Focal blood flow was measured in the lateral funiculus and center of the spinal cord in the rhesus monkey both before and after a 600 gm-cm injury at T-10. Measurements made by the hydrogen clearance technique showed that blood flow in the lateral funiculus more than doubled within 4 hours after injury, returned to normal by 8 hours, and remained in the normal range for 24 hours. At no time was a hypoperfusion in the lateral funiculus present. Blood flow in the center of the spinal cord, at the level of the lesion, began to fall within 1 hour following injury and continued to fall for 4 hours. These data challenge the notion that spreading ischemia of the white matter is an important factor in the pathophysiology of experimental spinal cord injury.

The response of SCBF to changes in pACO2 was tested in Rhesus monkeys under normotensive conditions. A sigmoid shaped response was demonstrated. At a pACO2 of 10 to 50 mm. Hg, SCBF remained constant and in the normal range. As the pACO2 was raised from 50 to 90 mm. Hg, SCBF increased. Further increases in the pACO2 above 90 mm. Hg failed to effect further changes in SCBF. We conclude from these data that SCBF is somewhat less responsive than CBF to changes in pACO2. Next, the effect of changes in MAP on SCBF was studied under normocapnic conditions. SCBF remained constant and in the normal range with an MAP of 50 to 135 mm. Hg. Above 135 mm. Hg, SCBF rose with further increases in MAP. With decreases in MAP below 50 mm. Hg, SCBF fell passively. It is our conclusion that autoregulation exists in the lateral white matter of the spinal cord and follows a pattern similar to that suggested for the cerebrum.

The authors used the hydrogen clearance method to measure focal spinal cord blood flow (SCBF) in the rhesus monkey over a wide range of mean arterial blood pressures (MAP) in an attempt to test the hypothesis of autoregulation. The MAP was either lowered by bleeding or raised by the intravenous infusion of norepinephrine or angiotensin. The SCBF remained constant and in the normal range with an MAP of 50 to 135 mm Hg, indicating the presence of autoregulation. Below 50 mm Hg, SCBF fell passively with further decreases in MAP. At MAP values above 135 mm Hg, vasodilatation occurred which resulted in a breakthrough of autoregulation and marked increases in SCBF with further increases in the MAP.

S U M M A R Y Ventriculocisternal perfusion is regarded as a precise method of measuring the rate of formation of cerebrospinal fluid (CSF) but it possesses inherent potential sources of error. Using the technique to measure CSF formation rate in the rhesus monkey, we have observed rate changes when none were expected. Most puzzling has been the steady decline of CSF formation rate at 4%/0 each hour during the final five hours of a seven hour perfusion although variables known to affect CSF formation remained stable. In addition, alterations in rate caused by artefacts were observed in experiments in which craniospinal blood volume was changed by sudden changes of either PCO2 or central venous pressure. Mobilisation or sequestration of incompletely equilibrated CSF is believed responsible. In other experiments, a small increase of intracranial pressure produced by increasing outflow resistance was quickly followed by an apparent reduction of CSF formation. We have concluded that to assess accurately the effect a variable has on the rate of CSF formation, one must control perfusion time and craniospinal blood volume as well as intracranial pressure.

Simple hydrogen-sensitive polarographical electrodes of thin platinum wire were inserted into the torcular Herophili of Rhesus monkeys. Hydrogen was administered by inhalation for ten minutes, after which the hydrogen clearance was recorded from torcular blood. At a Paco 2 of 32 mm Hg (SD ± 2.3), flow in the fast flow compartment was 102 ml/100 gm per minute (SD ± 19.1), and flow in the slow flow compartment was 28 ml/100 gm per minute (SD ± 5.8). Mean total cerebral blood flow was 52 ml/100 gm per minute (SD ± 10.5). Coefficient of variation was less than 10%. Our experience suggests that one may reliably measure average total cerebral blood flow in the experimental setting by following the clearance of hydrogen from torcular blood. The method is relatively simple, inexpensive and radiation-free. It can be easily combined with the standard hydrogen clearance technique for measuring local tissue blood flow, thereby permitting the simultaneous recording of both local and total brain blood flow.