No abstract

The effects of local, i.v. and volatile anaesthetic agents on locomotion of human blood leucocytes were studied in vitro. Blood neutrohpils and monocytes and PHA-activated lymphocytes were allowed to migrate in filters towards standard chemotactic agents and the effect of adding anaesthetic agents to the system was measured. The results showed that locomotion of all cell types was depressed reversibly by all classes of anaesthetics used at clinical concentrations. The pattern of depression varied according to the cell type under study and the class of anaesthetic used. The action of anaesthetics on chemically stimulated locomotion of leucocytes was analysed. It was concluded that the principal action of these drugs is primarily on the mechanism of locomotion itself, rather than on the capacity of the cells to detect and respond to concentration gradients of attractants. Serum albumin can protect against the inhibitory action of anaesthetics.

No abstract

No abstract

The binding to neutrophil leukoyctes of human serum albumin (HSA), which is chemokinetic for leukocytes, i.e. influences their rate of locomotion, and of alkali-denatured HSA, which is chemotactic for leukocytes, i.e. influences their direction of locomotion, was studied. Native serum albumin showed low affinity binding to the neutrophil surface. Denatured serum albumin showed saturable binding with a Ka of approximately 1-(6) litres per mole to about 10(6) binding sites per cell. Another protein chemotactic factor, alpha5-casein, gave similar binding. These results exclude that chemotactic reactions to denatured proteins are mediated in a completely non-specific manner and suggest the presence on the cell of a restricted number of defined recognition sites. Binding was reduced following treatment of the cells with either of two lipid-specific bacterial toxins, perfringolysin, the theta-toxin of Clostridium perfringens, an oxygen-labile cholesterol-specific toxin, and Staphylococcus aureus Sphingomyelinase C. Both have previously been shown to reduce chemotactic reactions and both were used at doses which did not reduce cell viability. These results suggest an important, and possiblly direct, role for membrane lipid in the binding sites for chemotactic factors. Visual analysis of the behaviour of perfringolysin-treated neutrophils showed that these cells were still capable of chemotactic locomotion. The cells appeared to be less efficient than normal in detecting chemotactic gradients only when at a distance from the gradient source, a finding which is consistent with reduced binding of the chemotactic factor to the cell surface.

No abstract

No abstract

Metabolic acidosis is a common metabolic derangement present in the acute medical patient. A thorough and structured investigative approach is required as there are many causes and management is reliant on identifying these. In particular calculation of the anion gap with correction for albumin level and use of the delta ratio can be helpful in complex cases especially in patients where a combination of metabolic derangements may be present.