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PubMed1982

Antigen-specific suppression of type II collagen-induced arthritis by collagen-coupled spleen cells.

The induction of arthritis in Wistar-Lewis rats was suppressed by i.v. injections of spleen cells coupled to native type II collagen, beginning 14 days before intradermal injection of native type II collagen in incomplete Freund's adjuvant and continuing at 7-day intervals for the next 3 weeks. Cells coupled to native type I collagen or to denatured type II collagen were ineffectual, suggesting antigen-relevant cells were required for suppression. The phenomenon appeared to be mediated by a humoral effector mechanism; IgG antibody titers but not hemagglutinating antibody titers or delayed-type hypersensitivity to collagen were decreased by the injection of type II collagen-coupled cells. These data demonstrate the potential of antigen-specific immunotherapy for autoimmune disease.

Animals↗
PubMedDate not supplied

The peripheral analgesic effect of tramadol in reducing propofol injection pain: a comparison with lidocaine.

BACKGROUND AND OBJECTIVES: Tramadol and metoclopramide have a local anesthetic effect similar to lidocaine following intradermal injection. When metoclopramide was retained in the venous system for 1 minute, it was found to be as effective as lidocaine in reducing propofol injection pain. Using this metoclopramide model, the effects of tramadol in reducing pain on propofol injection was investigated. METHODS: One hundred five patients were randomly allocated to receive 50 mg tramadol (group T), 60 mg lidocaine (group L), or normal saline (group NS) as pretreatment to reduce pain on propofol injection. Following venous occlusion with a tourniquet (70 mm Hg), one of the drugs was intravenously administered. Venous retention of the drug was maintained for 1 minute. Immediately after the tourniquet release, intravenous injection of 100 mg propofol (10 mL) at a rate of 0.5 mL/s followed. Pain assessment was made after each injection. RESULTS: Transient minor injection pain and local skin reactions were significantly greater with tramadol than with lidocaine (P < .05). Both tramadol and lidocaine significantly reduced the incidence and intensity of propofol injection pain when compared with normal saline (P < .05). CONCLUSIONS: Using -minute retention in veins, both tramadol and lidocaine significantly reduced propofol injection pain. A local anesthetic activity is postulated.

Adult↗
PubMed1995

Alpha 1-adrenoceptor-mediated sympathetically dependent mechanical hyperalgesia in the rat.

The model of rolipram (a type IV phosphodiesterase inhibitor) induced prolongation (> 3 days) of the mechanical hyperalgesia produced by the intradermal injection of prostaglandin E2 in the hairy skin of the hindpaw of the rat, measured by the Randall-Selitto paw-withdrawal test, was employed to study mechanisms involved in the contribution of the sympathetic postganglionic neuron to mechanical hyperalgesia. Lumbar surgical sympathectomy prevented rolipram-induced prolongation of prostaglandin E2 hyperalgesia. Decentralization of sympathetic postganglionic neurons innervating the hindpaw did not, however, effect rolipram-induced prolongation of prostaglandin E2 hyperalgesia. Phentolamine, an alpha-adrenoceptor antagonist, and prazosin, an alpha 1-selective adrenoceptor antagonist, when given systemically or intradermally at the site of injection of prostaglandin E2 and rolipram, blocked rolipram-induced prolongation of prostaglandin E2 hyperalgesia. Intrathecal administration of phentolamine and prazosin were, however, without effect on rolipram-induced prolongation of prostaglandin E2 hyperalgesia. Yohimbine, an alpha 2-adrenoceptor antagonist given systemically, intradermally or intrathecally also did not produce any alteration in rolipram-induced prolongation of prostaglandin E2 hyperalgesia. We propose that sympathetic postganglionic neurons are involved in rolipram-induced prolongation of prostaglandin E2 hyperalgesia and that this form of sympathetically dependent hyperalgesia, which is independent of activity in preganglionic sympathetic neurons, is mediated by a peripheral alpha 1-adrenergic mechanism.

Adrenergic alpha-1 Receptor Agonists↗
PubMed2001

Systemic distribution of Staphylococcus aureus following intradermal footpad challenge of broilers.

