Brain parenchyma PO2, PCO2, and pH during and after hypoxic, ischemic brain insult in dogs.

OBJECTIVES: 1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult.
DESIGN: Prospective, controlled, animal study in an acute experimental preparation.
SETTING: Physiology laboratory in a university medical school.
SUBJECTS: Fourteen mongrel dogs (20 to 35 kg), anesthetized, room-air ventilated.
INTERVENTIONS: Anesthesia was induced with thiopental and maintained after intubation using 1% to 1.5% halothane in room air (FiO2 0.21). Mechanical ventilation was established to maintain end-tidal PCO2 approximately 35 torr (-4.7 kPa). Intravenous, femoral artery, and pulmonary artery catheters were placed. The common carotid arteries were surgically exposed, and ultrasonic blood flow probes were applied. A calibrated intracranial pressure probe was placed through a right-side transcranial bolt, and a calibrated intracranial chemistry probe with optical sensors for PO2, PCO2, and pH was placed through a left-side bolt into brain parenchyma. Brain insult was induced in the experimental group (n = 6) by hypoxia (FiO2 0.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arterial pressure [MAP] approximately 40 mm Hg produced with isoflurane approximately 4%). After 45 mins, carotid artery occlusion was released, FiO2 was reset to 0.21, and anesthetic was returned to halothane (approximately 1.25%). The control group (n = 5) had the same surgical preparation and sequence of anesthetic agent exposure but no brain insult.
MEASUREMENTS AND MAIN RESULTS: Monitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored at 1-min intervals, and intracranial pressure, MAP, arterial hemoglobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for which data were collected at 15-min intervals for 7 hrs. Arterial and mixed venous blood gas analyses were done at approximately 1-hr intervals. Baseline data agreed closely with other published results: brain parenchyma PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09. Postcalibration data were accurate, indicating stability and durability over several hours. In six experiments, during the brain insult, brain parenchyma PO2 decreased to 16 +/- 2 torr (2.1 +/- 0.3 kPa), brain parenchyma PCO2 increased to 105 +/- 44 torr (14 +/- 5.9 kPa) (p < .05), and brain parenchyma pH decreased to 6.75 +/- 0.08 (p < .05). Intracranial pressure (ICP) remained nearly constant (baseline 16 +/- 6 to 14 +/- 5 mm Hg at the end of the brain insult). Cerebral perfusion pressure (CPP = MAP - ICP) decreased (baseline 95 +/- 15 to 28 +/- 8 mm Hg; p < .05). On release of brain insult stresses, ICP increased to 30 +/- 9 mm Hg and CPP increased to 71 +/- 19 mm Hg (p < .05). A biphasic recovery was observed for brain parenchyma pH, which had the slowest recovery of the monitored variables. On average, brain parenchyma pH gradually returned toward baseline, and was no longer significantly different from baseline 3 hrs after release of insult stresses. Brain parenchyma PCO2 continued to decrease rapidly after brain insult and then remained approximately 52 +/- 10 torr (approximately 6.9 +/- 1.3 kPa) (p < .05). Brain parenchyma PO2 increased from a minimum at the end of brain insult to a maximum of 43 +/- 17 torr (5.7 +/- 2.3 kPa) within 1.25 hrs (p < .05), and then gradually decreased to approximately 35 +/- 10 torr (approximately 4.7 +/- 1.3 kPa). Cerebral perfusion pressure gradually decreased as ICP increased 3 to 5 hrs after insult.
CONCLUSIONS: Intracranial chemistry probes with optical sensors demonstrated stable, reproducible monitoring of brain parenchyma PO2, PCO2, and pH in dogs for periods lasting > 8 hrs. Significant changes in brain p