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PubMedDate not supplied

Induction of syngeneic intradermal and orthotopic epidermal carcinomas in hairless Skh-1 mice as a reproducible model for experiments.

Epidermoid carcinomas, clinically and histologically similar to human squamous cell carcinomas (SCC), were obtained in hairless Skh-1 mice. Tumor cells originated from chemically-induced skin cancers. We developed three models of orthotopic skin tumors: (1) intradermal injection of a tumor cell suspension, (2) superficial abrasion of the skin, cell grafting and application of a hydrocolloid dressing, (3) skin incision, seeding and application of a hydrocolloid dressing. Intradermal injection was 100% successful. Skin incision, displaying histological evidence of rapid invasive tumor growth, was 75% successful. Though skin tumor growth after abrasion was only 20% successful, the tumor histogenesis exactly imitated human SCC development. These carcinomas provide research models for further experiments such as photodynamic therapy or antiangiogenesis therapy.

Animals↗

PubMed1957

Histamine release and pain production by xanthosine and related compounds.

Xanthosine (5 to 50 mug.) caused pain on intradermal injection in all human subjects tested: in about half the subjects it also gave a flare. Inosinic acid, uric acid, allantoin, alloxan and theophylline caused pain, but not a flare by intradermal injection in man. Xanthine caused both pain and flare. A number of related compounds in similar doses caused neither pain nor flare. Inosine, inosinic acid, and guanosine, but not xanthosine, were powerful histamine liberators in animals. The lowering of the cat blood pressure, depression of the activity of the guinea-pig ileum and stimulation of guinea-pig uterus by adenosine were confirmed.

Adenosine↗

PubMed2006

Safety of sodium fluorescein for in vivo study of skin.

BACKGROUND/PURPOSE: Epicutaneous labeling or intradermal injection of the fluorescent sodium fluorescein is being used increasingly to investigate skin conditions in vivo when using non-invasive devices such as confocal scanning laser microscopy. Sodium fluorescein was used intravenously for decades for the examination of the vasculature of the ocular fundus (fluorescein angiography) and as eye drops for diagnosis of corneal erosions. The objective of this article is to systematically review the literature on fluorescein and conclude its safety in cutaneous research to support research planning and evaluations by ethics committees. METHODS: A number of databases and the literature about safety and toxicity of fluorescein in animal and human studies were searched and analyzed. RESULTS: Side effects or adverse events reported in the literature were related to intravenous bolus injection. Transient nausea and vomiting may occur. Other adverse events such as vasovagal reaction, cardiac or respiratory effects and anaphylaxes are extremely rare but may be fatal. Intradermal injection may cause mild itch or pain; systemic adverse event was reported. Epicutaneous labeling is associated with no reported problem. A typical local dose is several magnitudes of order smaller than a typical intravenous dose. CONCLUSION: Fluorescein has been used for many years in medicine for diagnostic purposes and is widely safe, albeit intravenous bolus injection may cause serious adverse reactions. In the literature, we could not trace reports of local or systemic side effects of topical sodium fluorescein except itch and pain on intradermal injection, however, dependent on the fluorescein preparation used. Local dermal application of fluorescein for in vivo study of skin may be considered widely safe.

Administration, Oral↗

PubMed2000

Involvement of blockade of leukotriene B(4) action in anti-pruritic effects of emedastine in mice.

The anti-pruritic activity of emedastine difumarate was studied in mice. Emedastine (0.03-0.3 mg/kg) inhibited scratching induced by intradermal injection of histamine (100 nmol/site). Scratching induced by substance P (100 nmol/site) and leukotriene B(4) (0.03 nmol/site), but not by serotonin (100 nmol/site), was also suppressed by emedastine (0.03-0.3 mg/kg). Intradermal injection of substance P increased the cutaneous concentration of leukotriene B(4), which was not affected by emedastine. These results suggest that the inhibition by emedastine of substance P-induced itch-associated response is mediated by the blockade of leukotriene B(4) action. Anti-leukotriene B(4) action, as well as the anti-histamine action, may contribute to the anti-pruritic effects of emedastine.

