Traumatic brain injury (TBI) can trigger disturbances of cerebral pressure autoregulation that can translate into the generation of secondary insults and increased morbidity/mortality. Few therapies have been developed to attenuate the damaging consequences of disturbed autoregulatory control, although some suggest that hypothermia may exert such protection. Here we reexamine this issue of traumatically induced autoregulatory disturbances and their modulation by hypothermic intervention, examining these phenomena in two different models of TBI. Adult rats were subjected to either impact acceleration injury (IAI) or lateral fluid percussion injury (LFPI) followed by the insertion of cranial windows to assess the pial arteriolar cerebral autoregulatory vascular response to the post-traumatic induction of sequential reductions of arterial blood pressure. The potential for continued pial vasodilation in response to declining blood pressure was directly measured post-injury and compared with that in injured groups subjected to 33° C of hypothermia of 1-2 h duration initiated 1 h post-injury. We observed that the TBI resulted in either impaired or abolished cerebral vascular dilation in response to the sequential declines in blood pressure. Following IAI there was a 50% reduction in the vasculature's ability to dilate in response to the induced hypotension. In contrast, following LFPI, the vascular response to hypotension was abolished both ipsilateral and contralateral to the LFPI. In animals sustaining IAI, the use of 1 h post-traumatic hypothermia preserved vascular dilation in response to declines in blood pressure in contrast to the LFPI in which the use of the same strategy afforded no improvement. However, with LFPI, the use of 2 h of hypothermia provided partial vascular protection. These results clearly illustrate that TBI can alter the cerebral autoregulatory vascular response to sequentially induced hypotensive insult, whereas the use of post-traumatic hypothermia provides benefit. Collectively, these studies also demonstrate that different animal models of TBI can evoke different biological responses to injury.