Lipid Peroxidation as a Cause of Cerebral Vasospasm

Sano, Keiji; Asano, Takao; Tanishima, T; Sasaki, Tatsuya

doi:10.1080/01616412.1980.11739582

Cited by 115 publications

(40 citation statements)

References 22 publications

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“…Apart from lipid peroxidation, oxidation of cellular proteins and nucleic acids also occurs (Bayir and Kagan, 2001;Chan, 2001). Previous research indicates that free radicals have been implicated directly in a number of pathologic events of the central nervous system, including increased blood-brain barrier permeability (Easton and Fraser, 1998), vasogenic oedema (Hall et al, 1992), posttraumatic microvascular damage (Kontos and Hess, 1983), and subarachnoid haemorrhage-induced vasospasm (Sano et al, 1980).…”

Section: Antioxidant Properties Of Melatoninmentioning

confidence: 99%

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Seifman

Adamides

Nguyen

et al. 2008

J Cereb Blood Flow Metab

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Oxidative stress plays a significant role in secondary damage after severe traumatic brain injury (TBI); and melatonin exhibits both direct and indirect antioxidant effects. Melatonin deficiency is deleterious in TBI animal models, and its administration confers neuroprotection, reducing cerebral oedema, and improving neurobehavioural outcome. This study aimed to measure the endogenous cerebrospinal fluid (CSF) and serum melatonin levels post-TBI in humans and to identify relationships with markers of oxidative stress via 8-isoprostaglandin-F 2a (isoprostane), brain metabolism and neurologic outcome. Cerebrospinal fluid and serum samples of 39 TBI patients were assessed for melatonin, isoprostane, and various metabolites. Cerebrospinal fluid but not serum melatonin levels were markedly elevated (7.28±0.92 versus 1.47±0.35 pg/mL, P < 0.0005). Isoprostane levels also increased in both CSF (127.62 ± 16.85 versus 18.28 ± 4.88 pg/mL, P < 0.0005) and serum (562.46±50.78 versus 126.15±40.08 pg/mL (P < 0.0005). A strong correlation between CSF melatonin and CSF isoprostane on day 1 after injury (r = 0.563, P = 0.002) suggests that melatonin production increases in conjunction with lipid peroxidation in TBI. Relationships between CSF melatonin and pyruvate (r = 0.369, P = 0.049) and glutamate (r = 0.373, P = 0.046) indicate that melatonin production increases with metabolic disarray. In conclusion, endogenous CSF melatonin levels increase after TBI, whereas serum levels do not. This elevation is likely to represent a response to oxidative stress and metabolic disarray, although further studies are required to elucidate these relationships.

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Section: Antioxidant Properties Of Melatoninmentioning

confidence: 99%

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Seifman

Adamides

Nguyen

et al. 2008

J Cereb Blood Flow Metab

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“…2,4 -6 Free radicals can alter brain hemodynamics by causing vasoconstriction 7,8 and increase thromboxane A 2 (TXA 2 ). 9 -13 Although TXA 2 has been implicated in peroxidation-induced vasoconstriction, 9 -12 the mechanisms of TXA 2 production by brain vasculature during oxidant stresses remain unknown.…”

mentioning

confidence: 99%

Augmented Vasoconstriction and Thromboxane Formation by 15-F _2t -Isoprostane (8-Iso-Prostaglandin F _2α ) in Immature Pig Periventricular Brain Microvessels

