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To investigate the role of cerebral hypoxia as a causative factor in the alteration of the qEEG during hyperventilation, qEEG changes caused by progressive hypocapnia were compared with qEEG changes due to progressive normobaric hypoxia in two parallel groups of 12 and 10 healthy male subjects (age 20-27 years), respectively. In the first group, qEEG records were obtained before and during hyperventilation to pCO2 levels of 4.0, 3.0 and 2.0 kPa. In the second group, the qEEG samples were taken before and during hypoxia with hemoglobin oxygen saturations of 80, 70 and 60%. In both groups, blood flow velocity in the middle cerebral artery was also recorded. Hyperventilation caused an exponential increase in slow activity and a decrease in alpha power. No shift in the alpha mean frequency and alpha peak frequency was observed, except with the pCO2 level of 4.0 kPa, which caused an increase in both variables. Hypoxia with a hemoglobin oxygen saturation of 60% caused a much less pronounced increase in slow activity. No change in total power in the alpha band was found, but both the alpha peak frequency and alpha mean frequency decreased. Lesser degrees of hypoxia caused only minimal EEG changes. Blood flow velocity was decreased by hyperventilation but increased by hypoxia. It is concluded that the EEG changes observed during hyperventilation must mainly or totally be attributed to factors other than cerebral hypoxia.

This study tested the hypothesis that hypocapnia superimposed upon hypotension produces a further reduction in cerebral blood flow velocity (CBFV). In 12 newborn piglets, CBFV was measured continuously by Doppler ultrasound through an artificial fontanelle. Hypotension was induced by removing 30 ml/kg of blood. Increasing the ventilator rate reduced the average arterial carbon dioxide tension from 5.5 to 2.0 kPa. When mean arterial pressure (MAP) was held steady at 45 mm Hg or above, hypocapnia produced a substantial drop in CBFV but, in all the piglets with MAP below 38 mm Hg, hypocapnia failed to change CBFV by 10%. Hypocapnia produced an increase in lactate in sagittal sinus blood but cerebral venous hypoxanthine concentrations were not affected by hypocapnia. Hyperventilation (without haemorrhage) produced a significant drop in MAP, preventable by infusing colloid. Hypocapnia itself does not further reduce CBFV in the hypotensive piglet. However, the pressure effect of hyperventilation may significantly impair the cerebral circulation.

We noninvasively evaluated the effects of nicardipine on cerebral vascular responses to hypocapnia and blood flow velocity in the middle cerebral artery of 10 patients aged 17-60 (mean +/- SD 46.1 +/- 11.8) years. During fentanyl/diazepam/nitrous oxide anesthesia, mean blood flow velocity in the middle cerebral artery was measured and cerebral vascular reactivity to hypocapnia induced by hyperventilation was assessed before and during the administration of nicardipine. Mean blood flow velocity was measured using transcranial Doppler ultrasonography, and the cerebral vascular reactivity was expressed as the percentage change in mean blood flow velocity per unit change in end-tidal PCO2. During the administration of 5.1 +/- 1.3 micrograms/kg/min nicardipine, which caused a 26% reduction in mean arterial blood pressure, mean blood flow velocity increased significantly from 57.2 +/- 19.2 to 64.2 +/- 21.6 cm/sec (p less than 0.01, paired t test), whereas cerebral vascular reactivity showed no significant change (4.0 +/- 1.2% and 4.9 +/- 2.5%, respectively). In conclusion, during fentanyl/diazepam/nitrous oxide anesthesia in patients, cerebral vascular reactivity to hypocapnia was maintained and nicardipine-induced hypotension resulted in increased middle cerebral artery blood flow velocity with maintenance of carbon dioxide reactivity to hypocapnia.

Time course variations in the ventilation and gas exchange functions of the lungs, gas composition and acid-base equilibrium of blood were investigated in 22 male test subjects, aged 27-49 years, who were kept in the head-down position (-8 degrees) and rocked in parallel swings. The subjects susceptible to motion sickness developed lung hyperventilation and concomitant alveolar-arterial hypocapnia and respiratory alkalosis which may potentiate a symptom-complex of vestibular disorders. To control hypocapnia, the subjects used a hypercapnic breathing mixture (4% CO2, 96% air). This eliminated the above changes in the gas composition and acid-base equilibrium of blood, and in 7 out of 10 subjects alleviated vestibular symptoms and elongated the time of motion tolerance. In addition, the prophylactic effect of hypercapnic exposure showed individual variations which seem to be associated with individual sensitivity of the respiratory center to hypercapnic stimulation.

The effect of hypocapnic alkalosis (HA) on nicardipine-induced cerebral vasodilatation was studied in 2 groups of patients undergoing stereotaxic brain biopsy under general anaesthesia. Arterial diameter (AD) was measured in 16 different locations on a carotid arteriogram (lateral view), and intracranial pressure (ICP) was recorded with an intraventricular catheter. At time T0, in normocapnia an arteriogram was performed in both groups. The first group (GI) was then studied in hypocapnia (T1) and following an injection of nicardipine (T2), while the second group (GII) was studied first after injection of nicardipine (T1) and then in hypocapnia (T2). Groups GI (n = 6; 44 y) and GII (n = 6; 46 y) were similar with regard to age, blood pressure, heart rate and PaO2 at all three phases of the study. HA caused a 9.5% decrease in AD (GI.T1) compared to baseline values, and a 15.2% decrease when preceded by injection of nicardipine (GII.T2). In the latter case the decrease was 3% in comparison with baseline. Nicardipine increased AD by 14.7% (GII.T1) and by 18.5% when preceded by HA (GI.T2), but the rise (7.3%) was not significant in comparison with the baselines value. The changes variations were similar whether the entire arterial trunk or only the supraclinoid region were studied. HA decreased ICP by 44% (GI.T1) and by 50% after nicardipine (GII.T2). Nicardipine did not cause an increase in ICP. Nicardipine and HA antagonise each others vasomotor effects, as previously shown in the baboon using nimodipine.

Nicotinamide adenine dinucleotide fluorescence, cortical reflectance, cortical blood flow, and electroencephalograms were recorded from squirrel monkey brains before, during, and after focal transient cerebral ischemia produced by the temporary clipping of the middle cerebral artery. After release of the occluding clip, the monkeys were followed through an N2-breathing cycle and then to death from anoxia. The effects of controlled variations in arterial carbon dioxide tensions (PaCO2) and mean arterial blood pressures (MABP) were investigated in normal and in ischemic brain. In normal brain, with preserved autoregulation, NADH fluorescence was constant through a wide range in Paco2, MABP, and cortical blood flow. In ischemic brain, NADH levels increased, correlated closely with decreased cortical blood flow and EEG abnormalities, and became dependent on MABP. Artifacts in fluorescent measurements were reduced by: monochromators for excitation, emission, and reflected light; low intensity vertical excitation energy and high sensitivity recording instrumentation; and a small avascular (123 microns) field.