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PubMed2005

Use of preservative-free lidocaine for cataract surgery in a patient allergic to "caines".

Although many patients have been labeled allergic to local anesthetics (LAs), true allergic reactions to LAs are rare. An 81-year-old woman with a history of procaine (Novocaine) allergy presented for cataract surgery. Skin testing showed sensitivity to amide and ester LAs. Further testing with preservative-free lidocaine was negative, suggesting the patient was allergic to ester LAs and preservatives found in amide anesthetic preparations. Cataract extraction was subsequently and uneventfully performed in both eyes with topical anesthesia using preservative-free lidocaine.

Aged↗
PubMed2001

From cocaine to ropivacaine: the history of local anesthetic drugs.

In 1850, about three centuries after the conquest of Peru by Pizzaro, the Austrian von Scherzer brought a sufficient quantum of coca leaves to Europe to permit the isolation of cocaine. As suggested by his friend Sigmund Freud, descriptions of the properties of the coca prompted the Austrian Koller to perform in 1884 the first clinical operation under local anesthesia, by administration of cocaine on the eye. The use of cocaine for local and regional anesthesia rapidly spread throughout Europe and America. The toxic effects of cocaine were soon identified resulting in many deaths among both patients and addicted medical staff. Local anesthesia was in a profound crisis until the development of modern organic chemistry which led to the synthesis of pure cocaine in 1891. New amino ester local anesthetics were synthesized between 1891 and 1930, such as tropocaine, eucaine, holocaine, orthoform, benzocaine, and tetracaine. In addition, amino amide local anesthetics were prepared between 1898 and 1972 including nirvaquine, procaine, chloroprocaine, cinchocaine, lidocaine, mepivacaine, prilocaine, efocaine, bupivacaine, etidocaine, and articaine. All of these drugs were ostensibly less toxic than cocaine, but they had differing amounts of central nervous system (CNS) and cardiovascular (CV) toxicity. Bupivacaine is of special interest because of its long duration of action and history of clinical application. Synthesized in 1957, the introduction of bupivacaine on the market in 1965 paralleled the progressive and cumulative reports of CNS and CV toxicity, leading to the restriction of its use and the identification of a special therapy-resistant CV toxicity. Numerous experimental studies were conducted to identify the fine cellular mechanism of this toxicity, which refines our understanding of the action of local anesthetics. The identification of optically active isomers of the mepivacaine family led to the selection of ropivacaine, a pure S-(-) enantiomer, whose toxicology was selectively and extensively studied before its introduction on the market in 1996. During the rapid and extensive use of ropivacaine in the clinic, unwanted side-effects have been found to be very limited.

Amides↗
PubMed1997

Hydrolytic profile for ester- or amide-linkage by carboxylesterases pI 5.3 and 4.5 from human liver.

Carboxylesterases (EC 3.1.1.1) from human liver were purified using Q-Sepharose, Sephadex G-150, isoelectrofocusing and Con A-Sepharose. The calculated molecular mass of the pI 5.3 enzyme was 120 kDa and 61 kDa from the results of Sephadex G-150 gel filtration and SDS-polyacrylamide gel electrophoresis (PAGE), respectively, suggesting that this enzyme is a dimer. On the other hand, carboxylesterase pI 4.5, with a molecular mass of 64 kDa, was a monomer. The activities of both enzymes were inhibited by typical serine enzyme inhibitors. Amino acid sequence analysis of the purified enzymes pI 5.3 and 4.5 showed high homology with rabbit carboxylesterase form 1 and 2, respectively. The results also suggested that carboxylesterase pI 5.3 is identical to the deduced amino acid sequence from cDNA for HU1, and that carboxylesterase pI 4.5 is identical to the deduced amino acid sequence from the cDNA registered as human carboxylesterase (hCE-2) in GenBank. We first purified carboxylesterase pI 4.5 and investigated its hydrolytic activity upon various drugs. The two enzymes differed in substrate specificity. Prodrugs of angiotensin-converting enzyme inhibitors, such as delapril and imidapril, were converted to active metabolites by carboxylesterase pI 5.3, but not by carboxylesterase pI 4.5. The hydrolysis velocity of temocapril by carboxylesterase pI 5.3 was 12-fold faster than by carboxylesterase pI 4.5. In contrast, aspirin, oxybutynin and procaine were hydrolyzed by only carboxylesterase pI 4.5. We also found that an amide-linkage in drugs, except for that in aniracetam, was not a good substrate for the two enzymes. Consequently, carboxylesterases pI 5.3 and 4.5 may be involved in the metabolism of various drugs containing an ester-linkage.

