 demonstration of ganglion cells in the carotid plexus 

 (81). There is surprisingly little evidence in favor of 

 a tonic constrictor effect on cerebral vessels, at least 

 that which may be mediated by way of the known 

 sympathetic innervation to the head (38, 96). Studies 

 on the effects of stellate ganglion blockade in man 

 (38, 87), although showing expected evidence of 

 paralysis of the sympathetics to the eye and a dilata- 

 tion of cutaneous vessels, have failed to show any 

 change in cerebrovascular tone or in cerebral blood 

 flow in the conditions studied. 



The possibility of spasm of cerebral vessels, often 

 suggested by certain clinical syndromes and beauti- 

 fully demonstrated by cerebral embolization in 

 animals (7, 108), has not yet been definitively demon- 

 strated in man. Although arteriographic evidence 

 suggestive of spasm has been obtained (17), such 

 studies are difficult to control rigorously. Most of the 

 clinical evidence for spasm is equally compatible 

 with an explanation on the basis of multiple minor 

 thromboses (23) or transitory systemic hypotension 

 in a critically narrowed vessel (13, 16, 72). 



Humoral Control 



The effect of humoral agents is clearer and more 

 readily demonstrated. Cerebral blood flow shows an 

 excellent correlation with the carbon dioxide tension 

 of arterial blood (-,4, V. ( >~,, ~') ] I hi* has been con- 

 firmed in a large number of studies on animals and 

 man using a wide variety of techniques. In man the 

 inhalation of 7 per cent carbon dioxide tends to 

 double the cerebral circulation (56), while hyper- 

 ventilation produces a marked decrease (54) 



The elleets of oxygen are quite the reverse of those 

 of carbon dioxide. High concentrations of oxygen 

 exert a mild constricting effect and low oxygen con- 

 centrations dilate cerebral vessels, according to 

 studies in normal man (56) and in lower animals. 

 Exposure to several atmospheres of Oxygen produces 

 a greater decrease in cerebral blood How on the basis 

 of a more marked constriction (62) The studies 

 with carbon dioxide and oxygen suggest thai these 

 metabolic gases may be the important regulators of 

 cerebral circulation, maintaining an optimal local 



Circulation to meet local metabolic needs. This prob- 

 lem was dealt with in greater detail in the preceding 

 chapter by Schmidt 