We conducted an experiment with broilers to determine if prior exposure to Staphylococcus aureus would facilitate the systemic infiltration of this pathogen following intradermal footpad challenge with live S. aureus. Litter-raised broilers were sensitized at 3 and 4 wk of age with s.c. injections in the neck with heat-killed S. aureus diluted in polyethylene glycol (PEG). Equal numbers of control birds were injected at the same times with PEG. At 7 wk of age, chicks previously sensitized to killed S. aureus or injected with PEG were injected intradermally in the right footpad with PBS or live S. aureus. The left footpads of all birds were injected with PBS. The difference in thickness between the right and left footpads was determined at 0, 24, and 48 h postchallenge. Blood, liver, spleen, lung, and synovial fluid were collected six times between 1 and 48 h postchallenge to determine the recovery of S. aureus. Sensitized and non-sensitized birds showed footpad swelling following challenge with live S. aureus in the right footpad (P < 0.001). Injection of PBS did not induce footpad swelling. Birds injected in the footpads with live S. aureus as compared to PBS had significantly higher isolation rates of S. aureus in the spleen, liver, and blood; however, recovery of S. aureus from S. aureus-sensitized and PEG-injected birds was not significantly different. Time postchallenge (1, 3, 7, 11, 24, and 48 h) had no significant effect on the recovery of S. aureus. It was concluded that the intradermal challenge of the footpad with S. aureus resulted in systemic infiltration of S. aureus into the spleen, liver, and blood. Prior exposures to killed S. aureus as compared to PEG controls did not affect the systemic distribution of S.

Analysis of Variance↗
PubMed2001

Intraoperative lymphatic mapping and sentinel node identification with blue dye in patients with vulvar cancer.

OBJECTIVE: To determine the effectiveness of intraoperative lymphatic with blue dye alone as a means of localizing sentinel nodes in patients with vulvar cancer. METHODS: All patients undergoing primary surgical treatment for vulvar cancer were eligible for this prospective study. Isosulfan blue dye was injected intradermally at the edge of the primary tumor closest to the adjacent groin. Bilateral dye injections and groin dissections were performed if the tumor was within 2 cm of the midline. RESULTS: Fifty-two patients were enrolled in the study between 1993 and 1999. The median age was 58 years. Eighty-seven percent of the patients had T1 or T2 lesions, and 92% had nonsuspicious lymph nodes on palpation. Sixty-seven percent of the patients had squamous cell carcinoma; the remaining patients had melanoma or adenocarcinoma. The sentinel node was identified in 46 of the 52 patients (88%), comprising 22 of the 25 patients with lateral tumors and 24 of the 27 patients with midline lesions. The sentinel node was successfully identified in 57 of the 76 (75%) dissected groins. Sentinel node identification in the groin was hampered by the effects of prior excisional biopsy vs punch biopsy (11 of 25 vs 8 of 51, P = 0.007) and by the lateral vs midline location of the tumor (22 of 25 groins vs 35 of 51 groins, P = 0.067). During the first 2 years (1993-1994), a sentinel node could not be identified in 4 of the 25 (16%) patients and 13 of the 36 (36%) groins dissected, compared with 2 of the 27 (7%) of patients treated and 6 of the 40 (15%) groins dissected from 1995 through 1999 (P = 0.034). A total of 556 nodes were removed (median, 7 per groin), of which 83 (median, 1 per groin) were sentinel. The sentinel node was not identified in 2 of the 12 groins that proved to have metastatic disease. Both events occurred in the first 2 years of the study. There were no false-negative sentinel nodes. Since 1995, we have successfully identified the sentinel node in 16 of the 16 patients (25 of 25 groins) with T1 or T2 primary lesions, squamous histology, and nonsuspicious groin nodes on physical examination. CONCLUSIONS: Experience and careful patient selection can permit sentinel node identification with blue dye injection alone in more than 95% of patients with vulvar cancer.

Adolescent↗
PubMed1997

Synergistic interactions between neuropeptide and histamine on the capillary permeability in rat skin: evaluation by reflectance spectrophotometry.

Effects of neuropeptides on capillary permeability and their interactions with histamine (HIS) in rat skin were investigated. The capillary permeability was measured continuously by reflectance spectrophotometry after intravenous (iv) injection of Evans blue dye. The capillary permeability was increased dose-dependently by the intradermal injection of HIS (0.3-100 microg/site) and substance P (SP; 25-250 ng/site). Calcitonin gene-related peptide (80-800 ng/site) elicited a significant but less increase than did SP. Capsaicin (30 microg/site) also increased capillary permeability slightly but significantly, suggesting the release of endogenous neuropeptides. Both diphenhydramine (DPH; 3 mg/kg, iv) and cimetidine (CIM; 30 mg/kg, iv) reduced HIS-induced responses. DPH also reduced the SP-induced response significantly, but CIM did not. An SP antagonist, [D-Pro2, D-Trp7,9]-SP (1.3 mg/kg, iv), reduced not only SP- but also HIS-induced responses. Furthermore, the HIS-induced response was attenuated by pretreatment with epicutaneous capsaicin for 4 days, depleting endogenous SP. These results delineate the synergistic interactions between SP and HIS in rat skin and suggest the participation of neuropeptides in increasing capillary permeability.

