Period of Hyperbaric Oxygen Delivery Leads to Different Degrees of Hepatic Ischemia/Reperfusion Injury in Rats.

BACKGROUND: This study evaluated the morphology of the rat liver when hyperbaric oxygen (HBO) was used at various stages of ischemia and reperfusion. METHODS: Thirty-two male Wistar rats, subjected to 30 minutes of hepatic ischemia and 30 minutes of reperfusion, were randomly assigned as follows: GIR (n = 8), control without HBO; GHBO/I (n = 8), in which HBO was applied only during ischemia; GHBO/R (n = 8), HBO only during reperfusion; and GHBO/IR (n = 8), HBO during both ischemia and reperfusion. Feasibility scores of hepatocytes were determined by assessing 8 items related to liver injury. RESULTS: The histologic injury score of the hepatic specimens was significantly lower in the GHBO/I group (79.0 ± 0.1) compared with the GIR group (135.0 ± 0.1). HBO was not effective when applied during reperfusion (GHBO/R, 151.3 ± 0.1) or during the ischemia plus reperfusion period (GHBO/IR, 131.0 ± 0.1). The sum was significantly higher (P < .05) in HBO-treated animals during the reperfusion period (ie, in the GHBO/R group compared with any of the other groups). CONCLUSIONS: A favorable effect was obtained when HBO was administered early during ischemia. HBO given in later periods of reperfusion was associated with a more severe sum index percentage of liver damage.

The mitochondrial DNA C3303T mutation can cause cardiomyopathy and/or skeletal myopathy.

OBJECTIVE: Several mutations in mitochondrial DNA have been associated with infantile cardiomyopathy, including a C3303T mutation in the mitochondrial transfer RNA(Leu(UUR)) gene. Although this mutation satisfied generally accepted criteria for pathogenicity, its causative role remained to be confirmed in more families. Our objective was to establish the frequency of the C3303T mutation and to define its clinical presentation. STUDY DESIGN: Families with cardiomyopathy and maternal inheritance were studied by polymerase chain reaction/restriction fragment length polymorphism analysis looking for the C3303T mutation. RESULTS: We found the C3303T mutation in 8 patients from 4 unrelated families. In one, the clinical presentation was infantile cardiomyopathy; in the second family, proximal limb and neck weakness dominated the clinical picture for the first 10 years of life, when cardiac dysfunction became apparent; in the third family, 2 individuals presented with isolated skeletal myopathy and 2 others with skeletal myopathy and cardiomyopathy; in the fourth family, one patient had fatal infantile cardiomyopathy and the other had a combination of skeletal myopathy and cardiomyopathy. CONCLUSIONS: Our findings confirm the pathogenicity of the C3303T mutation and suggest that this mutation may not be rare. The C3303T mutation should be considered in the differential diagnosis of skeletal myopathies and cardiomyopathy, especially when onset is in infancy.