Original communication| Volume 16, ISSUE 3, P381-398, September 1944

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Acute physiologic responses in experimental head injury with special reference to the mechanism of death soon after trauma

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      • 1.
        1. The acute physiologic responses to injury may be minimal, moderate, or profound. In moderate and profound injuries usually there is a sudden increase in blood pressure with respiratory loss, unconsciousness (no reaction to painful stimuli), loss of palpebral and corneal reflexes, and frequent generalized rigidity followed by limpness. In moderate injuries the animal survived or died, in the group with profound injuries death was almost invariable.
      • 2.
        2. Under morphine analgesia the ability to respond to pain was considered an adequate sign of consciousness. In some animals vasoconstrictor stimulation and respiratory pause coexisted with normal response to pain.
      • 3.
        3. Loss of corneal reflexes represents a more profound response to injury than unconsciousness. Some animals were frequently observed to be unconscious with active palpebral and corneal reflexes.
      • 4.
        4. The acute changes in blood pressure, respirations, and reflexes following trauma to the head are due to stimulation or paralysis of medullary centers.
      • 5.
        5. The acute hypertension following trauma is caused by peripheral vasoconstriction as shown in experiments on adrenalectomized and yohimbinized animals and those in which the lower cervical spinal cord was sectioned. A drop in blood pressure following trauma was seen in some experiments. Dissolution of the vasomotor center by .22 rifle caused failure without an initial presser response.
      • 6.
        6. Respiratory paralysis is a common manifestation in severely injured dogs. However, in some with presser response there was little or no change in respirations and in others with respiratory paralysis there was little or no change in vasomotor activity. Increase in respiratory rhythm associated with other evidences of medullary stimulation was possible but infrequent.
      • 7.
        7. Evidences of vagal paralysis were common in most of the moderately and severely injured animals. Vagal stimulation with bradycardia was seen in some moderately and severely injured dogs.
      • 8.
        8. The depressor centers mediated through the vagoglossopharyngeal complex may have been stimulated to cause a drop in blood pressure in some experiments but it is felt that the vasomotor failure is mainly due to a failure of the vasomotor center in the medulla.
      • 9.
        9. Electroencephalographic studies of the cortex with simultaneously observed evidences of medullary paralysis reveal that the cortical activity may be unhampered even though the medulla is badly damaged and vice versa.
      • 10.
        10. In the experimental animal, death from acute trauma was due to paralysis of the vasomotor center.
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