Vascular disruption and local tissue ischemia have long been recognized as important aspects of secondary damage following acute traumatic spinal cord injury. Ischemia and resultant cellular energy failure is thought to contribute to the propagation of many other important pathophysiologic processes, and in this regard has been argued by some to be the most critical component of secondary damage (Amar and Levy, 1999). Mechanical disruption of the microvasculature causes petechial hemorrhage and intravascular thrombosis, which in combination with vasospasm of intact vessels and edema at the injury site can lead to profound local hypoperfusion and ischemia (Tator and Fehlings, 1991). This is primarily a microvascular phenomenon, with the larger caliber vessels such as the anterior spinal artery normally being spared (Koyanagi et al., 1993). Human post-mortem studies have demonstrated that vascular perfusion is substantially worse in the grey matter than in the white matter, which may be related to the disruption and/or thrombosis of the sulcal arterial network that centrifugally supplies much of the grey matter (Tator and Koyanagi, 1997). The high metabolic requirements of neurons make the grey matter exquisitely sensitive to ischemia injury, which can be compounded by the loss of autoregulatory mechanisms which normally maintain fairly constant microvascular hemodynamics within the spinal cord during systolic blood pressure fluctuations (Senter and Venes, 1979). The loss of autoregulation makes the cord vulnerable to further ischemic insult from systemic hypotension (Kobrine et al., 1975).