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Objective: The harmful effects of hyperoxemia have been reported in critically ill patients with various disorders, including those with brain injuries. However, the effect of hyperoxemia on aneurysmal subarachnoid hemorrhage (aSAH) patients is unclear. In this study the authors aimed to determine whether hyperoxemia during the hyperacute or acute phase in patients with aSAH is associated with delayed cerebral ischemia (DCI) and poor neurological outcome., Methods: In this single-center retrospective study, data from patients with aSAH treated between January 2011 and June 2017 were reviewed. The patients were classified into groups according to whether they experienced DCI (DCI group and non-DCI group) and whether they had a poor outcome at discharge (poor outcome group and favorable outcome group). The background characteristics and time-weighted average (TWA) PaO2 during the first 24 hours after arrival at the treatment facility (TWA24h-PaO2) and between the first 24 hours after arrival and day 6 (TWA6d-PaO2), the hyperacute and acute phases, respectively, were compared between the groups. Factors related to DCI and poor outcome were evaluated with logistic regression analyses., Results: Of 197 patients with aSAH, 42 patients experienced DCI and 82 patients had a poor outcome at discharge. TWA24h-PaO2 was significantly higher in the DCI group than in the non-DCI group (186 [141-213] vs 161 [138-192] mm Hg, p = 0.029) and in the poor outcome group than in the favorable outcome group (176 [154-205] vs 156 [136-188] mm Hg, p = 0.004). TWA6d-PaO2 did not differ significantly between the groups. Logistic regression analyses revealed that higher TWA24h-PaO2 was an independent risk factor for DCI (OR 1.09, 95% CI 1.01-1.17, p = 0.037) and poor outcome (OR 1.17, 95% CI 1.06-1.29, p = 0.002)., Conclusions: Hyperoxemia during the first 24 hours was associated with DCI and a poor outcome in patients with aSAH. Excessive oxygen therapy might have an adverse effect in the hyperacute phase of aSAH.

Object: In the experimental setting, hypothermia has been demonstrated to attenuate the damaging consequences of stroke and traumatic brain injury (TBI). Laboratory studies of TBI have focused primarily on the use of early hypothermic intervention, with little consideration of the potential efficacy of more delayed but prolonged hypothermia, which would constitute a more clinically relevant approach. In this investigation, the authors evaluated whether delayed, prolonged hypothermia after TBI protected the cerebral microcirculation., Methods: Male Sprague-Dawley rats were equipped with cranial windows for direct visualization of the pial arterial circulation and then subjected to impact-acceleration brain injury. The rats were randomly divided into four experimental groups: Group 1 consisted of normothermic animals; in Group 2 the rats received a 1-hour period of hypothermia (32 degrees C) 30 minutes posttrauma, followed by slow rewarming (32-37 degrees C/90 minutes); and in Groups 3 and 4 the rats received a more delayed induction (at 1 hour postinjury) of either 1 hour (Group 3) or 2 hours (Group 4) of hypothermia, followed by the slow rewarming. The pial arteriolar responses to acetylcholine (ACh) or hypercapnia were measured until up to 6 hours postinjury. With this approach the authors found that the normothermic group demonstrated severely impaired vasoreactivity in terms of ACh-dependent dilation and CO2 reactivity in comparison to baseline values (p < 0.001). In contrast, hypothermia of short duration that was initiated early (30 minutes postinjury) conferred significant cerebrovascular protection (p < 0.001), yet this protection was reduced when the onset of this 1-hour hypothermic period was postponed to 1 hour postinjury. Nevertheless, reduced protection could be significantly improved (p < 0.001) with prolongation of the hypothermic period to 2 hours., Conclusions: The results of this study show that early as well as delayed but prolonged hypothermia attenuate the impaired vascular responsiveness seen after TBI, indicating the potential clinical usefulness of this treatment.

Object: Although considerable attention has been focused on the use of posttraumatic hypothermia, little consideration has been given to the issue of posthypothermic rewarming and its potentially damaging consequences. In this communication, the authors examine the issue of rapid posthypothermic rewarming compared with gradual rewarming while exploring the potential utility of cyclosporin A (CsA) administration for attenuating any rapid rewarming-induced axonal change., Methods: Male Sprague-Dawley rats were subjected to impact-acceleration injury and then their body temperature was lowered to 32 degrees C for 1 hour postinjury. After hypothermia, rewarming to normothermic levels was accomplished either within a 20-minute period (rapid rewarming) or over a 90-minute period (slow rewarming). Some animals in the rapid rewarming group received intrathecal infusion of either CsA or its vehicle, whereas the rats in the slow rewarming group received vehicle alone. Both the CsA and its vehicle were administered immediately before initiation of rewarming. Twenty-four hours postinjury the animals' brains were processed for visualization of amyloid precursor protein (APP), a marker of traumatic axonal injury. The APP-positive axonal density in the gradually rewarmed group receiving vehicle was statistically significantly reduced in comparison with the rapidly rewarmed, vehicle-treated group. For the group undergoing rapid rewarming and treatment with CsA, a statistically significant reduction was also found in the density of the APP profiles compared with the rapidly rewarmed, vehicle-treated group., Conclusions: The results of this study show that rapid rewarming exacerbates traumatically induced axonal injury, which can be significantly attenuated by administering CsA.