Amino Acid Sequence↗
PubMed1998

Memory-impairing effects of local anesthetics in an elevated plus-maze test in mice.

Post-training intracerebroventricular administration of procaine (20 micrograms/microliter) and dimethocaine (10 or 20 micrograms/microliter), local anesthetics of the ester class, prolonged the latency (s) in the retention test of male and female 3-month-old Swiss albino mice (25-35 g body weight; N = 140) in the elevated plus-maze (mean +/- SEM for 10 male mice: control = 41.2 +/- 8.1; procaine = 78.5 +/- 10.3; 10 micrograms/microliter dimethocaine = 58.7 +/- 12.3; 20 micrograms/microliter dimethocaine = 109.6 +/- 5.73; for 10 female mice: control = 34.8 +/- 5.8; procaine = 55.3 +/- 13.4; 10 micrograms/microliter dimethocaine = 59.9 +/- 12.3 and 20 micrograms/microliter dimethocaine = 61.3 +/- 11.1). However, lidocaine (10 or 20 micrograms/microliter), an amide class type of local anesthetic, failed to influence this parameter. Local anesthetics at the dose range used did not affect the motor coordination of mice exposed to the rota-rod test. These results suggest that procaine and dimethocaine impair some memory process(es) in the plus-maze test. These findings are interpreted in terms of non-anesthetic mechanisms of action of these drugs on memory impairment and also confirm the validity of the elevated plus-maze for the evaluation of drugs affecting learning and memory in mice.

Analysis of Variance↗
PubMed1989

Synthesis of macromolecular prodrugs of procaine, histamine and isoniazid.

The attachment of various drugs bearing -NH2 groups to poly-alpha,beta-aspartic acid as a biodegradable carrier afforded in good yields macromolecular prodrugs which were characterized with respect to composition and drug load by spectroscopic and analytical methods. N-Ethyl-N'-(3-dimethylaminopropyl)carbodiimide hydrochloride (EDC) in an aqueous medium proved to be useful in the attachment reaction. Isoniazid, procaine and histamine were covalently coupled as pendant groups onto poly-alpha,beta-aspartic acid via an amide bond. In principle, controlled release of the aforementioned drugs can be achieved by biodegradation of the polymer or by cleavage of covalently bound polymer-drug conjugates.

Chemical Phenomena↗
PubMed1987

[Allergy to local anesthetics].

Patch testing with the local anaesthetics benzocaine and caine mix frequently yields positive reactions. Their relevance with regard to local anaesthesia is not clear. We therefore performed prick and intracutaneous tests with a battery of local anaesthetics in a group on 104 patients with known contact allergic reactions to these substances. Prick testing always yielded negative results. Intracutaneous testing showed also only rare positive immediate and delayed hypersensitivity reactions. In addition, a clear correlation was seen between the sensitizing potential and chemical structure of the local anaesthetics. Substances with amide structure never showed, with the exception of butanilicaine, any positive reaction in contrast to procaine exhibiting an ester structure. From our results, it can be concluded that contact allergic patients can be subjected to injection local anaesthesia without a significant risk of allergic reaction. In addition, the results show the importance of the route of administration for the manifestation of an allergic reaction.

Anesthetics, Local↗
PubMed1993

Relative neural toxicity of local anesthetics.

In rat sciatic nerve, relative neural toxicity and relative motor nerve conduction blockade were assessed for two amide-linked local anesthetics (etidocaine and lidocaine) and two ester-linked local anesthetics (chloroprocaine and procaine). As measures of neural toxicity, nerve fiber injury and edema were assayed by light microscopic examination of nerve tissue sampled 2 days after perineural (next to the sciatic nerve) injection of various concentrations of the local anesthetics. Both nerve injury and edema increased with concentration of local anesthetics, but injury was frequently present in nerve fascicles with little or no edema. In parallel studies, the amplitude of the electrical activity elicited from the interosseous muscles of the foot following ipsilateral electrical stimulation at the sciatic notch was monitored for up to 15 minutes to assess the extent of motor nerve blockade. The resulting log concentration-response curves were analyzed for differences in potency. Both for injury and for conduction block, the order of decreasing potency was: etidocaine, lidocaine, chloroprocaine, procaine. These results are not consistent with the proposal that ester-linked agents are more likely than other local anesthetic agents to cause nerve injury.