Animals↗

PubMed1989

Pharmacological modulation by cetirizine and atropine of the histamine- and methacholine-induced wheals and flares in human skin.

This study was planned to verify whether different methods for the measurement of skin reactivity, i.e. wheal and flare area, wheal thickness, skin capacitance and transepidermal water loss, were or were not able to discriminate between intradermally injected agonists (histamine and methacholine). For evaluating agonist/antagonist interactions, we adopted a cross-over, double-blind, placebo-controlled study designed to compare the effects of cetirizine and atropine. The intradermal injection of agonists elicited the appearance of wheal and flare reactions and, after histamine, the skinfold thickness was significantly increased. Skin capacitance and transepidermal water loss measurements reflected sweat gland activation after methacholine injection but were, respectively, not or less affected by histamine dry skin prick test or saline; hence, both methods appear very sensitive for in vivo testing of cholinomimetic agents. Cetirizine inhibited all the specific skin modifications induced by histamine challenge, wheals, flares and increased thickness, without affecting the methacholine-induced perspiration. This would further support the H1 specificity of this anti-H1 agent in vivo. However, at the agonist/antagonist ratios tested in view of the safety of the test persons, we were unable to objectivate methacholine blockade by atropine.

Adult↗

PubMed2000

Botulinum toxin treatment for symptomatic Frey's syndrome.

Gustatory sweating, or Frey's syndrome, usually occurs after surgery or trauma to the parotid gland as a result of inappropriate parasympathetic cholinergic innervation of cutaneous sympathetic receptors. Numerous medical and surgical treatments have been proposed to prevent or treat this condition. The results, overall, have been unsatisfactory. Botulinum toxin is a relatively new treatment modality for Frey's syndrome. We review the literature and present our experience with 7 patients successfully treated with intradermal injections of botulinum toxin (Botox). Our technique and dosing are described. In all treated patients gustatory sweating ceased in the area injected with botulinum toxin. In 6 patients, symptoms reappeared, and additional injections were needed up to 4 times, at 6- to 8-month intervals. All patients now have been free of symptoms for a long period of time (mean 12.1 months). We strongly recommend intradermal injections of botulinum toxin as a safe, efficacious treatment for gustatory sweating.

Aged↗

PubMed1995

Intradermal actions of hypertonic saline involve neural and vascular mechanisms.

The aim of this study was to investigate whether the wheal and flare responses to intradermal injection of hypertonic (4.5%) saline (HTS) were inhibited by local injection of 1% lignocaine. Eight normal subjects were studied on one occasion. Lignocaine (0.125 ml) was infiltrated at four sites on one forearm and normal saline on the other. Five minutes later, duplicate intradermal injections of 30 microliters of histamine (22.5 nmol ml-1), substance P (1 nmol ml-1), HTS and normal saline were given coded and in random order, one of each pair to each forearm. Lignocaine inhibited flare responses to histamine, substance P and HTS by 56% (P < 0.01), 78% (P < 0.01) and 77% (P < 0.05) respectively suggesting similar involvement of an axon reflex. Wheal to histamine was inhibited by 31% (P < 0.02) and to substance P by 33% (P < 0.05) but not to HTS. This suggests that the mechanism of wheal response to HTS differs from that of histamine and substance P.

Anesthetics, Local↗

PubMedDate not supplied

The synthesis of bradykinin-azoprotein and its effectivity.

Some authors succeded in binding the bradykinin in form of a haptene by an azo-bridge to the human gammaglobulin as a vehicle. In this way, the bradykinin has been supplemented to a complete antigen. The bradykinin as a strongly vasoactive substance causes--after a local intradermal injection--an intensive circumscribed increase of the permeability of the capillaries. If such animals receive an intravenous or intracardiac injection of a 1% Evans blue solution, there is a strong blue colouring in the place where the bradykinin has been applied. The guinea pigs and the rabbits which had been immunized by bradykinin-azo-protein showed a significant decrease in the local accumulation of the Evans blue-solution,, which must be attributed to the immunologic neutralization of the intradermally injected bradykinin by an anti-bradykinin-antibody. The intradermally injected bradykinin is neutralized by the bradykinin-antibody. The intravenous or intracardiac injection of bradykinin causes a strong bronchoconstriction in the guinea pig. In those animals which have been pretreated with bradykinin-azo-protein, either there was no asthmatic dyspnoea at all or a decrease of the bronchial reaction would be found. This result very probably is also caused by the production and the activity of anti-bradykinin antibodies.

