The configuration of the intracranial pressure (ICP) pulse wave represents a complex sum of various components. Amplitude variations of an isolated component might reflect changes in a specific intracranial structure. Fifteen awake patients suffering from hydrocephalus, benign intracranial hypertension, or head injury underwent ICP monitoring through a ventricular catheter and were subjected to three standardized maneuvers to alter the intracranial dynamics: head elevation, voluntary hyperventilation, and cerebrospinal fluid (CSF) withdrawal. A 12 degrees head elevation and fractionated CSF withdrawal caused a mild ICP drop and a proportionate amplitude reduction of all the wave components. Voluntary hyperventilation caused a comparable fall in ICP, and a disproportionate reduction in the amplitude of the wave components, especially the P2 component. It is postulated that the decrease in amplitude of the P2 component reflects the reduction of the cerebral bulk caused by hyperventilation. Head elevation and CSF withdrawal caused a decrease of global ICP but no specific changes in any intracranial structure, and consequently the configuration of the pulse wave remained unchanged. The establishment of relationships between anatomical substrate and particular wave components is promising since potentially it could be useful for monitoring conditions such as vasoparalysis, impaired cerebrovascular reactivity, and cerebral edema.

The effect on the cerebral blood flow (CBF) (27:1-6,1972)

The upper limit of autoregulation of cerebral blood flow was studied in ten young baboons. Blood pressure was increased by infusing angiotensin, and cerebral blood flow was measured by the intracarotid 133 xenon injection method. Autoregulation was maintained until blood pressure was 30-40% above resting values. At this blood pressure level, cerebrovascular resistance reached a maximum. Any additional increase in blood pressure resulted in an increase in cerebral blood flow and a decrease in cerebrovascular resistance; this situation is designated the "breakthrough of autoregulation." In four baboons subjected to unilateral sympathetic denervation, autoregulation of cerebral blood flow was studied bilaterally; no difference in the upper limit of autoregulation was found between the intact and the sympathectomized hemisphere. The breakthrough of autoregulation supposedly plays an important role in the pathogenesis of acute hypertensive encephalopathy. The old concept of hypertensive cerebral vasospasm has been revised in recent years, and it is now generally recognized that acute hypertensive encephalopathy is caused by focal overdistention of brain arterioles with lesions of the blood-brain barrier. However, whether this condition is associated with a high cerebral blood flow in the clinical syndrome has not been investigated. KEY WORDSinduced hypertension breakthrough of autoregulation hypertensive encephalopathy cerebrovascular resistance angiotensin 133 xenon clearance• When blood pressure rises, cerebral blood flow is held constant by autoregulatory constriction of the cerebral resistance vessels. Some recent communications have described the existence of an upper limit of autoregulation. When blood pressure rises beyond this limit, autoregulation is exhausted; a forced arteriolar dilation and an increase in cerebral blood flow occur. This situation is called the "breakthrough of autoregulation" (l) and has been observed in hypercapnic dogs (2), in man by the arteriovenous oxygen difference method (3), and, in a limited study, in man by the intracarotid criticism because of the unphysiological experimental conditions (2), the use of an indirect method for assessment of cerebral blood flow (3), and the limited number of experiments performed (4). The present study was undertaken to obtain conclusive evidence on the upper limit of autoregulation. Normocapnic baboons were used, and cerebral blood flow was measured by the intracarotid 133 Xe injection method. The involvement of sympathetic nerves in the regulation of cerebral blood flow during acutely induced hypertension was also evaluated. MethodsThe study was carried out in ten young adult baboons {Papio cynocephalus or Papio anubis) weighing 10-14 kg. Three of the baboons were studied 2 weeks after a unilateral cervical sympathectomy, and one baboon was studied immediately after an acute cervical sympathetic block. The baboons were anesthetized with phencyclidine (12 mg, im) and sodium thiopental (7.5 mg/kg, iv). They were intubated and connected to ...