Administration, Cutaneous↗
PubMed1992

In vivo transfection of bovine leukemia provirus into sheep.

Bovine leukemia virus is horizontally transmitted mainly through infected cells by direct blood transfer. In this report, a cloned bovine leukemia virus (BLV) provirus was examined for its infectivity by direct inoculation into sheep. One hundred micrograms of plasmid DNA containing a complete provirus was mixed with a cationic liposome solution and injected intradermally into five sheep at three different locations. Seroconversion occurred 1 to 2 months after injection as demonstrated by immunodiffusion, indirect ELISA (for the gp51 envelope protein), and blocking ELISA (for gp51 and the major capsid protein, p24). These results demonstrate that BLV infection can be efficiently initiated by direct transfection into sheep. This approach should thus facilitate investigation of the involvement of BLV genetic determinants in the induction of leukemia in ruminants.

Animals↗
PubMed1981

Leukotriene B4: an inflammatory mediator in vivo.

Leukotriene B4 (LTB4 isomer III), which promotes the movement and aggregation of leucocytes in vitro also stimulates the chemo-attraction of leucocytes and their adherence to vascular endothelium in vivo. These effects were observed directly in the hamster cheek pouch preparation and on histological examination of sections from the rabbit mesentery. Intravenous injection of LTB4 (isomer III) into the rabbit resulted in a profound but transient neutropenia. Intradermal injection of LTB4 (isomer III) in the rabbit produced a rapid accumulation of neutrophils and this effect was also observed in skin chambers applied over abrasions on the rabbit back or the human forearm.

Animals↗
PubMed1982

The speckled epidermal nuclear immunofluorescence of mixed connective tissue disease seems to develop as an in vitro phenomenon.

The pathogenesis of speckled epidermal nuclear immunofluorescence in patients with mixed connective tissue disease (MCTD) was studied by reproducing this reaction in guinea-pigs, using serum samples containing high titre antibody to ribonucleoprotein (RNP). Immunofluorescence studies on specimens obtained from guinea-pig skin into which serum samples containing high titre RNP antibody had been injected intradermally, revealed positive epidermal nuclear staining for IgG. This speckled immunofluorescence was demonstrable immediately after injection and remained so for 24 or 48 h. The pattern of fluorescence was similar in all cases, and there was no penetration of RNP antibody through the cell membrane. The epidermal nuclear fluorescence was not detected with sera at a dilution of 1:100 or more. These results provide strong evidence that the epidermal nuclear immunofluorescence observed in patients with high titre antibody to RNP develops as an in vitro phenomenon.

Animals↗
PubMed2005

A highly immunogenic trivalent T cell receptor peptide vaccine for multiple sclerosis.

BACKGROUND: T cell receptor (TCR) peptide vaccination is a novel approach to treating multiple sclerosis (MS). The low immunogenicity of previous vaccines has hindered the development of TCR peptide vaccination for MS. OBJECTIVE: To compare the immunogenicity of intramuscular injections of TCR BV5S2, BV6S5 and BV13S1 CDR2 peptides in incomplete Freunds adjuvant (IFA) with intradermal injections of the same peptides without IFA. METHODS: MS subjects were randomized to receive TCR peptides/IFA, TCR peptides/saline or IFA alone. Subjects were on study for 24 weeks. RESULTS: The TCR peptides/IFA vaccine induced vigorous T cell responses in 100% of subjects completing the 24-week study (9/9) compared with only 20% (2/10) of those receiving the TCR peptides/saline vaccine (P =0.001). IFA alone induced a weak response in only one of five subjects. Aside from injection site reactions, there were no significant adverse events attributable to the treatment. CONCLUSIONS: The trivalent TCR peptide in IFA vaccine represents a significant improvement in immunogenicity over previous TCR peptide vaccines and warrants investigation of its ability to treat MS.

Adult↗
PubMed1988

A study on demyelinating effect of galactocerebroside in experimental allergic encephalomyelitis.

