Abstract
Previous investigators have suggested that the systemic arterial pressure (SAP) elevation evoked by elevated intracranial pressure (ICP) — the Cushing response — is due to hypoxia [1], ischemia [2, 3], pressure upon or distortion of the brainstem [4], or a combination of these stimuli. Because of the apparent inseparability of the possible stimuli, efforts to identify the essential stimulus, and thereby the nature of its origin, have been frustrated. Cushing originally proposed ischemia of the medulla as the fundamental stimulus [2]. That the response could be triggered by localized pressure on the dorsal surface of the medulla has also been recognized [5]. Hypoxia was implicated when the typical Cushing response was augmented during asphyxia [1]. While recent works have placed more emphasis upon the pressure/distortion concept, hypoxia has not been eliminated as an essential component of the response. In order to determine the effect of hypoxia upon the Cushing response, the following study was done.
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