A clinical case is reported indicating that intracranial pressure (ICP) rises with cross-clamping of the thoracic aorta (CCTA) in humans and does not fall if arterial blood pressure (BP) is lowered by nitroprusside. Hantler and Knight (Anesthesiology 1982;56:146-147) also reported a similar case. We investigated this phenomenon prospectively, measuring ICP, aortic arch BP, and right atrial pressure in 10 halothane-anesthetized New Zealand White rabbits ventilated to pH 7.45-7.55. When CCTA was applied, BP and ICP rose significantly (by paired t test, p ≤ 0.01), although right atrial pressure did not change. After removal of the cross-clamp and a period of stabilization, BP was elevated to the same level as that attained with CCTA with phenylephrine. Although phenylephrine induced BP elevation, neither ICP nor CVP changed significantly from control or recovery measurements. In six animals, after applying CCTA, BP was lowered to control levels with nitroprusside (in combination with CCTA). Nitroprusside was effective in lowering BP to control level, but ICP remained elevated as long as the cross-clamping continued. With no rise in central venous pressure, venous engorgement is an unlikely mechanism for ICP elevation. Time constants of ICP change are too short to invoke increased cerebral spinal fluid production or decreased absorption. BP does not rise above the expected range for autoregulation, but recruitment of either arterial capacitance vessels or of a neuroreflex arc, or the effects of cord ischemia disrupting cerebral autoregulation may be the cause of an acute increase cerebral blood volume.
|Original language||English (US)|
|Issue number||5 II SUPPL.|
|State||Published - Jan 1 1988|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)