An experimental allergic encephalomyelitis was induced by bovine myelin basic protein (MBP) and bovine galactocerebroside (GC) on male guinea pigs. Animals were divided into five experimental and one control groups. Among the five experimental groups, three were inoculated with 75 micrograms, 150 micrograms and 300 micrograms of MBP, respectively, to see the dose dependency of demyelination. The fourth group was inoculated with mixture of 75 micrograms of MBP and 180 micrograms of GC and the fifth group with 180 micrograms GC. All inocula was injected intradermally in emulsion state mixed with equal amount of complete Freund adjuvant. Control group was injected with adjuvant only. Clinical symptoms began to appear from 15th day after inoculation and animals were sacrificed on maximum neurologic deficit or 4 to 5 days after the onset of symptoms. Demyelination was observed in 6 out of 8 animals inoculated with MBP/GC mixture, while only 3 out of 24 animals inoculated with various dosage of MBP showed demyelination. The difference was statistically significant. Serum antibodies to MBP and GC were measured by ELISA method. All of the eight animals inoculated with MBP/GC mixture and two animals inoculated with GC had low titer of anti-GC antibodies, while all animals inoculated with MBP, MBP alone or MBP/GC mixture, had high titer of anti-MBP antibodies. Therefor it is concluded that the demyelination is augmented by GC and is not significantly dose-dependent on MBP.

Animals↗
PubMed2003

[Sentinel node radiolocalisation and predictive value in lip squamous cell carcinoma].

PURPOSE: Is to evaluate the role of the sentinel node (SN) radiolocalisation and its prognostic value in state T2N0M0 squamous cell carcinomas (SCC) of the lip. MATERIALS AND METHODS: Between November 1999 and June 2002 we enrolled 11 consecutive patients (8m,3f) affected with lower lip SCC (7 pts.), labio-commissure (3 pts.) and upper lip (1 pt). Lymphoscintigraphy was performed three hours before surgery. After topical anaesthesia (Lidocaine spray 10%), 30-50MBq of Nanocoll-Tc99m diluted in a 0.3 ml physiological solution was injected intradermally, divided into two peri-lesional points. Planar static acquisition began immediately after the injection in order to visual lymph drainage pathways (lateral and/or anterior view, 512x512 matrix, 5 min. pre set time, LEGP collimator). All patients underwent only selective lymph adenectomy of the SN. RESULTS: SN were visible in all patients within 5 minutes after the injection. In all patients the SNs were observed in the submandibular area (I neck level) in three patients a second SN was localized in latero cervical area (II neck level). All patients were staged SN negative. The average disease free interval for patients who underwent a selective lymph adenectomy of the SN was 20 months with continuing follow-up. CONCLUSIONS: We must stress the importance of performing an immediate exploratory dynamic or static scintigraphy within the first minutes of the radio tracer injection, in order to acquire a precise SN localisation and an accurate mapping of the tumour lymphatic pathways. SN radio localisation is especially beneficial in T2N0 stage patients where immediate lymphadenectomy is not necessary. It also saves time and cuts costs, which are specific goals in the current climate of health service management. Although our results are encouraging, a larger data base from multi centre trials with a five year follow-up would confirm the validity of our approach.

Carcinoma, Squamous Cell↗
PubMed1976

Basophil-sensitizing antibody response to herpes simplex viruses in rabbits.

Antibodies to herpes simplex virus type 1 and type 2 were detected in the sera of rabbits by release of histamine from basophils sensitized in vitro with the sera. The time course of the appearance of the antibodies, the dose-response curve of the release of histamine in relation to antigen concentration, the sedimentation characteristics of the antibodies in sucrose gradients, and the ability to destroy the sensitizing capacity of the sera with heat suggest that the antibodies being assessed were of the IgE class. These antibodies were induced in animals injected intradermally, intramuscularly, and i.p. with live virus. The antibodies were detected 1 week after primary injection and a similar time course of antibody appearance was observed after a second or third injection. The same cross-reactivity between type 1 and type 2 virus observed with IgG antibody was also observed with IgE antibody.

Animals↗
PubMed2003

Gene expression analysis of atopic dermatitis-like skin lesions induced in NC/Nga mice by mite antigen stimulation under specific pathogen-free conditions.

