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Leptomeningeal adhesion formation frequently complicates operations and diseases of the central nervous system. Chronic adhesive arachnoiditis may follow intraspinal surgery for disc, tumor, and closure of myelomeningocele, eventually producing pain and declining neurological status of the patient. Reoperation for scar removal is seldom successful as the arachnoidal adhesions reform. Poloxamer 407 (P407) has been shown to reduce postoperative peritoneal adhesion formation in rats and golden hamsters. In a rabbit model, we investigated the potential of P407 to prevent the production of arachnoidal adhesions and nerve root scarring following laminectomy and surgical meningeal injury. The lumbar spinal roots of 8 New Zealand white rabbits were surgically isolated under magnification. One root sleeve axilla was opened and immediately closed with 10-0 suture (control site) and a second root sleeve axilla was opened, P407 injected, and closed with 10-0 suture (treatment site). Five of 7 rabbits treated with P407 and followed for 7–42 days showed no arachnoidal adhesions at the level of the nerve root. Four New Zealand white rabbits had the lamina removed, and the dura over the spinal cord was opened at two sites separated by one to two lumbar segments. At one site P407 was inserted beneath the dura following durotomy, and the other site was opened in a similar fashion and immediately closed without the insertion of P407. There was a 50% reduction in leptomeningeal adhesion formation with the use of P407. P407 may be useful in neurosurgery for the prevention of arachnoidal adhesions.

The potential for hypothermia to prevent or ameliorate ischemic injury to the central nervous system is well known. To determine if a more prolonged period of metabolic suppression with blood substitution is possible, a method was developed to lower body temperature to near the freezing point. Eight adult mongrel dogs underwent closed-chest extracorporeal circulation with both external and internal body cooling. As they were cooled, progressive hemodilution was employed until complete exsanguination and blood substitution with an aqueous solution was accomplished. Continuous circulation and a core temperature at a mean of 1.7 degrees C were maintained from 2 1/2 to 3 hours. After rewarming to 20 degrees C, the animals were autotransfused and allowed to recover. Of the eight animals, two died due to technical factors related to cardiac defibrillation. Of the six surviving animals, five survived over a long period and one died on the 10th postoperative day with hepatorenal failure resulting from a presumed blood transfusion incompatability reaction. All six showed normal neurological function and kennel behavior, except one dog with mild weakness of a hindlimb. When the dogs were sacrificed 1 to 2 months postoperatively, all organs were histologically normal. Specifically, there was no gross or microscopic evidence of ischemic or hypoxic injury to any central nervous system structures. This pilot study demonstrates that it is possible to successfully achieve complete exsanguination, blood substitution, and ultraprofound body temperature, while continuous circulation of the blood substitute is maintained. With the capability of controlling and repeatedly performing washout of the extracellular environment and by reaching lower temperatures, it may be possible to attain greater cellular metabolic suppression. This perhaps will extend the allowable times for circulatory arrest procedures. In addition, "bloodless ischemia" may be beneficial in removing both blood substances and formed elements which may mediate organ ischemia. With replacement of blood at warm temperatures, coagulopathy is avoided. This preliminary evidence demonstrates potential in the combination of ultraprofound hypothermia and complete blood component substitution. However, further study is required to confirm the potential of achieving circulatory arrest of longer duration.

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