Alpha-Globulins↗

PubMed1992

Pituitary adenylate cyclase activating polypeptide is a potent vasodilator in humans.

The vasodilator effect of the novel peptide pituitary adenylate cyclase activating polypeptide (PACAP) was investigated in humans. Forearm blood flow was measured in six healthy men by venous occlusion plethysmography. Infusion of PACAP into the brachial artery at 0.01, 0.1, 1, 3, and 10 pmol/min produced a dose-related increase in forearm blood flow in the cannulated arm from 2.8 +/- 0.6 to 8.6 +/- 2.4 ml/100 ml/min at the highest dose (mean +/- SEM, p less than 0.05). In a subsequent experiment, where the highest dose of PACAP was repeated after a 36 min interval, there was no tachyphylaxis of the forearm blood flow response, with the forearm blood flow increasing by 129 +/- 9% during the first infusion and 128 +/- 31% during the second infusion (N.S.). In further experiments, microvascular blood flow was measured by a laser-Doppler flow probe to compare the effects of intradermally injected PACAP, vasoactive intestinal polypeptide (VIP), and calcitonin gene-related peptide (CGRP). When injected into the skin of normal volunteers at 10(-12) to 10(-11) mol/site, each peptide caused a rapid flare lasting 2-3 min, which became erythematous after 5 min. At 10(-12) mol/site, intradermally injected PACAP and VIP caused a maximum increase in skin blood flow at 15 min of 379 +/- 96 and 307 +/- 121% (% increase above basal +/- SEM), respectively, and these responses were not significantly affected by oral aspirin (600 mg) taken 1.5 h beforehand. The vasodilation induced by PACAP at 10(-12) mol/site lasted approximately 6 h, whereas the effect of the same dose of CGRP and VIP lasted less than 2 h. These data suggest that PACAP is a potent and long-lasting vasodilator in humans.

Adult↗

PubMed1989

Cutaneous inflammation: effects of hydroxy acids and eicosanoid pathway inhibitors on vascular permeability.

Four metabolic products of arachidonic acid lipoxygenation, 5-hydroxyeicosatetraenoate (5-HETE), 12-HETE, 15-HETE, 5(S),12(S)-DiHETE, were injected intradermally into depilated dorsae of albino guinea pigs. The presence of intravenously injected 125I-bovine serum albumin (10uCi/kg) in 13-mm punch biopsy specimens served as a marker for altered vascular response; histologic changes were evaluated at 6 and 24 h after the injection in 1-micron-thick sections. Thirty minutes after the injections of 15 nanomoles and 60 nanomoles of 5-HETE, the ratios of radioactivity in HETE-injected to that in buffer-injected sites were 1.35 +/- 0.06 (mean +/- SE) and 2.80 +/- 0.27, respectively. Corresponding effects of 15-HETE were 1.39 +/- 0.17 and 1.63 +/- 0.21, respectively. Values for 60 nanomoles of 12-HETE and 5,12-DiHETE were intermediate in comparison with the above eicosanoids. The most notable histologic changes were a neutrophilic infiltrate induced by 12-HETE at 6 and 24 h, and neutrophilic and eosinophilic infiltrates in response to 5,12-DiHETE injection at 6 and 24 h. Effects of topically applied eicosanoid pathway inhibitors were also evaluated, using intradermally injected sodium arachidonate (AA) as agonist. Three mixed cyclooxygenase/lipoxygenase inhibitors, BW755C, phenidone, and nordihydroguaiaretic acid, suppressed vascular response by 9%, 9%, and 6% for 150 nmol of AA, and by 9%, 13%, and 12% for 300 nmol of AA, respectively. The cyclooxygenase inhibitor, indomethacin, induced suppressions of 39% for 150 nmol AA and 22% for 300 nmol AA, respectively. These data demonstrate that metabolites of both cyclooxygenase and lipoxygenase eicosanoid pathways are involved in alteration in vascular response accompanying cutaneous inflammation.

