Effects of mannitol on cerebral blood flow, blood pressure, blood viscosity, hematocrit, sodium, and potassium.

In our miniature swine model of brain retraction ischemia under conditions simulating the neurosurgical operating room, we studied the effects of bolus mannitol (2 g/kg) administration on cerebral blood flow, blood pressure, blood viscosity, hematocrit, sodium, and potassium serially for 4 hours following administration, at which time a second bolus was administered. Both viscosity and hematocrit were significantly decreased transiently following both the first and second boluses. Sodium was decreased for 30 minutes following the first bolus, 15 minutes following the second bolus, and increased at 150 minutes and later following the second bolus. There was a mild decrease in blood pressure and a mild increase in cerebral blood flow following mannitol, but little difference between the first hour following a bolus (when the viscosity and hematocrit were decreased) and hours 2-4 (when they were near baseline). Mannitol's effects on blood pressure and cerebral blood flow probably depend on factors in addition to its effects on blood viscosity and hematocrit. The results are discussed in light of previous findings that bolus mannitol administration may improve cerebral blood flow in ischemia, but does not appear to benefit the preservation of brain electrical activity.

Retraction brain ischaemia: cerebral blood flow, evoked potentials, hypotension and hyperventilation in a new animal model.

Undue intraoperative brain retraction can cause significant neurosurgical morbidity. By combining brain retractor blade pressure measurement with monitoring of brain electrical activity, one can determine the limits of safe brain retraction and then test systematically various therapeutic interventions. Cortical evoked potential (EP) mapping and laser-Doppler cerebral blood flow (CBF) measurement were undertaken during brain retraction in the miniature swine (Sus scrofa). Forelimb somatosensory EP recording during subtemporal retraction simulated the pterional and subtemporal approaches, respectively. Retraction pressure of 30 mmHg usually resulted in a 50% decrement in EP amplitude after 10 to 20 minutes in normotensive, normocapnic adult animals. Recovery of EP occurred within 5 to 10 minutes of retraction release. The effects of animal age, induced hypotension (nitroprusside, MAP approximately 40), and induced hypocapnia (hyperventilation, PaCO2 approximately 28) on EP preservation during retraction were then investigated, with data reported here from 23 animals (8 to 35 kg). By Spearman rank correlation coefficients, early loss of EP was associated with the following: lower MAP (p approximately 0.0001), lower CBF (p approximately 0.0005), lower PaCO2 (p less than 0.001), and older age (p approximately 0.01). These results indicate (1) retractors should be relaxed every 10-15 minutes whenever possible (for at least 5 minutes), and (2) hypotension, in particular, but also hypocapnia (hyperventilation) should not be used indiscriminately. Details of this new model of retraction ischaemia are presented.

Retraction brain ischaemia: mannitol plus nimodipine preserves both cerebral blood flow and evoked potentials during normoventilation and hyperventilation.

In our miniature swine model simulating operating room brain retraction, we investigated the effects of mannitol plus nimodipine on cerebral blood flow (CBF) and evoked potentials (EP) ipsilateral and contralateral to retraction, in comparison with either agent alone, during both normoventilation and hyperventilation. We here report results in 27 animals with intravenous mannitol (2 g kg-1 over 15 min) and/or nimodipine (1 microgram kg-1 min-1 constant infusion). Mannitol plus nimodipine was superior both to controls and to either mannitol alone or nimodipine alone in preserving EP amplitude ipsilateral to retraction during both normoventilation and hyperventilation. Mannitol alone was effective in normoventilation at preserving EP, while nimodipine alone was effective in hyperventilation. No significant asymmetries in CBF or EP were seen with mannitol plus nimodipine in either normoventilation or hyperventilation. By five minutes postretraction CBF had returned to preretraction values for all groups, and EP amplitude had returned also except for hyperventilated controls. In this model of brain retraction, mannitol plus nimodipine is superior to either agent alone in maintaining both CBF and EP when normoventilation and hyperventilation are employed. The results are discussed in terms of the possible mechanisms for the different and complementary effects of mannitol and nimodipine.