Hydrogen gas reduces brain injury in a global cerebral ischemia model

• Autorzy: Ostrowski R.P. , Mansell C. , Zhang J. H.
• Języki publikacji: EN

Abstrakty

EN

Transient global cerebral ischemia-reperfusion injury can occur during acute severe hypotensive states and in cardiac arrest that is followed by resuscitation. This transient reduction in perfusion causes an insult to selective hippocampal neuronal populations via an apoptotic mechanism. Hydrogen gas has a neuroprotective effect and could be used as a pharmacologic agent of beneficial effect. As such we set out in this study to describe the effect of the inhalation of 2.9% hydrogen enriched air following an ischemia-reperfusion injury. A 2-vessel occlusion model was used to induce global cerebral ischemia for 6 minutes while maintaining a hypotensive state with a mean arterial pressure of 30 mm Hg through reversible exsanguinations in male Sprague-Dawley rats (280–330 g). The study included three groups: global ischemia without treatment (GI, n=6), global ischemia with hydrogen (GI + H2, n=6 ) and sham surgery (Sham, n=6). Rats in the treatment group received 2.9% inhalational hydrogen for 1 hour starting 15 minutes following reperfusion. Neurobehavioral testing was performed on day one and T-maze testing prior to being euthanized on days 3 or 7. Treated rats demonstrated an improved outcomes in spontaneous alternations, seizure incidence and survivability. Quantitative Nissl histology and TUNEL of the CA-1 region of the hippocampus showed increased cell survival in the treatment group. We conclude that treatment with inhalational hydrogen following ischemia-reperfusion injury could be low cost method of decreasing the effects of neuronal cell death.

Słowa kluczowe

EN

hydrogen gas; neuroprotective effect; inhalation; brain injury; cerebral ischaemia model; ischaemia-reperfusion injury; rat; animal model; neuronal cell; apoptosis; treatment

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2013
• Tom: 73
• Numer: 1
• Opis fizyczny: p.185

Twórcy

autor

Ostrowski R.P.

• Department of Experimental and Clinical Neuropathology, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Mansell C.

• Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, California, USA

autor

Zhang J. H.

• Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, California, USA