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.
Changes in cerebrospinal fluid formation rate (VF) with hypocapnia were measured by the ventriculocisternal perfusion technique in 24 rhesus monkeys anesthetized with nitrous oxide. In addition cerebral blood flow (CBF) was measured by the hydrogen clearence methods, Vf in control animals declined at a mean rate of 2.3 mul/min each hour during the last 4.5 h of a 7-h perfusion although variables known to effect Vf remained stable. Three hours after perfusion began, Vf of normocapnic controls was 41.4 mul/min +/- 5.4; CBF, 59P ML/100 G PER MIN. When Pco(2) was reduced to half of control, Vf fell to 35.6 mul/min +/- 6.3 and CBF fell by 27%. When Pco(2) was doubled, Vf fell to 33.1 mul/min +/- 5.3 and CBF increased threefold. The difference in Vf id significant only for the hypercapnic group (p=0.01). When animals were used as their own controls, three were no significant differences in Vf with hypercapnia compared to normocapnia. These results indicated that in the monkey variations of Pco(2) within broad physiologic limits, which are sufficient to cause large changes in CBF, have little effect of Vf.
The authors studied the effect of high cervical cord section on the phenomenon of autoregulation in the rhesus monkey with the hydrogen clearance method to measure focal spinal cord blood flow (SCBF). Laminectomies were performed at T7-11 and C1-2. The spinal cord was completely severed at C1-2. Under normocapnic conditions, SCBF was then measured in the thoracic spinal cord over a wide range of blood pressures (MAP). The MAP was either lowered by bleeding or raised by the intravenous infusion of angiotensin. Autoregulation was found to be intact between 50 and 125 mm Hg, following a pattern similar to the one observed in the intact animal.
The hydrogen clearance method was used to measure total and focal cerebral blood flow (CBF) in the monkey before and for 5 hours after a simulated subarachnoid hemorrhage (SAH). Some monkeys also received 0.2 to 1.0 mg/kg phentolamine intracisternally 3 hours after SAH. Results show that SAH did not change cerebrovascular resistance, but as cerebral perfusion pressure decreased, CBF fell transiently. Phentolamine injected intracisternally 3 hours after SAH produced a significant fall in arterial blood pressure; cerebrovascular resistance did not change but CBF decreased significantly. These data indicate that intracisternal phentolamine cannot be considered potentially useful to treat ischemic encephalopathy after SAH.
The hydrogen clearance method was used to measure local and total cerebral blood flow (CBF) in the rhesus monkey before and for five hours after a simulated subarachnoid hemorrhage (SAH). CBF remained stable after SAH unless SAH was associated with a fall in cerebral perfusion pressure. In addition, cerebrovascular resistance did not increase after SAH. These results suggest that vasoactive agents in fresh whole blood, and the arterial spasm they produce when added to cerebrospinal fluid (CSF), play only a limited role in the pathogenesis of ischemic encephalopathy that follows an SAH.
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