Heme oxygenase in experimental intracerebral hemorrhage: the benefit of tin-mesoporphyrin

Journal of Neuropathology and Experimental Neurology
A H KoeppenJoanne Smith

Abstract

The prognosis of intracerebral hemorrhage (ICH) is unfavorable. Beyond immediate mass effect and tissue destruction, ICHs cause additional neuronal loss in a "perifocal reactive zone." Heme in ICH induces heme oxygenase-1 (HO-1), and the action of this enzyme on heme yields ferrous iron, biliverdin, and carbon monoxide. Iron is ultimately converted to ferritin and hemosiderin. Free iron is tissue-toxic, and inhibition of HO-1 should provide protection against additional damage. Experimental ICHs were made in adult rabbits by the stereotaxic injection of autologous blood, and the induction of HO-1 and increase in ferritin were followed by confocal immunofluorescence microscopy. Heme diffused rapidly through perivascular spaces, and HO-1 reaction product first occurred in perivascular cells and microglia. At this stage, HO-1 and ferritin showed extensive colocalization. As ICH resolution progressed, HO-1 immunoreactivity faded while ferritin and hemosiderin continued to accumulate. This process was accompanied by a gradient of destruction of neuronal cell bodies and dendrites in the perifocal reactive zone. In an effort to inhibit HO-1, repeated intravenous injections of tin-mesoporphyrin IX (SnMP) were given to ICH-bearing rabbi...Continue Reading

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