Safety of high volume lipid emulsion infusion: a first approximation of LD50 in rats.

Background: Lipid infusion reverses systemic local anesthetic toxicity. The acceptable upper limit for lipid administration is unknown and has direct bearing on clinical management. We hypothesize that high volumes of lipid could have undesirable effects and sought to identify the dose required to kill 50% of the animals (LD(50)) of large volume lipid administration.

Epinephrine impairs lipid resuscitation from bupivacaine overdose: a threshold effect.

Background: Lipid emulsion infusion reverses local anesthetic-induced cardiac toxicity, but the effect of adding epinephrine has not been studied. We compared escalating doses of epinephrine on recovery with lipid infusion in a rat model of bupivacaine overdose.

Methods: Rats anesthetized with isoflurane received an IV bolus of 20 mg/kg bupivacaine, producing asystole (zero time) in all animals.

Lipid emulsion is superior to vasopressin in a rodent model of resuscitation from toxin-induced cardiac arrest.

Objectives: Lipid emulsion infusion is an emerging antidotal therapy for toxin-induced cardiac arrest. To compare the efficacy of resuscitation from bupivacaine-induced asystole using lipid emulsion infusion vs. vasopressin, alone and with epinephrine.

Resuscitation with lipid versus epinephrine in a rat model of bupivacaine overdose.

Background: Lipid emulsion infusion reverses cardiovascular compromise due to local anesthetic overdose in laboratory and clinical settings. The authors compared resuscitation with lipid, epinephrine, and saline control in a rat model of bupivacaine-induced cardiac toxicity to determine whether lipid provides a benefit over epinephrine.

Methods: Bupivacaine, 20 mg/kg, was infused in rats anesthetized with isoflurane, producing asystole in all subjects.

Metabolic context affects hemodynamic response to bupivacaine in the isolated rat heart.

Previous studies have demonstrated that the local anesthetic bupivacaine selectively inhibits oxidative metabolism of fatty acids in isolated cardiac mitochondria. In the present investigation, we compare the development of bupivacaine cardiotoxicity during fatty acid and carbohydrate metabolism. Hearts from adult male Sprague-Dawley rats were excised and retrograde perfused with a solution containing fatty acid (oleate or octanoate) or carbohydrate substrates for cardiac metabolism.

Cytochrome oxidase deficiency protects Escherichia coli from cell death but not from filamentation due to thymine deficiency or DNA polymerase inactivation.

Temperature-sensitive DNA polymerase mutants (dnaE) are protected from cell death on incubation at nonpermissive temperature by mutation in the cydA gene controlling cytochrome bd oxidase. Protection is observed in complex (Luria-Bertani [LB]) medium but not on minimal medium. The cydA mutation protects a thymine-deficient strain from death in the absence of thymine on LB but not on minimal medium.

Cell death in Escherichia coli dnaE(Ts) mutants incubated at a nonpermissive temperature is prevented by mutation in the cydA gene.

Cells of the Escherichia coli dnaE(Ts) dnaE74 and dnaE486 mutants die after 4 h of incubation at 40 degrees C in Luria-Bertani medium. Cell death is preceded by elongation, is inhibited by chloramphenicol, tetracycline, or rifampin, and is dependent on cell density. Cells survive at 40 degrees C when they are incubated at a high population density or at a low density in conditioned medium, but they die when the medium is supplemented with glucose and amino acids.