Videodensitometric estimation of the protective effect of hyperbaric oxygen in the ischemic gerbil brain

Corkill, Guy; Housen, Karen Van; Hein, Larry; Reitan, John A.

doi:10.1016/0090-3019(85)90186-7

Cited by 23 publications

(7 citation statements)

References 10 publications

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“…1,2,6,8,17,18 With this paradigm, the final infarct size could be reduced by 38%, almost similar to a previously demonstrated reduction after permanent ligation of the MCA. 2 In vivo MR monitoring of ischemia could be important to study onset, duration, and effectiveness of any treatment paradigm.…”

Section: Schäbitz Et Al Neuroprotection Of Hbo Monitored By Mrisupporting

confidence: 85%

Neuroprotection by Hyperbaric Oxygenation After Experimental Focal Cerebral Ischemia Monitored by MRI

Schäbitz

Schade

Heiland

et al. 2004

Stroke

107

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Background-Hyperbaric oxygenation (HBO) after focal cerebral ischemia reduces infarct size and improves outcome when applied early after stroke. Here, we evaluated effects of HBO on permanent focal cerebral ischemia and applied magnetic resonance imaging (MRI) monitoring to study lesion evolution. Methods-Rats underwent permanent middle cerebral artery occlusion (MCAO). Two hours later, animals were treated with HBO (100% O 2 /2 atm; nϭ17) for 1 hour or treated with room air (nϭ17). Animals underwent serial MRI studies (DWI, PI, T2) beginning 90 minutes after MCAO. Neuroscore was assessed (5-point rating scale). Animals were euthanized and brains were 2,3,5-triphenyltetrazolium chloride (TTC)-stained for infarct volume calculation 120 hours after MCAO. Immunohistochemistry was performed with antibodies against c-FOS and 4-hydroxy-2-nonenal-modified proteins (HNE) to check for effects of oxidative stress caused by HBO treatment. Results-HBO reduced infarct volume by 38% (PϽ0.001). As shown by MRI, neuroprotection began 5 hours after ischemia and remained effective for 5 days. The relative regional cerebral blood flow was not different between groups at 3.5 and 5 hours after occlusion. There was less neurological deficit in HBO-treated animals compared with controls (PϽ0.05). Lipid peroxidation of cerebral vessels after HBO treatment as measured by HNE staining and pattern of c-FOS induction were not significantly different between groups at 3.5 and 8 hours after ischemia. Conclusion-As monitored by MRI HBO treatment reversed ischemic lesion size between 3 and 5 hours after ischemia and achieved a long-lasting neuroprotective effect without significant oxidative damage.

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Section: Schäbitz Et Al Neuroprotection Of Hbo Monitored By Mrisupporting

confidence: 85%

Neuroprotection by Hyperbaric Oxygenation After Experimental Focal Cerebral Ischemia Monitored by MRI

Schäbitz

Schade

Heiland

et al. 2004

Stroke

107

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“…Most showed a benefit to animals treated with HBO. Models of stroke examined cerebral ischemia with and without reperfusion through either temporary [7, 10, 11, 13, 14, 16, 17,59,60,61,62,63,64,65] (table 2) or permanent [6, 49, 50,65,66,67,68] (table 3) occlusion of cerebral arteries. Timing of temporary occlusions ranged from 20 min [11] to 24 h [59].…”

Section: Animal Studiesmentioning

confidence: 99%

“…This suggests that there may be a window of opportunity between 6 and 12 h after transient ischemia for HBO to be effective and raises concerns that beyond that window, HBO may actually be harmful. Permanent ischemia may have an even shorter window as studies treating within 2 h showed a benefit from HBO [6, 49, 51,66,67,68] whereas one study treating at 3 or 6 h after ischemia did not [65. ]…”

Section: Animal Studiesmentioning

confidence: 99%

“…Second, animal studies used primarily transient ischemia as a model for stroke, but clinical trials did not limit patients to those with thrombolysis or reperfusion, and since the bulk of patients do not undergo recanalization, these results are not comparable. Further, although most animal models that did evaluate HBO in permanent cerebral arterial occlusion reported benefit, most administered treatment almost immediately after ischemia [6, 50, 51,66,67,68]. Only one study evaluated HBO treatment within a window more consistent with patient care (3–6 h) and showed no benefit in permanent arterial occlusion [65].…”

Section: Limitations and Future Directionsmentioning

confidence: 99%

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Hyperbaric Oxygen Therapy of Cerebral Ischemia

Helms

Whelan

Torbey³

2005

Cerebrovasc Dis

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Background: Hyperbaric oxygen (HBO) therapy of cerebral ischemia has been evaluated in a number of human and animal studies; however, there is presently no consensus on its efficacy. Methods: We present a review of animal and human studies on HBO therapy of cerebral ischemia as well as present potential mechanisms of action of HBO. Results: Animal studies of HBO have shown promise by reducing infarct size and improving neurologic outcome. HBO has also been shown to inhibit inflammation and apoptosis after cerebral ischemia. Early reports in humans also suggested benefit in stroke patients treated with HBO. Recent randomized, controlled human studies, however, have not shown benefit, although all were limited by small sample size. Important differences between animal and human studies suggest HBO might be more effective in stroke within the first few hours and at a pressure of 2–3 ATA. Conclusions: The clinical usefulness of HBO in the treatment of cerebral ischemia is not yet certain. Attention to emerging pathophysiologic data should be taken into consideration in design of any future clinical trials of HBO in acute ischemic stroke.

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“…Table 2 summarizes reports on experimental brain ischemia in which HBO has been applied. 1 -425 - 36 In some experiments (protection models), 25 -32 the animal was receiving HBO treatment when the ischemia was induced; in other experiments (treatment models), 1 -4 -33 -36 HBO treatment was initiated at various intervals after ischemia. In general, the results of research in animals have suggested a promising role for the use of HBO.…”

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confidence: 99%

A pilot study of hyperbaric oxygen in the treatment of human stroke.

Anderson

Bottini

Jagiella

et al. 1991

Stroke

128

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We administered hyperbaric oxygen or air in a double-blind prospective protocol to 39 patients with ischemic cerebral infarction. We interrupted the study when we noticed what appeared to be a trend favoring the air-treated patients, whose neurological deficits were less severe (mean±SEM score on graded neurological examination: air, 25.6±4.9; oxygen, 34.5±7.5) and whose infarcts were smaller (air, 29.0±12.2 cm 3 ; oxygen, 49.2 ±11.7 cm 3 ) at 4 months. The trend, we decided, was probably an artifact of the randomization process. Nevertheless, we chose not to resume the trial because the treatment was difficult to administer by schedule (for various reasons the treatment protocol was broken in 15 of the 39 patients), was poorly tolerated (eight of the 39 patients refused to continue treatments), and did not produce dramatic improvement (Stroke 1991^2:1137-1142)

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Videodensitometric estimation of the protective effect of hyperbaric oxygen in the ischemic gerbil brain

Cited by 23 publications

References 10 publications

Neuroprotection by Hyperbaric Oxygenation After Experimental Focal Cerebral Ischemia Monitored by MRI

Neuroprotection by Hyperbaric Oxygenation After Experimental Focal Cerebral Ischemia Monitored by MRI

Hyperbaric Oxygen Therapy of Cerebral Ischemia

A pilot study of hyperbaric oxygen in the treatment of human stroke.

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