RESPIRATORY AND BLOOD PRESSURE RESPONSES TO STIMULATION OF PERIPHERAL AFFERENT NERVES.
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To study the acute effects of hyperbaric oxygen ventilation (HBO) on long-tract function following spinal cord trauma, the authors employed a technique for monitoring spinal cord evoked potentials (SCEP) as an objective measure of translesion neuronal conduction in cats subjected to transdural impact injuries of the spinal cord. Control animals subjected to injuries of a magnitude of 400 or 500 gm-cm occasionally demonstrated spontaneous return of translesion SCEP within 2 hours of injury when maintained by pentobarbital anesthesia and by ventilation with ambient room air at 1 atmosphere absolute pressure (1 ATA). Animals sustaining corresponding injuries but receiving immediate treatment with HBO at 2 ATA for a period of 3 hours following impact demonstrated variable responses to this treatment modality. Animals sustaining injuries of 400 gm-cm magnitude showed recovery of translesion SCEP in four of five cases, while animals sustaining injuries of 500 gm-cm magnitude responded to HBO treatment by recovery of SCEP no more frequently than did control animals. When the onset of HBO therapy was delayed by 2 hours following impact, there appeared to be no demonstrable protective effect on long-tract neuronal conduction mediated by HBO alone. The observations suggest that HBO treatments can mediate preservation of marginally injured neuronal elements of the spinal cord long tracts during the early phases of traumatic spinal cord injury. These protective effects may be based upon the reversal of focal tissue hypoxia, or by reduction of tissue edema. HBO treatment markedly diminished the protective effects of HBO on long-tract neuronal conduction following traumatic spinal cord injury.
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Experiments on nerves in situ and on isolated nerves provide no evidence that morphine interferes with impulse transmission in myelinated or nonmyelinated nerve fibres. The concentrations used in experiments on isolated nerves were 10- to 100-times as high as those required to depress transmission at autonomic nerve-effector cell junctions. Examination of the resting membrane potential, the action potential and the positive after-potential, the conduction velocity, the time courses of the recovery of the size of the action potential and of the excitability after a conditioning stimulus, the ability of the axons to sustain repetitive activity and the posttetanic hyperpolarization gave no indication that morphine affects either the mechanisms involved in the initiation of the propagated impulse or those leading to restoration of the resting state after activity. Analgesic drugs, such as pethidine and methadone which have a local anaesthetic action, may cause a reversible decrease in the size of the compound action potential and in the conduction velocity of A-B and C fibres.
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