Abstract
The mechanism of increased susceptibility of the traumatized brain to hypoxemia (HYP) was investigated by measuring the local cortical blood flow (LCBF) by hydrogen clearance. Following pentobarbital anesthesia and head injury (HI) using a repetitive acceleration/deceleration injury, five surviving cats were ventilated to maintain arterial PCO 2 (28.3 ± 1.8 Torr, mean ± SEM). Three control (C) animals received no head injury. LCBF (ml/min/100 g) measurements at two cortical locations were made between 30 and 60 min postinjury, at 10 min and 40 min of HYP ( P aO 2 = 29.5 ± 2.6 Torr), and at 30-min intervals for 4.5 hr after HYP. Before HYP, LCBF was not different in cortical areas in C (84 ± 12 ml/min/100 g) and HI (81 ± 17 ml/min/100 g) animals. In C animals LCBF increased to 141 ± 10 after 10 min of HYP and remained elevated at 40 min ( P < 0.05). Ten minutes post-HYP, LCBF fell to 56 ± 8 ml/min/100 g. Hypoxemia did not increase LCBF significantly in HI animals (87 ± 17 ml/min/100 g). Post-HYP, LCBF in HI animals remained unchanged. In 78% of HI LCBF measurements, clearances following a brief H 2 inhalation were faster than clearances following tissue equilibration with H 2. This may be due to nonhomogeneous tissue perfusion in HI animals. In conclusion, after head injury there may be an attenuated microvascular blood flow response to hypoxemia and flow inhomogeneities which will accentuate tissue hypoxia.
Published Version
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