Hypoxic Brain Tissue following Subarachnoid Hemorrhage

Hoffman, William E.; Wheeler, Peggy; Edelman, Guy; Charbel, Fady T.; Torres, Norman J.; Ausman, James I.

doi:10.1097/00000542-200002000-00026

Cited by 54 publications

(33 citation statements)

References 18 publications

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“…Due to the occurred inflammatory reactions with blood product after SAH, it has been reported that SAH can decrease pH in brain tissue related to the severity of the bleeding. Compared to control patients, the pH of brain tissue was significantly decreased in those with severe hemorrhage after SAH, but had no noticeable change in those with low Fisher grade hemorrhage [30,31]. In this case, pirfenidone is expected to provide more effective treatment to those patients with severe bleeding and complications after SAH.…”

Section: Loading and Release Of Sah Drugmentioning

confidence: 88%

Functionalized graphene oxide as a drug carrier for loading pirfenidone in treatment of subarachnoid hemorrhage

Yang

Wang

Han

et al. 2015

Colloids and Surfaces B: Biointerfaces

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Section: Loading and Release Of Sah Drugmentioning

confidence: 88%

Functionalized graphene oxide as a drug carrier for loading pirfenidone in treatment of subarachnoid hemorrhage

Yang

Wang

Han

et al. 2015

Colloids and Surfaces B: Biointerfaces

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“…25 The mechanism for this may be a combination of deranged metabolism and impaired homeostatic mechanisms, both related to a low CBF state. pH b has been shown to be a useful marker for assessing the severity of focal cerebral injury 25,26 and outcome in patients with traumatic brain injury. 27 Where pH b fell Ͻ7.0, patients had a significantly higher hospital mortality, and it has been suggested that derangement of …”

Section: Discussionmentioning

confidence: 99%

Hypertonic Saline In Patients With Poor-Grade Subarachnoid Hemorrhage Improves Cerebral Blood Flow, Brain Tissue Oxygen, and pH

Al-Rawi

Tseng

Richards

et al. 2010

Stroke

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Background and Purpose— Delayed cerebral ischemia and infarction due to reduced CBF remains the leading cause of poor outcome after aneurysmal subarachnoid hemorrhage. Hypertonic saline (HS) is associated with an increase in CBF. This study explores whether CBF enhancement with HS in patients with poor-grade subarachnoid hemorrhage is associated with improved cerebral tissue oxygenation. Methods— Continuous monitoring of arterial blood pressure, intracranial pressure, cerebral perfusion pressure, brain tissue oxygen, carbon dioxide, pH, and middle cerebral artery flow velocity was performed in 44 patients. Patients were given an infusion (2 mL/kg) of 23.5% HS. In 16 patients, xenon CT scanning was also performed. CBF in a region surrounding the tissue oxygen sensor was calculated. Data are mean±SD. Results— Thirty minutes postinfusion, a significant increase in arterial blood pressure, cerebral perfusion pressure, flow velocity, brain tissue pH, and brain tissue oxygen was seen together with a decrease in intracranial pressure ( P <0.05). Intracranial pressure remained reduced for >300 minutes and flow velocity elevated for >240 minutes. A significant increase in brain tissue oxygen persisted for 240 minutes. Average baseline regional CBF was 33.9±13.5 mL/100 g/min, rising by 20.3%±37.4% ( P <0.05) after HS. Patients with favorable outcome responded better to HS in terms of increased CBF, brain tissue oxygen, and pH and reduced intracranial pressure compared with those with an unfavorable outcome. A sustained increase in brain tissue oxygen (beyond 210 minutes) was associated with favorable outcome ( P <0.023). Conclusion— HS augments CBF in patients with poor-grade subarachnoid hemorrhage and significantly improves cerebral oxygenation for 4 hours postinfusion. Favorable outcome is associated with an improvement in brain tissue oxygen beyond 210 minutes.

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“…In several studies, isoflurane, compared with other anesthetic agents, maintained stable cerebral blood flow and high tissue oxygenation 86,87 and, thus, does not cause false interpretations of tissue hypoxia. Indeed, the decrease in blood pressure and cerebral perfusion caused by the related anesthetic desflurane has been associated with increased brain oxygenation, 88 possibly as a result of its vasodilator properties and lower cerebral metabolic rate. 86,89 HIF-1␣ expression is induced by isoflurane in vitro 90 and in vivo, and this depends on activation of the extracellular signal-regulated kinases cascade.…”

Section: Hypoxia and Cerebralmentioning

confidence: 99%

CNS Hypoxia Is More Pronounced in Murine Cerebral than Noncerebral Malaria and Is Reversed by Erythropoietin

Hempel

Combes

Hunt

et al. 2011

The American Journal of Pathology

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Cerebral malaria (CM) is associated with high mortality and risk of sequelae, and development of adjunct therapies is hampered by limited knowledge of its pathogenesis. To assess the role of cerebral hypoxia, we used two experimental models of CM, Plasmodium berghei ANKA in CBA and C57BL/6 mice, and two models of malaria without neurologic signs, P. berghei K173 in CBA mice and P. berghei ANKA in BALB/c mice. Hypoxia was demonstrated in brain sections using intravenous pimonidazole and staining with hypoxia-inducible factor-1␣-specific antibody. Cytopathic hypoxia was studied using poly (ADP-ribose) polymerase-1 (PARP-1) gene knockout mice. The effect of erythropoietin, an oxygen-sensitive cytokine that mediates protection against CM, on cerebral hypoxia was studied in C57BL/6 mice. Numerous hypoxic foci of neurons and glial cells were observed in mice with CM. Substantially fewer and smaller foci were observed in mice without CM, and hypoxia seemed to be confined to neuronal cell somas. PARP-1-deficient mice were not protected against CM, which argues against a role for cytopathic hypoxia. Erythropoietin therapy reversed the development of CM and substantially reduced the degree of neural hypoxia. These findings demonstrate cerebral hypoxia in malaria, strongly associated with cerebral dysfunction and a possible target for adjunctive therapy.

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Hypoxic Brain Tissue following Subarachnoid Hemorrhage

Cited by 54 publications

References 18 publications

Functionalized graphene oxide as a drug carrier for loading pirfenidone in treatment of subarachnoid hemorrhage

Functionalized graphene oxide as a drug carrier for loading pirfenidone in treatment of subarachnoid hemorrhage

Hypertonic Saline In Patients With Poor-Grade Subarachnoid Hemorrhage Improves Cerebral Blood Flow, Brain Tissue Oxygen, and pH

CNS Hypoxia Is More Pronounced in Murine Cerebral than Noncerebral Malaria and Is Reversed by Erythropoietin

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