Hou

Gobeil

Peri

et al. 2000

Stroke

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Background and Purpose-Oxidant stress, especially in the premature, plays a major role in the pathogenesis of hypoxic-ischemic encephalopathies mostly manifested in the periventricular region. We studied the vasomotor mode of actions of the peroxidation product 15-F 2t -isoprostane (15-F 2t -IsoP) (8-iso-prostaglandin F 2␣ ) on periventricular region during development. Methods-Effects of 15-F 2t -IsoP on periventricular microvessels of fetal, newborn, and juvenile pigs were studied by video imaging and digital analysis techniques. Thromboxane formation and intracellular Ca 2ϩ were measured by radioimmunoassay and by using the fluorescent indicator fura 2-AM. Results-15-F 2t -IsoP-mediated constriction of periventricular microvessels decreased as a function of age such that in the fetus it was Ϸ2.5-fold greater than in juvenile pigs. 15-F 2t -IsoP evoked more thromboxane formation in the fetus than in the newborn, which was greater than that in the juvenile periventricular region; this was associated with immunoreactive thromboxane A 2 (TXA 2 ) synthase expression in the fetus that was greater than that in newborn pigs, which was greater than that in juvenile pigs. 15-F 2t -IsoP-induced vasoconstriction was markedly inhibited by TXA 2 synthase and receptor blockers (CGS12970 and L670596). Vasoconstrictor effects of the TXA 2 mimetic U46619 on fetal, neonatal, and juvenile periventricular microvessels did not differ. 15-F 2t -IsoP increased TXA 2 synthesis by activating Ca 2ϩ influx through non-voltage-gated channels in endothelial cells (SK&F96365 sensitive) and N-type voltage-gated channels (-conotoxin sensitive) in astrocytes; smooth muscle cells were not responsive to 15-F 2t -IsoP but generated Ca 2ϩ transients to U46619 via L-type voltage-sensitive channels. Conclusions-15-F 2t -IsoP causes periventricular brain region vasoconstriction in the fetus that is greater than that in the newborn, which in turn is greater than that in the juvenile due to greater TXA 2 formation generated through distinct stimulatory pathways, including from endothelial and astroglial cells. The resulting hemodynamic compromise may contribute to the increased vulnerability of the periventricular brain areas to oxidant stress-induced injury in immature subjects. (Stroke. 2000;31:516-525.)

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“…The most likely secondary injury process, which high-dose MP is thought to affect, is lipid peroxidation and hydrolytic destruction of neuronal and microvascular membranes, [3,14,17,18,27] a process that continues for several days after injury. [18,29,30] When secondary posttraumatic spinal cord injury is increased because of delayed treatment, it is likely to be more difficult to slow the postinjury cascade of neurodestructive events. Delayed reactions are also manifested as hemoglobin oxidation in subarachnoid clots after subarachnoid hemorrhage.…”

Section: Possible Mechanismsmentioning

confidence: 99%

“…Delayed reactions are also manifested as hemoglobin oxidation in subarachnoid clots after subarachnoid hemorrhage. [30] Single-bolus dosing does not attenuate posttraumatic spinal ischemia, [11,12,22] and in experiments in which 48MP dosing was used [13] it was not compared with 24-hour regimens. With even longer delays in treatment to longer than 8 hours in NASCIS II, we observed reduced recovery with 24MP treatment compared with placebo.…”

Section: Possible Mechanismsmentioning

confidence: 99%

Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up

Bracken¹,

Shepard²,

Holford³

et al. 1998

FOC

121

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Object A randomized double-blind clinical trial was conducted to compare neurological and functional recovery and morbidity and mortality rates 1 year after acute spinal cord injury in patients who had received a standard 24-hour methylprednisolone regimen (24MP) with those in whom an identical MP regimen had been delivered for 48 hours (48MP) or those who had received a 48-hour tirilazad mesylate (48TM) regimen. Methods Patients for whom treatment was initiated within 3 hours of injury showed equal neurological and functional recovery in all three treatment groups. Patients for whom treatment was delayed more than 3 hours experienced diminished motor function recovery in the 24MP group, but those in the 48MP group showed greater 1-year motor recovery (recovery scores of 13.7 and 19, respectively, p = 0.053).A greater percentage of patients improving three or more neurological grades was also observed in the 48MP group (p = 0.073). In general, patients treated with 48TM recovered equally when compared with those who received 24MP treatments. A corresponding recovery in self care and sphincter control was seen but was not statistically significant. Mortality and morbidity rates at 1 year were similar in all groups. Conclusions For patients in whom MP therapy is initiated within 3 hours of injury, 24-hour maintenance is appropriate. Patients starting therapy 3 to 8 hours after injury should be maintained on the regimen for 48 hours unless there are complicating medical factors.

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Lipid Peroxidation as a Cause of Cerebral Vasospasm

Cited by 115 publications

References 22 publications

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Augmented Vasoconstriction and Thromboxane Formation by 15-F _2t -Isoprostane (8-Iso-Prostaglandin F _2α ) in Immature Pig Periventricular Brain Microvessels

Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up

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Lipid Peroxidation as a Cause of Cerebral Vasospasm

Cited by 115 publications

References 22 publications

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Augmented Vasoconstriction and Thromboxane Formation by 15-F 2t -Isoprostane (8-Iso-Prostaglandin F 2α ) in Immature Pig Periventricular Brain Microvessels

Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up

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Augmented Vasoconstriction and Thromboxane Formation by 15-F _2t -Isoprostane (8-Iso-Prostaglandin F _2α ) in Immature Pig Periventricular Brain Microvessels