Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IVFE infusion can impair lung function in healthy adults, premature infants, and adults with pre-existing lung injury, and in experimental animals with acute injury. Although all observed IVFE-related lung dysfunction was initially attributed to the temporally associated hyperlipemia, this explanation may in fact be correct only with fat overload syndrome. When serum triglyceride levels are in a more appropriate range, all subsequent studies have shown the same alterations in lung function unrelated to triglyceride increases and indomethacin-related blocking of lung function impairment, despite comparable serum triglyceride increases. Furthermore, our studies with Liposyn demonstrated the most significant increases in serum triglyceride levels, but the smallest PaCO2 and PaO2 changes. In general, the lung function abnormalities associated with IVFE infusion have thus been caused by increases in VA/Q inequalities. Although elucidation of the relationship between IVFE-related increased PG production and secondary VA/Q changes may be of significant physiologic import, the PaO2 and PaCO2 changes even with pre-existing lung injury have generally not been of sufficient magnitude to be of much clinical significance. The IVFE-related increases in plasma PG concentrations may, however, still have significant nonpulmonary clinical effects related to known or postulated consequences of increased plasma PG concentrations, including effects on ductus arteriosus patency, retinal and cerebral blood flow, and immune competence.
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PMID:Fat emulsions and lung function. 308 79

The purpose of this study is to better understand how hyperlipidemia alters the modulating action of prostaglandin E1 (PGE1) on platelet function. Using our previously characterized rat model of atherogenesis, we demonstrate that the parenteral lipid emulsions, Lipofundin-S and Liposyn, significantly (p < or = 0.05) enhance baseline platelet aggregation. In addition, dose response curves show that in all animals, PGE1 substantially inhibits platelet aggregation at 10(-7) to 10(-6) M, while significantly stimulating platelet function at lower doses. However, at all PGE1 concentrations, aggregation values are higher in platelets from lipid-treated vs. control rats, showing that hyperlipidemia significantly reduces the ability of high concentrations of PGE1 to inhibit platelet activity, based on the absolute values of the controls. Also, dose response curves for PGE1 on platelet aggregation show a marked similarity in shape for control ratsvs. normal humans. Thus, this study demonstrates that hyperlipidemia significantly alters the platelet modulating action of prostaglandin E1, and it shows that PGE1 can either inhibit or stimulate platelet activity in both rat and human platelets.
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PMID:The effect of parenteral lipid emulsion-induced hyperlipidemia on prostaglandin E1 modulation of platelet function. 801 Aug 86