Anesthetics, Local↗
PubMed1996

[Allergic reactions to local anesthetics].

In this article type I and type IV allergic reactions evoked by local anaesthetics are discussed. Contact dermatitis (type IV) reactions are mainly caused by local anaesthetics of the ester-type like procaine. Both contact dermatitis and anaphylactic reactions (type I) can be caused by anaesthetics of the amide-type (e.g. lidocaine), but these reactions are rare. Intra- and epicutaneous tests can be useful to prove allergy, but sometimes provocation tests are necessary. Many reactions are not caused by an allergic mechanism.

Anaphylaxis↗
PubMed2001

Inhibition of the Na,K-ATPase of canine renal medulla by several local anesthetics.

The ATPase activity of Na,K-ATPase-enriched membranes from canine renal medulla was determined in the absence of local anesthetic and in the presence of procaine, chloroprocaine, bupivacaine, mepivacaine, lidocaine, and two quaternary derivatives of lidocaine (QX-222 and QX-314) at 37( composite function)C. Chloroprocaine (IC(50)= 13 mM) had slightly greater potency than procaine (IC(50)= 17.7 mM). Bupivacaine (IC(50)= 6.7 mM) was more potent than its congener mepivacaine (IC(50)> 10 mM, the solubility limit). QX-222 (IC(50)> 600 mM) and QX-314 (IC(50)= 132 mM) had less potency than lidocaine (IC(50)= 30.4 mM). This study supports the interpretation that the uncharged forms of local anesthetics are much more potent inhibitors of Na,K-ATPase activity than the cationic forms.

Amides↗
PubMed1997

Structure-affinity relationships and stereospecificity of several homologous series of local anesthetics for the beta2-adrenergic receptor.

UNLABELLED: Local anesthetics inhibit binding of ligands to beta2-adrenergic receptors (beta2ARs), and, as a consequence, inhibit intracellular cAMP production. We hypothesized that among homologous local anesthetics, their avidity at inhibiting binding of tritiated dihydroalprenolol (3H-DHA) to beta2ARs would increase with increasing length of alkyl substituents and would demonstrate stereospecificity. Specific binding of 3H-DHA to human beta2ARs was assayed in the presence of six different members of the 1-alkyl-2,6-pipecoloxylidide class of local anesthetics (including mepivacaine, ropivacaine, and bupivacaine), the R(+) and S(-) bupivacaine enantiomers, lidocaine, prilocaine, etidocaine, procaine, and tetracaine. Avidity of binding to beta2ARs increased with increasing length of the alkyl chain (pKi values = 2.4, 3.6, 4.3, 4.1, 4.1, 5.9 for the methyl [mepivacaine], ethyl, S(-)propyl [ropivacaine], butyl [bupivacaine], pentyl, and octyl derivatives, respectively). We found no evidence for bupivacaine stereospecificity (pKi values = 4.3 and 4.9 for the S(-) and R(+) isomers, respectively). Other amide and ester local anesthetics also showed increasing potency with increasing length of alkyl substituents (pKi values = 3.6, 3.8, and 4.3 for lidocaine, prilocaine, and etidocaine; 4.2 and 5.6 for procaine and tetracaine, respectively). The correlation between increased inhibition of beta2AR binding and alkyl chain length resembles the correlation between local anesthetic potency at nerve block and increased alkyl chain length. The lack of clear stereospecificity is consistent with the relatively low potency these agents demonstrate at inhibition of beta2AR binding. Finally, the relatively potent inhibition of beta2ARs by etidocaine, tetracaine, and bupivacaine suggests that their propensity for cardiovascular depression after accidental intravenous overdose could result from beta2AR or beta1AR blockade and inhibition of cAMP production. IMPLICATIONS: Local anesthetics demonstrate a rank order of avidity for displacing ligands from beta2-adrenergic receptors such that larger molecules displace ligands at lower concentrations than smaller local anesthetic molecules. This relationship between molecular size and receptor avidity could explain the greater propensity for cardiovascular toxicity of relatively large local anesthetics such as bupivacaine.

Adrenergic beta-2 Receptor Antagonists↗