The Clinical Significance of the Experimental Results
H. Cushing 141 first observed that an increase in ICP up to a certain level can result in a concomitant elevation of blood pressure. This event is generally known as the “Cushing reflex” or “Cushing response” and is interpreted as a central regulatory mechanism 286, 183, 178 which maintains adequate cerebral circulation by elevating blood pressure to a certain level above ICP. Johnston et al. demonstrated this effect convincingly 169 with an experiment in baboons: ICP was artificially increased by infusion of fluid into the cisterna magna. At ICP levels between 50 and 100 mm Hg, MABP rose an average of 64%, ranging from 28% to 91% in eight baboons. This hypertension ran parallel with marked increases in CBF (measurement with the xenon-clearance technique), ranging from 26% to 85%. This response of hypertension and high perfusion occurred in all animals except one at ICP levels below that of control MABP and accompanied by failure of autoregulation. With a further increase in ICP, CBF decreased as a linear function of cerebral perfusion pressure. The authors also confirmed an ICP of 50 mm Hg as a critical level, below which CBF remains normal. The occurrence of the Cushing response has recently been considered to depend on sympathico-adrenal discharge at an ICP level around mean or even systolic blood pressure 77.
KeywordsBrain Edema Sodium Nitroprusside Carotid Stenosis Severe Head Injury Neurosurgical Patient
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