Can liver transplantation achieve similar effects at high altitudes compared with plains: case report.
ABSTRACT In orthotopic liver transplantation, particular emphasis must be placed on the unique physiologic, pathologic, and clinical features in residents living in areas at high vs low altitude. Hypobaric hypoxia, hypothermia, heavy radiation, high wind speed, and superevaporation at high altitudes may lead to various diseases. These features have progressive effects on cardiopulmonary and central nervous system functions. A high concentration of red cells in the circulation is likely to result in an increased incidence of hepatic artery and portal vein thrombosis. The immune system is also affected at high altitudes. Exposure to high altitude, which is associated with decreased oxygen pressure, can result in oxidation-reduction stress, enhanced generation of reactive oxygen and nitrogen species, and related oxidative damage to lipids, proteins, and DNA. Our male patient with liver cirrhosis caused by chronic hepatitis B virus infectionunderwent orthotopic liver transplantation in Tibet with a successful outcome and good long-term survival.
Article: Altitude-related illness.[Show abstract] [Hide abstract]
ABSTRACT: There are a number of conditions which can be grouped together as ARI. Many represent potentially fatal pathophysiological states that are rapidly reversible if identified and treated properly. Physiological alterations that result from the hypobaric hypoxia of altitude include cerebral vasodilatation, altered ventilatory patterns, pulmonary vasoconstriction, decreased cardiac output, and altered fluid and electrolyte balance. The various altitude-related illnesses represent a spectrum of conditions with overlapping presentations. The symptoms of AMS and HACE represent a continuum of disease that appears to be related to alterations in cerebrovascular autoregulation. High-altitude retinal hemorrhage may be related to similar vascular events in the retinal circulation. Although the etiology of HAPE remains unclear, it is likely that alterations of pulmonary vascular tone and flow play an important roles in its production. Knowledge regarding ARI is important in planning prophylaxis and instituting therapy. Gradual ascent and acclimatization are the mainstays of prophylaxis. Pharmacological prophylaxis is available for those who are prone to severe AMS. Prompt recognition, descent, and administration of oxygen constitute the major therapies for severe ARI. The ability to perform these three tasks can rapidly reverse a potentially fatal illness.American Journal of Emergency Medicine 06/1985; 3(3):217-26. · 1.70 Impact Factor
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ABSTRACT: The chemokine monocyte chemoattractant protein (MCP)-1 plays a role in regulating the lymphocyte and macrophage infiltrate in ovarian cancer, but macrophages also accumulate in necrotic areas of the tumors where there is little MCP-1 expression (Negus, R. P. M. et al., Am. J. Pathol. 1997. 150: 1723-1734). Necrotic regions are likely to be hypoxic. In this study we show that hypoxia inhibits MCP-1-induced migration of THP-1 monocytic cells and human macrophages. In contrast, lymphocytes from peripheral blood migrate normally to an MCP-1 gradient in hypoxic conditions. The inhibition of monocyte migration by hypoxia is rapid and reversible. At the exposure times studied (30-90 min) hypoxia does not affect expression of the MCP-1 receptor CCR2B and cells exposed to hypoxia still respond to MCP-1 with an elevation of intracellular calcium. Although hypoxia is known to modulate gene expression, the inhibition of migration reported here was not due to the production of soluble factors, and mRNA expression of macrophage migration inhibitory factor was unchanged. Hypoxia-induced inhibition of chemotaxis was not limited to MCP-1. Hypoxia also inhibited the chemotactic response to macrophage inflammatory protein-1alpha, RANTES and the chemoattractant N-formyl-met-leu-phe, but hypoxic cells were still able to phagocytose opsonized red blood cells. We suggest that inhibition of migration by hypoxia is not due to gene regulation but is a reflection of metabolic changes in the cell. Transient hypoxia may regulate the distribution of macrophages in tumors and other inflammatory conditions.European Journal of Immunology 08/1999; 29(7):2280-7. · 4.97 Impact Factor
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ABSTRACT: The neutrophil (PMN) is regarded as a key component in the hyperinflammatory response known as the systemic inflammatory response syndrome. Acute respiratory distress syndrome (ARDS) and subsequent multiple organ failure (MOF) are related to the severity of this hyperinflammation. ICU patients who are at highest risk of developing MOF may have acute hypoxic events that complicate their hospital course. This study was undertaken to evaluate the effects of acute hypoxia and subsequent hypoxemia on circulating PMNs in human volunteers. Healthy subjects were exposed to a changing O2/N2 mixture until their O2 saturation (SaO2) reached a level of 68% saturation. These subjects were then exposed to room air and then returned to their baseline SaO2. PMNs were isolated from pre- and post-hypoxemic arterial blood samples and were then either stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or PMA alone, or they were primed with L-alpha-phosphatidylcholine, beta-acetyl-gamma-O-alkyl (PAF) followed by fMLP activation. Reactive oxygen species generation as measured by superoxide anion production was enhanced in primed PMNs after hypoxemia. Protease degranulation as measured by elastase release was enhanced in both quiescent PMNs and primed PMNs after fMLP activation following the hypoxemic event. Adhesion molecule upregulation as measured by CD11b/CD18, however, was not significantly changed after hypoxemia. Apoptosis of quiescent PMNs was delayed after the hypoxemic event. TNFalpha, IL-1, IL-6, and IL-8 cytokine levels were unchanged following hypoxemia. These results indicate that relevant acute hypoxemic events observed in the clinical setting enhance several PMN cytotoxic functions and suggest that a transient hypoxemic insult may promote hyperinflammation.Shock 05/2002; 17(4):269-73. · 2.61 Impact Factor