PubMed · 8759600
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M S Chattman. 1996. Shoulder reduction.. https://doi.org/10.1016/s0196-0644(96)70073-2
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The purpose of this study is to characterize the effects of local anaesthetics on Na,K-ATPase activity. The ATPase activity of Na, K-ATPase-enriched membranes from canine renal medulla was determined in the absence and in the presence of lidocaine, procaine, tetracaine, benzocaine, bupivacaine, prilocaine, and procainamide at 37 and 25 degrees C. All of these local anaesthetics, except benzocaine, inhibit the activity of the Na,K-ATPase of canine renal medulla at both 25 and 37 degrees C. Benzocaine inhibits Na,K-ATPase activity at 37 degrees C, but stimulates activity at 25 degrees C. The influence of lidocaine on stimulation of Na,K-ATPase activity by Na(+) and K(+) was investigated. Lidocaine increases the apparent K(0.5) of the Na,K-ATPase for both Na(+) and K(+) and decreases the V(max) values for both ions. IC(50) values for lidocaine increase with increasing concentrations of both Na(+) and K(+). The data indicate that lidocaine diminishes the affinity of the Na,K-ATPase for Na(+) and K(+) and that binding of Na(+) or K(+) decreases the potency of lidocaine as an inhibitor of the Na,K-ATPase. Lidocaine markedly decreases the affinity of the Na,K-ATPase for ouabain, but only slightly diminishes the maximum amount of ouabain bound. Unprotonated lidocaine is apparently a more potent inhibitor than is the protonated form.
Local anesthetics impair certain functions of neutrophils, and phospholipase D (PLD) is considered to play an important role in the regulation of these functions. To understand the mechanisms by which local anesthetics suppress the functions of neutrophils, we examined the effects of local anesthetics on PLD in neutrophil-like differentiated human promyelocytic leukemic HL60 cells. Tetracaine, a local anesthetic, inhibited formyl-methionyl-leucyl-phenylalanine (fMLP)- and 4beta-phorbol 12-myristate 13-acetate (PMA)-induced PLD activation, but potentiated fMLP-stimulated phospholipase C activity. All four local anesthetics tested suppressed PMA-induced PLD activation to different extents, and the order of their potency was tetracaine > bupivacaine > lidocaine > procaine. In a cell-free system, tetracaine suppressed guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS)-induced PLD activation as well as PMA-induced PLD activation. Western blot analysis revealed that tetracaine prevented the membrane translocation of PLD-activating factors, ADP-ribosylation factor, RhoA, and protein kinase Calpha. Tetracaine also inhibited the activity of recombinant hPLD1a in vitro. These results suggest that local anesthetics suppress PLD activation in differentiated HL60 cells by preventing the membrane translocation of PLD-activating factors, and/or by directly inhibiting the enzyme per se. Therefore, it could be assumed that local anesthetics would suppress the functions of neutrophils by inhibition of PLD activation.
Previous work in our laboratory indicates that the nuclear matrix protein lamin B is a "prompt" heat shock protein, which increases significantly when human U-1 melanoma and HeLa cells are exposed to 45.5 degrees C for 5-40 min. Using Western blotting, we found that the lamin B content in U-1 and HeLa cells increased to a greater extent during post-heat incubation at 37 degrees C than during the heat dose itself. When HeLa cells were heated at 45.5 degrees C for 30 min, and then incubated at 37 degrees C for up to 7 h, lamin B content was increased significantly (1.69-fold maximum increase at 3 h) compared to unincubated heated cells. Also, thermotolerant HeLa cells showed a greater increase (up to 1.72-fold) in lamin B content during subsequent heating compared to nontolerant cells. The increase in lamin B content in thermotolerant cells, or when heated cells were incubated at 37 degrees C, was also observed in U-1 cells. HeLa cells heated in the presence of glycerol (a heat protector) showed a 1.21-1.72-fold increase in lamin B content compared to cells heated for 10-30 min without glycerol. In contrast, lamin B content decreased 1.23-1.85-fold when cells were heated for 10-30 min in the presence of procaine (a heat sensitizer) compared to cells heated without procaine. These data suggest that lamin B may play an important role in the heat shock response, and that modulation of lamin B content by heat sensitizers or protectors may play a role in regulation of heat sensitivity.