Pulmonary hypertension (PHT) associated with chronic heart failure (CHF) is a risk factor of right ventricular failure after heart transplantation (HT). Our aim was to study pulmonary vascular changes in patients with CHF and to assess any correlation with haemodynamic data. Methods: We studied 17 HT recipients with preoperative CHF who died shortly after HT. Preoperative haemodynamic information was obtained immediately before HT. Vascular lesions in muscular arteries were assessed by linear morphometry. Haemodynamic data were correlated with the morphologic changes. Results: Mean transpulmonary gradient (TPG) was 8.9F4.5 mm Hg and pulmonary vascular resistance (PVR) was 2.25F1.34 Wu. According to the threshold for at-risk PHT (TPGN12 mm Hg or PVRN2.5 Wu), six patients had at-risk PHT. Medial thickness was 23.82F7.23% in patients with at-risk PHT and 17.16F3.24% in patients without at-risk PHT ( p=0.018). Conclusions: Medial hypertrophy of muscular pulmonary arteries is more common and severe than expected in patients with CHF, even in patients without at-risk PHT. This structural change could explain why PHT, even in range of values not excluding HT, is a risk factor for right ventricular failure after HT and influences post-HT haemodynamic behaviour.

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This study presents morphological and biochemical evidence of programmed cell death (PCD) in Entamoeba histolytica induced by exposure of trophozoites to the aminoglycoside antibiotic G418. Morphological characteristics of PCD, including cell shrinkage, reduced cellular volume, nuclear condensation, DNA fragmentation and vacuolization were observed, with preservation of trophozoite membrane integrity. PCD is orchestrated biochemically by alterations in intracellular ion fluxes. In G418-treated trophozoites, overproduction of reactive oxygen species (ROS), decreased intracellular K + , increased cytosolic calcium, and decreased intracellular pH levels were observed. However, externalization of phosphatidylserine was not detected. These results suggest that amoebae can undergo PCD under stress conditions, and that this PCD shares several properties with PCD reported in mammals and in a variety of unicellular organisms. INTRODUCTIONEntamoeba histolytica, the causal agent of amoebiasis, is a protozoan parasite that resides in the colon of infected humans. The invasive trophozoites adhere to mucus and epithelial cells, proliferate by binary fusion, and release proteolytic factors that destroy the intestinal mucosa, resulting in amoebic dysentery. In one in 10 patients with intestinal E. histolytica infection, the trophozoites migrate through the portal vein to the liver and give rise to amoebic abscesses, the main cause of death by this parasite (Espinosa-Cantellano & Martínez-Palomo, 2000). The apoptosis of host cells such as macrophages induced by contact with E. histolytica trophozoites has been widely studied, and it is considered an important feature of the host-parasite relationship (Ragland et al., 1994;Berninghausen & Leippe, 1997).Programmed cell death (PCD) has been considered a critical mechanism of development, differentiation and control of cellular proliferation in metazoans. However, increasing evidence indicates that PCD is also present in unicellular organisms. Forms of PCD such as apoptosis, apoptosis-like processes and necrosis-like processes have been identified in several bacteria (Lewis, 2000), yeast (Madeo et al., 1999), the slime mould Dictyostelium discoideum (Cornillon et al., 1994), the dinoflagellate Peridinium gatunense (Vardi et al., 1999), the euglenoid Euglena gracilis (Scheuerlein et al., 1995), the ciliate Tetrahymena thermophila (Christensen et al., 1995), and the protozoan parasites Trypanosoma, Leishmania (Nguewa et al., 2004) and Plasmodium (Al-Olayan et al., 2002). Recently, results reported by Ramos et al. (2007) have suggested the induction of an apoptotic-like process by nitric oxide species in E. histolytica. Apoptosis is the result of a genetic program that induces cellular and biochemical changes, including caspase activation, externalization of phosphatidylserine (PS), an increase in intracellular Ca 2+ and mitochondrial dysfunction, as well as physical changes such as cell shrinkage, alteration in cell volume, cytoplasmic blebbing and vacuolization, chromatin conden...

Our data suggest that physical activity and resveratrol may be of great importance for the prevention of age-related diseases, but that their organ-dependent effect must be taken into consideration to design a better intervention.