Intracranial volume-pressure relationships during experimental brain compression in primates: 3. Effect of mannitol and hyperventilation

Abstract

SY N OP SI S In 10 anaesthetized and ventilated baboons a steady level of raised intracranial pressure was achieved by graduated inflation of an extradural balloon. Measurements were made of the ventricular fluid pressure, and of the change in this pressure after injection of 0 05 ml into the ventricle, the volume-pressure response. This response was studied at normocapnia and at hypocapnia (induced by hyperventilation), and before and after the intravenous administration of mannitol under normocapnic and hypercapnic conditions. During hypocapnia, ventricular fluid pressure and the volume-pressure response were reduced equally. Mannitol, however, caused a greater reduction in the volume-pressure response than in ventricular fluid pressure. The intravenous administration of mannitol therefore produces a beneficial effect on intracranial capacitance which is greater than observation of intracranial pressure alone indicates.In a previous experimental study it was established that a measure of the reserve capacity of the intracranial contents to compensate for volume addition to the cranium may be obtained by observing the response of the ventricular fluid pressure (VFP) to an induced change in the volume of the lateral ventricle. During continuous brain compression in baboons this measurement, termed the volume-pressure response (VPR), was found to correlate closely with VFP (before induced ventricular volume change) and with balloon volume (Leech and Miller, 1974a). Measurement of the VPR also provides useful information in patients during continuous monitoring of intracranial pressure .In the present study, measurements of VFP and VPR were used to explore the effect on intracranial volume-pressure relationships of two methods in clinical use for the reduction of raised intracranial pressure, hypertonic mannitol solution, and induced hypocapnia. Intravenous mannitol was administered not only at normocapnia but also at hypercapnia, and the results compared with those observed during hypocapnia, produced by imposed hyperventilation. EXPERIMENTAL METHODSTen anaesthetized ventilated baboons (body weight 8 to 11 5 kg) were studied. The anaesthesia, surgical preparation, and methods of recording systemic arterial pressure (SAP) and VFP have been described previously (Leech and Miller, 1974a). The VPR was calculated from the change in mean VFP after an injection into the lateral ventricle of 0-05 ml normal saline over one second. Cerebral blood flow (CBF) was measured from the right cerebral hemisphere by the intracarotid 133Xe technique (Rowan et al., 1970) over a 10 minute period of isotope clearance. Arterial blood gases were checked throughout the study with a direct reading electrode system.

Intracranial volume-pressure relationships during experimental brain compression in primates: 2. Effect of induced changes in systemic arterial pressure and cerebral blood flow

“…This interesting phenomenon has been noted previously by one of the authors. Lofgren (1974) has also shown that increases in arterial carbon dioxide tension, which produce cerebral arteriolar dilatation, do not affect the elastance, and this has been confirmed by the present authors (Leech and Miller, 1974b) using the different method of measuring elastance already described. These findings tend to argue against the theory that arterial pressure increases elastance during venous compression because of a rise in mean intravascular pressure, since CO2 will also increase mean intravascular pressure during venous compression by reducing arterial/ arteriolar resistance and permitting the head of pressure to be transferred downstream.…”

“…This interesting phenomenon has been noted previously by one of the authors. Lofgren (1974) has also shown that increases in arterial carbon dioxide tension, which produce cerebral arteriolar dilatation, do not affect the elastance, and this has been confirmed by the present authors (Leech and Miller, 1974b) In any patient with raised intracranial pressure, the occurrence of arterial hypertension, whether spontaneous or therapeutically induced, will lead to a pronounced increase in brain elastance. This implies that any increase in intracranial volume will then result in a large rise in intracranial pressure.…”

Cerebral Autoregulation in Unconscious Patients with Brain Injury

“…I n brain tumours a restoration of the autoregulation after steroids has been described ( REULEN et al 1972 . In postischaemic periods and during ICP increase, arterial hypertension will have a deleterious effect, and may provoke brain oedema (LEECH & MILLER 1974, FENSKE et al 1975.…”

Intracranial pressure pulse amplitude during changes in head elevation: a new parameter for determining optimum cerebral perfusion pressure?

“…The importance of the intracranial volume-pressure relationship for understanding the pathophysiology of raised ICP and ICPPA has been demonstrated in several studies [4,27,28,30,32,43,49,51].…”