The displacement of membrane calcium by a local anesthetic (chlorpromazine)

Kwant, W.O.; Seeman, Philip

doi:10.1016/0005-2736(69)90194-1

Cited by 140 publications

(31 citation statements)

References 64 publications

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“…It antagonizes the binding of calcium and other ions to phospholipids (Feinstein, 1964;Blaustein & Goldman, 1966a). Local anaesthetics displace calcium from red blood cell membranes (Kwant & Seeman, 1969) and are competitive inhibitors of the .binding of mono-and divalent cations to submitochondrial particles (Scarpa & Azzi, 1968). A decrease in membrane permeability by local anaesthetics appears to be related to membrane phospholipase activity (Scherphof et al, 1972).…”

Section: Discussionmentioning

confidence: 99%

E. col/ ENDOTOXIN SHOCK IN THE DOG; TREATMENT WITH LIDOCAINE OR INDOMETHACIN

Fletcher

Ramwell

1978

British J Pharmacology

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1 Dogs treated with lidocaine (1 mg kg-' h-1) or indomethacin (1.5 mg/kg) before and after an LD60 dose (1 mg/kg) of E. coli endotoxin survived for at least 72 h.2 Although all dogs in both treated groups survived, only those treated with indomethacin were significantly protected against the fall in the arterial blood pressure 1 to 2 min following endotoxin administration.3 Endotoxin increased the plasma prostaglandin F2Q (PGF2,) concentration in the control and lidocaine-ireated groups, however, no increase was observed with indomethacin treatment. 4 Neither lidocaine nor indomethacin alone had any significant effect on the parameters measured in this model.5 Following the administration of endotoxin, lidocaine-treated animals had significantly decreased plasma fibrinogen concentrations when compared to the other groups.6 This study suggests that lidocaine, a local anaesthetic and a drug widely used for cardiac arrhythmias, might offer protection in endotoxin shock. ImtrodUctiomPrevious work in this laboratory (Fletcher, Herman & Ramwell, 1976a;Fletcher, Ramwell & Herman, 1976b;Fletcher & Ramwell, 1977) has documented increased plasma prostaglandin concentrations following the administration of endotoxin intravenously in dogs and primates. The increases in prostglandins were related in time to changes in circulatory function. Therapeutic doses of analgesic-antipyretic drugs given before and after administration of endotoxin diminished the early haemodynamic changes and prevented the increase in the prostaglandins, but failed to improve the survival in the lethal (LD1oo) baboon model. In contrast, in the LD50 dog model, these drugs did improve the survival and the early circulatory function while inhibiting the synthesis of the prostaglandins. Although the prostaglandins were elevated as early as 1 to 2 min after the endotoxin administration, their relationship to the pathophysiology of endotoxin shock is unclear.The analgesic-antipyretic drugs do improve circulatory function and survival in canine endotoxin shock but the exact mechanism by which they exert a beneficial effect is unknown. We demonstrated (Fletcher & Ramwell, 1977) that while indomethacin or aspirin

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Section: Discussionmentioning

confidence: 99%

E. col/ ENDOTOXIN SHOCK IN THE DOG; TREATMENT WITH LIDOCAINE OR INDOMETHACIN

Fletcher

Ramwell

1978

British J Pharmacology

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“…However, a side-effect of chlorpromazine, on calcium associated to membranes for example, cannot be excluded (9). CCCP, which inhibits mitochondrial Ca"+ uptake, has no effect on microsomes isolated from green spinach leaves in the presence or in the absence of calmodulin.…”

Section: Methodsmentioning

confidence: 97%

Distribution of Calmodulin-Stimulated Ca²⁺ Transport into Membrane Vesicles from Green Spinach Leaves

Stosic¹,

Penel²,

Marmé³

et al. 1983

Plant Physiol.

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A microsomal fraction isolated from green spinach leaves exhibited a Mg2+ and ATP-dependent 4GCa2+ uptake. Addition of 10 micromolar carbonyl cyanide ,n-chlorophenylhydrazine had no effect. The cationophore A23187 (10 micromolar) induced the release of 4"Ca2+ accumulated by membrane vesicles. Membranes prepared from lower epidermis showed the highest Ca2' accumulation activity. Microsomal fractions from petiole, lamina, and midrib were less active. The stimulation by bovine brain calmodulin was about 30% for the lower epidermis, 23.5% for midrib, and below 20% for petiole and lamina.