BACKGROUND: Atopic dermatitis (AD) is a chronic relapsing inflammation characterized by pruritic and eczematous skin lesions usually observed in patients with a familial history of atopic diseases, but its exact etiology is unclear. An animal model is indispensable for the analysis of the pathogenesis and the development of new drugs to treat this disease. Here, we compare changes in gene expression profiles in the AD-like skin lesions of NC/Nga or BALB/c mice stimulated intradermally by mite antigen under specific pathogen-free (SPF) conditions. METHODS: Mite Extract-Dp was injected intradermally into the right and left pinnae and into the skin of the back of NC/Nga or BALB/c mice in 2 places once per 3 days, and the clinical symptoms and the ear thickness were measured. On day 14 or day 28 after starting mite extract injection, we collected plasma and pinnae from NC/Nga or BALB/c mice. The amount of total immunoglobulin E (IgE) in plasma was assayed. We analyzed mRNA transcripts in pinnae using real-time quantitative PCR for the murine counterparts of several known allergy-related genes. Moreover, genome-wide gene expression in pinnae from NC/Nga mice was analyzed using high-density oligonucleotide arrays (GeneChip, Affymetrix). RESULTS: From 2 weeks after stimulation, marked skin inflammation was induced in the pinnae of NC/Nga but not BALB/c mice. However, IgE levels in sera rose equally in both strains. Quantitative PCR analysis and comprehensive GeneChip analysis of the AD-like pinna skin lesions revealed that their development was accompanied by changes in expression of more than 1,000 genes. These included cytokines, cytokine receptors, proteases, and adhesion molecules. Furthermore, genes thus far not reported in association with AD were also affected. CONCLUSION: From these results, the NC/Nga mouse model using mite sensitization under SPF conditions could be useful for elucidating the mechanisms of AD pathogenesis and developing more effective therapy for AD.

Animals↗
PubMed1997

Adenosine A3 receptors promote degranulation of rat mast cells both in vitro and in vivo.

OBJECTIVE: To investigate the effects of adenosine receptor agonists and antagonists on 5-HT release from rat isolated pleural mast cells and on plasma protein extravasation in the skin of conscious rats. In vitro METHODS: Rat isolated pleural mast cells were loaded with [14C] 5-HT, sensitised with mouse monoclonal anti-DNP and then challenged with human serum albumin-DNP. DNP-stimulated 5-HT release from mast cells was determined. In vivo METHODS: Rats, loaded intravenously with [125I] human serum albumin, were injected intradermally with adenosine agonists at sites on the back. 30 min later plasma protein extravasation at each injection site was determined. RESULTS: In isolated mast cells, each adenosine agonist enhanced DNP-induced 5-HT release, N6-(3-iodobenzyl)-5-(N-methyl-carboxamidoadenosine), (IB-MECA), being the most potent agonist. The adenosine A1/A2 antagonist, 8-phenyltheophylline (8-PT), had no effect on the response to IB-MECA. In contrast, 3-(4-amino-iodobenzyl)-8-[4-[[[carboxy]methyl]oxy]phenyl]-1-propylxanthi ne, (I-ABOPX), inhibited (pA2 6.2) the IB-MECA responses. In the skin of conscious rats, intradermal IB-MECA produced a marked plasma protein extravasation (PPE) which was mimicked by N6-2-(4-aminophenyl)-ethyladenosine (APNEA). The PPE produced by IB-MECA was not affected by either 8-PT or CGS15943A, but was virtually abolished by cyproheptadine and in rats pre-treated with Compound 48/80. CONCLUSIONS: These results indicate that stimulation of adenosine A3 receptors both enhances degranulation in vitro and directly produces degranulation of rat mast cells in vivo.

Adenosine↗
PubMed1994

Inhibition of the development of immediate hypersensitivity by staphylococcal enterotoxin B.

We investigated the ability of staphylococcal enterotoxin B (SEB) to modify the immediate hypersensitivity response induced in BALB/c mice following sensitization to ovalbumin (OVA), a response mediated by OVA-reactive V beta 8 T cells. Mice were sensitized by skin painting with OVA every second day over a period of 2 weeks. SEB, a potent activator of V beta 8+ T cells, was administered at the same site where OVA was applied (skin of the lower abdomen) following two different protocols. In protocol (A) SEB was injected intradermally 1 day before painting with OVA and on day 7; in protocol B, SEB was injected each time OVA was applied to the skin (eight times). SEB (but not SEA) altered the development of immediate hypersensitivity to OVA, as demonstrated by the reduction in allergen-specific IgE, decreased OVA-specific immediate skin test responsiveness, and prevented the development of increased airways responsiveness after bronchial challenge with OVA. Injections of SEB did not alter the proliferative responses of local draining lymph node cells or spleen mononuclear cells to OVA, indicating that administration of SEB did not inhibit the sensitization of OVA, but shifted the immune response away from an immediate type response (IgE/IgG1) to IgG2a, IgG2b and IgG3. Although both protocols of SEB treatment did not lead to a major deletion of the V beta 8 T cell population, they did reduce the proliferative response of V beta 8+ T cells to OVA. These data indicate that the bacterial toxin SEB is capable of modifying the immediate hypersensitivity response induced by OVA by altering the functional capacity of antigen-reactive V beta 8 T cells.

