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Arthur I. Kobrine, Delbert E. Evans and Hugo V. Rizzoli

✓ Blood flow in the spinal cord was measured in a group of monkeys over a wide range of artificially varied blood pressures after the administration of propranolol, a beta adrenergic blocker. Spinal cord blood flow was found to be constant and in the normal range between a mean system arterial blood pressure of 50 to 150 mm Hg. From 150 to 180 mm Hg spinal cord blood flow decreased. There was no breakthrough of autoregulation, previously seen in the untreated animal. It is suggested, therefore, that the previously observed breakthrough of autoregulation is a beta adrenergic-mediated phenomenon.

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Arthur I. Kobrine, Delbert E. Evans and Hugo V. Rizzoli

✓ Spinal cord blood flow (SCBF) was measured over a wide range of artificially varied mean systemic arterial blood pressures (MAP) in a group of monkeys with alpha adrenergic receptors blocked by the intravenous administration of phenoxybenzamine (Dibenzyline). The SCBF was found to vary linearly with changes in MAP. Autoregulation appeared to have been abolished. These data are cited as evidence for a dominant role of the sympathetic nervous system in control of the spinal circulation.

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Arthur I. Kobrine, Delbert E. Evans and Hugo V. Rizzoli

✓ In this experiment, the effects of ischemia on neural conduction in the monkey spinal cord were studied. In six monkeys generalized ischemia of the spinal cord was created by bleeding the animals to a hypotensive level below the lower limits of autoregulation in the spinal cord. The progressive development of spinal cord ischemia was documented by blood-flow measurement using the hydrogen clearance method. Physiological integrity of the spinal cord was monitored and recorded by the spinal evoked response. The spinal evoked response did not disappear until at least 10 minutes of profound ischemia. At levels of ischemia 20% to 25% of normal blood flow, the spinal evoked response was unchanged. It is concluded that long-tract neural conduction in the spinal cord is relatively resistant to the effects of ischemia.

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Delbert E. Evans, Arthur I. Kobrine and Hugo V. Rizzoli

✓ This study was undertaken to determine the cardiovascular response to compression of the spinal cord and to determine the autonomic mechanisms involved. The electrocardiogram and arterial blood pressure were recorded in anesthetized monkeys during inflation of a balloon catheter in the epidural space of the mid-thoracic region. Acute spinal cord compression resulted in a wide variety of severe cardiac arrhythmias and acute hypertension. The arrhythmias were found to result from hyperactivity of both the sympathetic and parasympathetic divisions of the autonomic nervous system.

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Experimental acute balloon compression of the spinal cord

Factors affecting disappearance and return of the spinal evoked response

Arthur I. Kobrine, Delbert E. Evans and Hugo V. Rizzoli

✓ Acute balloon compression of the thoracic spinal cord for 15, 7, 5, 3, and 1 minute in monkeys caused immediate disappearance of the spinal evoked response and complete focal ischemia of the compressed segment in all animals. Only the animals in the 1-minute group, however, demonstrated return of the evoked response. These data, coupled with data from previous experiments of slow balloon compression of the spinal cord and spinal cord ischemia, suggest that the major pathological substrate for neural dysfunction after balloon compression of the spinal cord, be it acute or slow, is physical injury of the neural membrane, irrespective of blood flow changes. These findings also suggest that the ability of that membrane to recover is related to rapidity and length of time of compression. Focal changes in blood flow do not appear to be significant in this mechanism.

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Delbert E. Evans, Arthur I. Kobrine, David C. LeGrys and Mark E. Bradley

✓ To investigate possible approaches to the prevention and treatment of neural damage induced by air embolism and other forms of acute cerebral ischemia, a model was used in which cerebral air embolism was produced by infusion of air (0.4 ml) into a vertebral artery of chloralose-anesthetized cats. Neurological function was assessed by measuring cortical somatosensory evoked responses in a group of 10 untreated animals and in a group of eight animals pretreated with intravenous lidocaine (5 mg/kg). In the untreated group, the primary somatosensory amplitude was reduced to 28% ± 9% (mean ± standard error) of the value before air embolism, with a return to 60% ± 8% 1 hour and 73% ± 12% 2 hours after embolism. In the group pretreated with lidocaine, the primary somatosensory amplitude was reduced to 68% ± 9% of the value before air embolism, with a return to 92% ± 3% 1 hour and 97 ± 2% 2 hours after embolism. Pretreatment with lidocaine also greatly attenuated the acute hypertension and the increase in intracranial pressure following air embolism. These results demonstrate that pretreatment with intravenous lidocaine significantly reduces the neural decrement and increases the recovery of neural function after acute cerebral ischemia induced by air embolism.

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Arthur I. Kobrine, Delbert E. Evans, David C. LeGrys, Lyn J. Yaffe and Mark E. Bradley

✓ A series of experiments was conducted to study the effect of systemic intravenous administration of lidocaine on neurological recovery after acute experimental spinal cord injury in cats. The spinal cord was injured by the rapid inflation of an epidural balloon at T-6. The physiological integrity of the spinal cord ceased within 2 seconds in all animals, as demonstrated by acute disappearance of the somatosensory evoked response (SER). There was essentially no return of the SER in the five untreated animals when monitored for 4 hours post-injury. All of the pathological specimens from these animals revealed severe central cord hemorrhage. Intravenous lidocaine was begun 15 minutes after the injury in five animals. Three of these animals had significant return of the SER. The pathological specimens from the lidocaine-treated animals revealed either mild or moderate central cord hemorrhage. The results of this experiment suggest that systemic lidocaine administration has a significant beneficial effect in the treatment of acute spinal cord injury.

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Delbert E. Evans, William A. Alter III, Stanley A. Shatsky and E. Neal Gunby

✓ The cardiovascular events resulting from experimental head injury were studied to determine the incidence of cardiac arrhythmias and to define the autonomic mechanisms responsible for these changes. Electrocardiograms and arterial blood pressure were recorded in anesthetized monkeys before and after the animals were subjected to temporoparietal head impact. Cardiac arrhythmias and hypotension occurred immediately following impact in every animal studied. Various atrioventricular nodal and ventricular arrhythmias were seen. Cholinergic blockade was found to prevent arrhythmias induced by head injury whereas adrenergic blockade was found to be ineffective.

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