Temporal changes in perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin after subarachnoid hemorrhage

Pluta, Ryszard; Afshar, John K. B.; Boock, Robert J.; Oldfield, Edward H.

doi:10.3171/jns.1998.88.3.0557

Cited by 126 publications

(78 citation statements)

References 52 publications

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“…aneurysmal SAH. 55 This result was consistent with an animal study by Pluta et al 56 However, because we did not perform re-imaging, it remains unknown whether the mild secondary increase of CSF oxyhemoglobin was due to micro-rebleeds. Quantitative techniques CSF spectrophotometry is semi-quantitative.…”

Section: The Uk Experiencesupporting

confidence: 81%

Spectrophotometry for Cerebrospinal Fluid Pigment Analysis

Petzold

Sharpe²,

Keir³

2006

NCC

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The use of spectrophotometry for the analysis of the cerebrospinal fluid (CSF) is reviewed. The clinically relevant CSF pigments -oxyhemoglobin and bilirubin -are introduced and discussed with regard to clinical differential diagnosis and potentially confounding variables (the four "T"s or: traumatic tap, timing, total protein and total bilirubin). The practical laboratory aspects of spectrophotometry and automated techniques are presented in the context of analytical and clinical specificity and sensitivity. The perceptual limitations of human color vision are highlighted and the use of visual assessment of the CSF is discouraged in light of recent evidence from a national audit in the United Kingdom. Finally, future perspectives including the need for longitudinal CSF profiling and routine spectrophotometric calibration are outlined.

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Section: The Uk Experiencesupporting

confidence: 81%

Spectrophotometry for Cerebrospinal Fluid Pigment Analysis

Petzold

Sharpe²,

Keir³

2006

NCC

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“…Similar conditions (i.e. presence of deoxyhemoglobin 71 and low pH 83 ) exist in the subarachnoid space after SAH. Therefore, the lower CSF nitrite levels after SAH and during development of vasospasm may be caused not only by decreased NO production by neuronal and endothelial NOS, but also by increased consumption of nitrite.…”

Section: Nitrite On Demand Local But Systemically Administered No Dmentioning

confidence: 86%

“…Although the pathogenesis of vasospasm after SAH is probably multifactorial, imbalance between vasoconstricting (endothelin-1, endotheliumderived constricting factor) and vasodilating influences on vascular tone in response to the presence of blood in the subarachnoid space almost certainly play an integrating role 54,71 . The above mentioned mechanisms of initiation, sustenance and resolution of delayed cerebral vasospasm open the possibility to develop vasospasm-preventing treatment with NO replacement and sequential, targeted therapy, which may yield a novel treatment for this life-threatening complication of SAH.…”

Section: No-based Prevention and Treatment Of Vasospasmmentioning

confidence: 99%

“…There is little doubt that ferrous hemoglobins (oxyhemoglobin and deoxyhemoglobin) slowly released from erythrocytes in the subarachnoid space oxidized and metabolized are directly and/or indirectly responsible for development of cerebral vasospasm 13,54,71 ( Figure 1). At the time of vasospasm, the nNOS-expressing (nitroxic nNOS-containing) neurons disappear from the arterial adventitia 75 , diminishing NO availability and resulting in vasoconstriction 70 (Figure 1).…”

Section: No and Pathomechanism(s) Of Delayed Cerebral Vasospasmmentioning

confidence: 99%

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RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Pluta

2008

Acta Neurochirurgica Supplement

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Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation and chemoregulation. Subarachnoid hemorrhage (SAH) interrupts this regulation of cerebral blood flow. Hemoglobin, gradually released from erythrocytes in the subarachnoid space, destroys nNOS-containing neurons in the conductive arteries. This deprives the arteries of NO, leading to initiation of delayed vasospasm. But such vessel narrowing increases shear stress, which stimulates eNOS. This mechanism normally would lead to increased production of NO and dilation of arteries. However, a transient eNOS dysfunction evoked by an increase in the endogenous competitive NOS inhibitor, asymmetric dimethylarginine (ADMA), prevents this vasodilation. eNOS dysfunction has been recently shown to be evoked by increased levels of ADMA in cerebrospinal fluid (CSF) in response to the presence of bilirubin-oxidized fragments (BOXes). A direct cause of the increased ADMA CSF level is most likely decreased ADMA elimination owing to disappearance of ADMA-hydrolyzing enzyme [dimethylarginine dimethylaminohydrolase II (DDAH II)] immunoreactivity in the arteries in spasm. This eNOS dysfunction sustains vasospasm. CSF ADMA levels are closely associated with the degree and time course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of pre-clinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.

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“…This idea is based on the evidence that DCI develops while the patient is on the intensive care unit where proof-of-concept studies on neuroprotectants and neuromonitoring can be performed. The risk for DCI correlates with the amount of blood in the initial computed tomography scan (Brouwers et al, 1993), and its onset coincides with the period of peak subarachnoid hemolysis (Pluta et al, 1998). Therefore, erythrocyte products in the subarachnoid space presumably cause DCI.…”

Section: Subarachnoid Hemorrhagementioning

confidence: 99%

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Lauritzen

Dreier

Fabricius

et al. 2010

J Cereb Blood Flow Metab

683

582

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Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

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Temporal changes in perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin after subarachnoid hemorrhage

Cited by 126 publications

References 52 publications

Spectrophotometry for Cerebrospinal Fluid Pigment Analysis

Spectrophotometry for Cerebrospinal Fluid Pigment Analysis

RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

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