Cardiovascular response to experimental spinal cord compression

Abstract

✓ Anesthetized, and unanesthetized decerebrate, cats were used to study the arterial pressor response to spinal cord compression. To produce a cervical compression it was necessary that the cervical cord be functionally connected to the thoracic cord, pressor response by the reverse was not true. A pressor response above 200 mm Hg systolic was associated with electrocardiographic (EKG) signs of left ventricular overload and ventricular ectopic beats. These changes were not prevented by atropine, hexamethonium, or propanolol. Both the pressor response and the EKG abnormalities were prevented by an alpha-adrenergic blocking agent. The authors conclude that alpha-adrenergically mediated arterial vasoconstriction is the effector mechanism in the pressor response to increased intracranial pressure or cord compression.