160 QUARTERLY JOURNAL OF MEDICINE 



an extended clinical trial, the importance of data dealing with the efficiency 

 of the kidney under conditions of lowered blood-pressure is obvious — with 

 regard to the differentiation of cases in which reduction of high pressure may be 

 permissible or desirable or the reverse. Some results of the clinical use of the 

 hepatic extracts have been described by Macdonald (8), by Major (13), and 

 by Major and Stephenson (15). Major (14) reported that in two cases of hyper- 

 tension the excretion of guanidine was not diminished, but rather increased, during 

 a period (several days) of blood-pressure lowering by hepatic extracts. Gruber, 

 Shackelford, and Ecklund (4) found that, when high arterial pressure was lowered 

 by pheno-barbital, no harmful effect was produced on the excretion of phenol- 

 sulphonephthalein. 



The latter, however, is a foreign substance, and might be thrown out by the 

 kidney independently of any but very extensive changes in blood-pressure, so 

 that, while the above investigation agrees, so far as phenolsulphonephthalein is 

 concerned, with the findings of the present investigation as regards urea, the 

 evidence obtained in the former inquiry is not necessarily valid as an argument 

 against the compensatory theory. 



Possible Compensatory Mechanisms. 



It is evident that elevated blood-pressure might be a compensatory adjust- 

 ment in the way of driving more blood through some vital organ, e. g. brain, 

 heart-muscle, or kidney : such might be needed where there is inadequacy of 

 blood-flow depending on alteration in its vascular channels, arterial or capillary, 

 or when, even apai*t from such alteration, a higher capillary pressure and more 

 rapid blood-flow would be beneficial in enhancing the functioning of an organ — 

 deficient from structural or other causes. 



There is the familiar instance of the mechanism by which an interference 

 with the normal blood-supply to the head (e. g. cerebral compression, experimental 

 closure of the carotids) promptly calls forth a rise of aortic pressure with an 

 obviously compensatory significance through excitation of the vasomotor centre, 

 causing constriction in the splanchnic and other areas, and diminution of the 

 activity of the vagus centre leading to increased action of the cardiac pump. 

 The recent experimental work of Anrep and Starling (1) by cross-circulation 

 experiments shows the converse action of increased blood-pressure in the head in 

 depressing the vasomotor centre, in addition to the well-known influence of such 

 pressure in stimulating the vagus centre and slowing the heart. 



L. Hill (6) wrote in 1900, ' The vasomotor centre is not only excited reflexly, 

 but responds to every change in the circulation through the spinal bulb. A rise 

 of pressure in the cerebral arteries provokes a fall of aortic tension ; conversely, 

 a fall of pressure in the cerebral arteries provokes a rise. In other words, 

 cerebral anaemia, however produced, excites the centre and increases vascular 

 tone, while cerebral hyperaemia decreases vascular tone.' 



In cases of high blood-pressure Starling (17) attaches much importance 