Allergens↗
PubMed1994

Pro-inflammatory and anti-inflammatory effects of the stable prostaglandin D2 analogue, ZK 118.182.

This study examined the pro- and anti-inflammatory effects of the stable prostaglandin (PG) D2 analogue, ZK 118.182 and the mechanism by which prostaglandins may exert their anti-inflammatory activity. Co-injected locally, ZK 118.182, like PGE2 and PGD2, dose-dependently increased plasma leakage induced by intradermal injection of bradykinin in rabbit skin. Infused i.v., ZK 118.182 (0.45 microgram/kg/min), a dose which did not affect systemic blood pressure, inhibited oedema formation in rabbit skin induced by the neutrophil-dependent agonists, formyl-methionyl-leucyl-phenylalanine (FMLP) and leukotriene B4 (LTB4). However, it did not modify plasma leakage induced by the neutrophil-independent mediators, bradykinin and platelet-activating factor (PAF). In contrast, neutrophil accumulation in response to LTB4 and FMLP was not affected in animals infused with ZK 118.182. In vitro, ZK 118.182, like PGE2 and PGD2 inhibited FMLP-induced superoxide anion (O2-) production by rabbit neutrophils. The compound, however, had minimal effects on O2- production induced by phorbol myristate acetate (PMA). ZK 118.182 inhibited to a small extent FMLP but not PMA-induced neutrophil adherence. These results show that depending on the route of administration, the PGD2 analogue, ZK 118.182, exhibits either pro- or anti-inflammatory effects. The anti-inflammatory effect may be related to the ability of the compound to inhibit increased microvascular permeability induced by neutrophil activation without interfering with neutrophil accumulation. This latter effect may be due to the analogue's capacity to suppress neutrophil secretion to a greater extent than neutrophil adherence.

Animals↗
PubMed1992

Effect of body locale and addition of epinephrine on the duration of action of a local anesthetic agent.

STUDY OBJECTIVE: Little information exists relating body locale to the duration of action of local anesthetics. We tested the duration of action of a local anesthetic with and without epinephrine at different body locales. PARTICIPANTS: Twenty healthy volunteers aged 27 to 48 years (mean, 32.0 years). INTERVENTIONS: In the first of two experiments (L), 20 subjects had 1 mL buffered 1% lidocaine injected intradermally on the forehead, hand, forearm, and calf. In the second experiment (LE), ten subjects were injected at the same sites with lidocaine containing epinephrine. METHODS: Subjects ranked anesthesia by reaction to pinprick from 0 (complete) to 20 (none) on a scale with testing done every 15 (L) or 30 (LE) minutes and continued until no anesthetic effect was present. Duration of effective and of any anesthesia were times until score of more than 5 and of more than 19, respectively. Mean duration of anesthesia was compared by analysis of variance (between body areas) and paired two-tailed t-test (L vs LE). Significance was taken as P less than or equal to .05. RESULTS: Anesthesia was significantly briefer for the face than for all other body locales by both indexes of duration and for both plain lidocaine and lidocaine with epinephrine (P less than .001 to P less than .05). Anesthesia with epinephrine lasted significantly longer than with lidocaine alone at all body locales and for duration of both effective or any anesthesia (P = .0001 to P = .001). Based on 95% confidence interval limits, the duration of anesthesia at other body locales is predicted to be 1.3- to 3.2-fold that on the face. Confidence interval analysis indicated that addition of epinephrine to lidocaine increases the duration of anesthetic action by 1.3- to 13.0-fold that of lidocaine alone. CONCLUSION: The duration of action of local anesthesia is considerably shorter for the face than for other body areas. Epinephrine significantly increases the duration of action of lidocaine at all body locales.

Adult↗