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Biomedical subjects

M S Liu

Publications and source records attributed to M S Liu.

At least 109 records · Page 6Linked to original sources
PubMed1981

In vitro effects of E coli endotoxin on K+-activated para-nitrophenylphosphatase activity and ouabain binding in dog hearts.

The in vitro effect of E coli endotoxin on the activity of K+-activated paranitrophenylphosphatase (K+-PNPPase), an enzyme which represents the partial activity of (Na+ + K+)-ATPase enzyme system, was studied in isolated adult dog heart myocytes. The results were correlated with ouabain-binding studies. Endotoxin had an inhibitory effect on the Vmax for K+ activation as well as the Vmax for Mg++ and para-nitrophenylphosphate (PNPP) saturation. The inhibition was concentration-dependent and noncompetitive with K+, Mg++, and PNPP and furthermore, reversible. Endotoxin did not displace the bound 3H-ouabain from receptor sites nor did it affect the capacity of ouabain binding, indicating that the total enzyme concentration was not altered. From these findings, it is concluded that endotoxin in vitro affects the myocardial (Na+ + K+)-ATPase enzyme system by decreasing the turnover number of the enzyme molecule. The ability of endotoxin to modify myocyte membrane-associated enzyme activity may be responsible for altered heart metabolism and function in endotoxemia.

4-Nitrophenylphosphatase↗
PubMed1981

Effect of E coli endotoxin on the leakage of 14C-sucrose from phosphatidylcholine liposomes.

The effect of E coli endotoxin on the leakage of 14C-sucrose from phosphatidylcholine liposomes in the absence or presence of Ca2+ was studied. Endotoxin decreased the leakage from liposomes from 27% to 4% in 5 hr when Ca2+ (1 mM) was incorporated into liposomes during sonication. The effect of endotoxin on the leakiness of liposomes was concentration dependent. Ca2+ alone increased the leakage of 14C-sucrose from liposomes. Mg2+ at concentrations higher than 5 mM exhibited an effect similar to that of Ca2+. These findings suggest that endotoxin increases the molecular packing of phosphatidylcholine bilayers in the presence of Ca2+ or Mg2+. A change in the physical state of membrane lipid bilayers induced by endotoxin may affect the function of biological membranes.

Calcium↗
PubMed1981

Influence of Escherichia coli endotoxin on palmitate, glucose, and lactate utilization by isolated dog heart myocytes.

The in vitro effects of E. coli 0127:B8 endotoxin on the oxidation of palmitate, glucose, and lactate by isolated, beating, adult dog heart myocytes were studied. The result were correlated with the in vitro effect of endotoxin on the transport of palmitate and glucose by using their respective analog, hexadecanol and 3-O-methyl-D-glucose. Endotoxin decreased palmitate but increased glucose and lactate oxidation in a dose-dependent manner. The changes in palmitate and lactate oxidation induced by endotoxin could not be corrected by addition of L-carnitine to the reaction mixture. The transport of hexadecanol or of 3-O-methyl-D-glucose was not affected by endotoxin. These results suggest that the endotoxin-induced alteration in palmitate and glucose oxidation by the heart is not the result of an impairment in metabolite transport, but rather a defect in the subsequent intracellular oxidative processes.

Animals↗
PubMed1979

Changes in surface charge density on liposomes induced by Escherichia coli endotoxin.

Changes in surface charge density of liposomes induced by E. coli endotoxin were studied by microelectrophoresis. Endotoxin altered the surface charge of phosphatidylcholine liposomes from neutral to negative. The negative charge of the endotoxin-phosphatidylcholine complex was neutralized electrostatically by binding with Ca2+ (2 mM). Phosphatidylcholine liposomes were made positive by addition of the positively charged detergent, hexadecyltrimethylammonium chloride. Endotoxin made the positively charged liposomes less charged. On the other hand, phosphatidylserine liposomes which were negatively charged became less charged in the presence of high concentration of endotoxin (8 mg/ml). The endotoxin effect on phosphatidylserine liposomes was abolished by EDTA (1 mM) but potentiated by CaCl2 (0.1--2 mM). These results indicate that endotoxin interacts with liposomes both hydrophobically and electrostatically.

Endotoxins↗
PubMed1979

Comparison of radiopaque perfluorocarbon and Ethiodol in lymphography.

Lymphangiography was performed on 40 adult cats, 39 dogs, 20 rabbits, and 12 rats of mixed sex using Ethiodol or radiopaque perfluorocarbon (BPC). Ethiodol was more radiodense than RPC, but imaging of lymph channels and nodes was satisfactory with the latter. RPC could be infused rapidly, while Ethiodol infusion was time consuming. RPC was biologically inert; Ethiodol produced both local and systemic inflammatory reactions. The lymph node distribution with RPC was more uniform and persisted for longer periods. It was concluded that RPC was an improvement over Ethiodol for lymphangiography.

Animals↗
PubMed1979

Effect of endotoxin on hepatic pyruvate kinase activity in normal and diabetic dogs.

The influence of endotoxic administration (0.5 mg/kg) on hepatic pyruvate kinase activity in normal (nondiabetic) and diabetic dogs was investigated. Pyruvate kinase activity was not affected four hours after endotoxin injection in nondiabetic dogs. However, it was stimulated by 288% in dogs that were made diabetic prior to the administration of endotoxin. Since pyruvate kinase activity in diabetic dogs without endotoxin treatment was not affected, these findings suggest that the stimulatory effect of endotoxin on pyruvate kinase activity in diabetic dogs may be associated with insulin deficiency and/or high ambient blood glucose level.

Animals↗
PubMed1978

Fatty acid and lactate metabolism by heart homogenates from alloxan-diabetic dogs.

Myocardial homogenates from control of alloxan-diabetic dogs were incubated in the presence of lactate or palmitate as the sole substrate. The rate of lactate oxidation of the homogenates from diabetic dogs was less than half of the oxidation rate of homogenates from control animals. The incorporation of labelled palmitate into triglyceride was greatly enhanced in the heart taken from diabetic animals. The tissue concentration of l-carnitine was twice and that of triglyceride was three times as high in the diabetic animals as in their control counterparts. Thus the myocardium of diabetic animals exhibited both altered substrate utilization and increased rate of triglyceride synthesis.

Adenosine Triphosphate↗