SUMMARY Continued expansion of an artificial space-occupying lesion produced further increases in mean supratentorial and infratentorial pressures associated with increases in mean arterial pressure, heart rate, and systemic vascular resistance-the 'Cushing' or systemic hypertensive response. These primary changes resulted in an increase in transtentorial pressure gradient and a decrease in arrhythmia index. Immediately before the onset of the systemic hypertensive response, supratentorial perfusion pressure was low, and the period of systemic hypertension did not appear to produce any worthwhile improvement in the perfusion pressure or in the blood flow in the supratentorial compartment. The studies demonstrated also that the systemic hypertensive response was a pre-terminal event and was followed rapidly by circulatory failure.Since the beginning of the nineteenth century, increased intracranial pressure and the mechanisms by which it acted have been the subjects of many investigations both in the experimental animal and in the clinical situation. As early as 1811, Ravina studied the effects of increased intracranial pressure after inserting glass windows in the skull. A few years later, Astley Cooper (1824) found that, in animals, mechanical pressure against the surface of the brain would produce a decrease in heart rate. In 1880, von Bergmann was able to induce a decrease in pulse rate and depression of respiration by increasing the intracranial pressure. In addition, he showed that when the intracranial pressure equalled the systolic arterial pressure in the carotid artery, death would follow. Since the observations of Kocher (1901) and Cushing (1901),

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SUMMARY Disadvantages associated with the use of ventricular catheters for the prolonged measurement of intracranial pressure have resulted in the search for an alternative technique. Measurement of pressure from the extradural space is one such possibility, but widespread acceptance of this procedure has been limited by the technical difficulties associated with this measurement and lack of information on the relationship between cerebrospinal fluid and extradural pressures. A study to investigate this relationship and to develop a simple and effective technique for measuring extradural pressure is described.In certain patients with head injuries and intracranial space-occupying lesions, acute rises in intracranial pressure producing brain shift or impairment of the cerebral circulation-with subsequent secondary brain damage-may occur before changes in vital signs are recognized. Furthermore, the reduction of intracranial pressure by means of one of the several methods currently available is too often unpredictable. For these reasons patient management may be greatly assisted, and more readily programmed, if intracranial pressure is directly monitored (Lundberg, Troupp, and Lorin, 1965;Johnston, Johnston, and Jennett, 1970 The aims of this study were: (1) to explore the relationship between extradural pressure, supratentorial subarachnoid pressure and ventricular pressure; (2) to assess the use of latex balloons as pressure-sensing devices in the extradural and subarachnoid spaces; (3) to evaluate a metal capsule, to be described, for clinical use in measuring extradural pressure over prolonged periods with minimal discomfort to the patient. METHODSANIMAL STUDIES The experiments were carried out on 12 dogs, but two baboons were also studied because the dura mater in these primates is more like that in man, being only loosely attached to the skull. The dogs were intubated after induction with thiopentone sodium, and anaesthesia maintained with nitrous oxide, oxygen, and halothane. Artificial ventilation to normocarbia and normoxia was achieved with the aid of muscle relaxants. Body temperature was maintained at 370 C. The baboons were premedicated with phencyclidine 0 5-1 mg/kg 514

SUMMARY Hypotension to a mean blood pressure of 33 mmHg for periods of 70 to 187 minutes was induced by increasing the inspired halothane concentration in 11 baboons which were already anaesthetized with 0.500 halothane, nitrous oxide, and oxygen. During hypotension, cerebral blood flow, measured by Xenon clearance and by a carotid electromagnetic flowmeter, decreased by more than half, and sagittal sinus oxygen saturation was 46%. Cerebral oxygen uptake fell from 5*15 to 3-56 ml./100 g/min at this deeper level of halothane anaesthesia. Cerebral hyperaemia developed after hypotension in those animals which regained a mean blood pressure greater than 70 mmHg. Acidbase measurements on CSF from the cisterna magna revealed no metabolic acidosis during or after hypotension. In all four animals with intact autoregulation before hypotension, this was absent or impaired afterwards.Controlled hypotension is used to diminish bleeding and to facilitate surgery. There is, however, a considerable disagreement about the safety of the technique; for example, Mayrhofer (1971) has written that: 'Induced hypotension, using ganglion-blocking drugs, should have been abandoned long ago as it is an unsafe and potentially dangerous technique', while Enderby (1972) has replied: 'We are today using this technique routinely and, moreover, have been doing so for more than 20 years'. When such divergent opinions are expressed, further investigation is indicated, and the present study was designed to elucidate the effect of controlled hypotension on cerebral blood flow, cerebral metabolism, and acid-base balance. Since it has been suggested (Nilsson and Siesjo, 1971) that hypotension with deep halothane anaesthesia may be safer than with other methods, because of the associated reduction in cerebral oxygen demand, it was decided to produce hypotension by this means in experimental animals. METHODSEleven baboons were premedicated with phencyclidine (0-8-1-0 mg/kg) and anaesthesia was induced and maintained with halothane, nitrous oxide, and 898 oxygen. After intramuscular injection of suxamethonium (50 mg) an endotracheal tube was inserted and the animals were artificially ventilated by a Palmer pump. Muscle relaxation was maintained by injecting pancuronium (I mg) intramuscularly at half-hourly intervals. End-tidal CO2 was monitored by an infrared gas analyser and ventilation was adjusted to maintain normocapnia. Endtidal halothane was measured intermittently by an ultraviolet halothane meter. The inspired oxygen was adjusted so that PaO2 remained above 100 mmHg. The temperature of the animal was kept at 370 C by automatically controlled heating lamps.Not all measurements were made on all animals and the animals were divided into three experimental groups as indicated in Table 1