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“…Ca++ binding was also measured by equilibrium dialysis. In a standard assay, 0.4 mg of protein in 0.4 ml was dialyzed for 40 hr at 12'C against 100 ml of a solution of 5 mM Tris -HC1 (pH 7.5)-0.1 mM CaCl2, to which was added 45Ca++ (to a specific activity of [25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40] cpm/nmol). Samples were dissolved in "Aquasol" (New England Nuclear) and counted in a scintillation spectrometer.…”

Section: Methodsmentioning

confidence: 99%

Isolation of a Calcium-Sequestering Protein from Sarcoplasmic Reticulum

MacLennan

Wong

1971

Proc. Natl. Acad. Sci. U.S.A.

490

214

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An acidic protein has been extracted from sarcoplasmic reticulum with KCI and deoxycholate. believe that it is a major binding site for calcium in sarcoplasmic reticulum. We propose that the protein be designated Calsequestrin. MATERIALS AND METHODSPreparation of the calcium-sequestering proteinStep 1. Sarcoplasmic reticulum was prepared from two 14.4-kg albino rabbits and was extracted with deoxycholate as described (8), except that dithiothreitol (1 mM) was present during the extraction and the supernatant, after centrifugation at 165,000 X g, was retained as the source of the binding protein. The deoxycholate extract (about 80 ml) was dialyzed, first for 4 hr and then for 18 hr at 12'C, against 3 liters of 5 mM Tris * HCl, pH 7.5. At 4 and 22 hr, insoluble protein was removed by centrifugation at 165,000 X g for 30 min.Step 2. The supernatant solution (35-to 40-ml aliquot) was passed through a 1.5 X 18 cm column of DEAE-cellulose and the column was eluted with 400 ml of 5 mM Tris -HCl, pH 7.5, that contained a linear gradient of KCl from 0 to 0.7 M. The last peak to be eluted, at a KCl concentration of about 0.48 M, was collected, concentrated by ultrafiltration under pressure (Amicon Diaflo apparatus) to 8 ml, and dialyzed overnight against a solution of 0.15 M KCl-0.01 M Tris -HCl, pH 8.0.Step 3. The dialyzed sample was passed through a 2.5 X 40 cm column of Sephadex G-200 equilibrated with 0.15 M KCl-0.01 AM Tris HCl, pH 8.0. Material absorbing at 280 nm was eluted in a sharp peak at the void volume, in a second symmetrical peak, and in a tail following the second peak. Fractions making up the second symmetrical peak were collected, concentrated by Diaflo filtration to 10 ml, and dialyzed overnight against 10 mM potassium phosphate, pH 7.0.Step 4. The dialyzed sample was applied to a column (7 g) of hydroxylapatite (Biogel HTP) equilibrated with 10 mM potassium phosphate pH 7.0. The column was eluted with 400 ml of a linear gradient of potassium phosphate from 10 to 600 mM. The last peak to be eluted, at a phosphate concentration of about 330 mM, was concentrated to 5 ml and dialyzed overnight against a solution of 5 mM Tris .HC1, pH 7.5. The solution, containing purified protein (about 1 mg per ml), was stored at -20°C. Analytical methodsCalcium transport was measured (10) at a protein concentration of 200 ug/ml. After 10 min at 24°C, 0.5 ml was filtered

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The displacement of membrane calcium by a local anesthetic (chlorpromazine)

Cited by 140 publications

References 64 publications

E. col/ ENDOTOXIN SHOCK IN THE DOG; TREATMENT WITH LIDOCAINE OR INDOMETHACIN

E. col/ ENDOTOXIN SHOCK IN THE DOG; TREATMENT WITH LIDOCAINE OR INDOMETHACIN

Distribution of Calmodulin-Stimulated Ca²⁺ Transport into Membrane Vesicles from Green Spinach Leaves

Isolation of a Calcium-Sequestering Protein from Sarcoplasmic Reticulum

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The displacement of membrane calcium by a local anesthetic (chlorpromazine)

Cited by 140 publications

References 64 publications

E. col/ ENDOTOXIN SHOCK IN THE DOG; TREATMENT WITH LIDOCAINE OR INDOMETHACIN

E. col/ ENDOTOXIN SHOCK IN THE DOG; TREATMENT WITH LIDOCAINE OR INDOMETHACIN

Distribution of Calmodulin-Stimulated Ca2+ Transport into Membrane Vesicles from Green Spinach Leaves

Isolation of a Calcium-Sequestering Protein from Sarcoplasmic Reticulum

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Distribution of Calmodulin-Stimulated Ca²⁺ Transport into Membrane Vesicles from Green Spinach Leaves