MR images enhanced with bis-gadolinium mesoporphyrins provide accurate sizing of irreversibly damaged myocardium with a strong and persistent signal enhancement in the reperfused myocardium.

No abstract

We report two infants with neonatal hypoglycaemic encephalopathy who were evaluated with diffusion-weighted imaging (DWI) and proton MR spectroscopy (MRS) as well as conventional MR. As in conventional MR, DWI and proton MRS revealed a predominance of abnormalities in the parieto-occipital lobes and underlying white matter including the splenium of the corpus callosum. In the acute phase of the disease, lesions on DWI showed restricted water diffusion and on DWI the characteristic lesions seemed to be more readily discernible than on conventional MRI. In the chronic phase, DWI demonstrated increased water diffusion in the affected areas showing atrophy on conventional MRI. Proton MRS revealed an increased lactate-lipid peak and a decreased NAA peak in the involved areas. DWI and proton MRS findings appear helpful in evaluating the extent and the presence of neuronal damage early in the course of neonatal hypoglycaemic encephalopathy.

Homing of intravenously administered iron oxide-labeled macrophages can be monitored with MR imaging and may provide a tool to investigate interactions between macrophages and the invading pathogens.

Using 1H-MRS, we evaluated the effects of growth hormone (GH) as a caspase inhibitor on hypoxic-ischemic injury in neonatal rat brains. The right common carotid arteries of rats were ligated, allowed to recover for 3 hr, and exposed to 8% oxygen for 2 hr. GH was given just prior to HI insult and animals were divided into four groups: control, intracerebroventricular (ICV), intracerebroventricular/intraperitoneal (ICV/IP), and intraperitoneal (IP). Localized in vivo 1H-MRS and TUNEL staining were performed 24 hr after HI injury. Lipid/N-acetyl aspartate (NAA) and lipid/creatine (Cr) ratios were used as apoptotic markers. Gross morphologic changes at 2 weeks were used to evaluate the effects of GH. The lipid/NAA ratio was lower in the ICV and ICV/IP groups than in the control, and the lipid/Cr ratio was lower in the ICV group than in the control. The number of TUNEL positive cells was decreased in the ICV and ICV/IP groups, and the degree of morphologic change indicative of brain injury was lower in the ICV group and somewhat lower in the ICV/IP group. The degree of morphologic change correlated with the lipid/NAA and lipid/Cr ratios. These findings suggest that GH exerts neuroprotective effects in cerebral hypoxic-ischemic injury.