Animals↗

PubMed1984

Skin and pulmonary models using coated bentonite particles for the study of the inflammation evoked by Paracoccidioides brasiliensis antigens in previously immunized mice.

Bentonite particles coated with polysaccharide antigen or crude soluble antigen of Paracoccidioides brasiliensis were injected intradermally or intravenously in mice. In control animals that were not pre-immunized with P. brasiliensis antigens, coated and uncoated bentonite caused minimal and nonspecific inflammation around the cutaneous injection site or around the bentonite thrombi in small lung vessels after intravenous injection. However, in mice previously immunized with P. brasiliensis antigens, the coated bentonite particles boosted the humoral and cellular immune responses to P. brasiliensis and evoked intense inflammatory reactions. Twelve days after intradermal injection, the inflammatory reaction around the bentonite was rich in neutrophils, macrophages, lymphocytes and plasma cells associated with young granulation tissue. In intravenously injected mice, the pulmonary inflammation was maximal at day 2, and was characterized by a florid neutrophilic and macrophagic cellular infiltration around bentonite thrombi; in some foci, there was incipient organization to mature granuloma. However, in both models, there was no formation of epithelioid granulomata, demonstrating that in paracoccidioidomycosis cellular immunity alone, without the presence of intact micro-organisms, may not be enough for the development of this type of granuloma.

Animals↗

PubMed1996

Possible role of protein kinase C in the sensitization of primate spinothalamic tract neurons.

The responsiveness of spinal cord nociceptive neurons to innocuous mechanical stimuli can be increased by the release of excitatory amino acids (EAAs) and peptides attributable to an injury-induced barrage of impulses. This sensitization of spinal dorsal horn neurons can also result from administration of phorbol ester by microdialysis, presumably by direct activation of protein kinase C (PKC). This study was designed to examine the effects of central sensitization of spinothalamic tract (STT) neurons produced by intradermal injection of capsaicin on the descending inhibition driven from the periaqueductal gray (PAG) and the possible role of PKC in this process in anesthetized monkeys. Sensitization of responses of STT cells to mechanical stimuli was induced by intradermal injection of capsaicin. PAG inhibition was significantly attenuated when sensitization of responses to mechanical stimuli occurred. However, perfusion of the spinal cord with NPC15437 (a selective PKC inhibitor) by microdialysis could prevent the sensitization of the responses to mechanical stimuli and the reduction in PAG inhibition of these responses induced by capsaicin injection. Results similar to those produced by capsaicin injection were observed when a PKC activator, phorbol ester (12-O-tetradecanoylphorbol-13-acetate), was infused within the dorsal horn by microdialysis. An inactive phorbol ester (4 alpha-phorbol 12,13-didecanoate) had no effect. These results provide evidence that the activation of PKC contributes to the development of central sensitization in dorsal horn neurons produced by chemical stimulation with capsaicin. Attenuation of the effectiveness of PAG inhibition takes place when the sensitization of dorsal horn cells develops, and PKC may play a significant role in this process.

Animals↗

PubMed2003

High-frequency interferon-gamma-secreting splenocytes specific for murine cytomegalovirus immediate-early-1 (IE-1) peptide 168YPHFMPTNL176 are insufficient to provide complete protection from viral challenge.

Infection of Balb/c mice with murine cytomegalovirus (MCMV) has been used extensively as a model system with which to study host mechanisms of immunity to cytomegaloviruses. In this model, the cytotoxic T-lymphocyte (CTL) response crucial for clearing infected cells is dominated by CTLs specific for the MCMV nonapeptide 168YPHFMPTNL176 encoded by the immediate-early 1 (IE-1) gene. The intradermal injection of plasmid pcDNA89 encoding IE-1 has been shown to offer some protection from viral challenge. In the present studies, the protective efficacy of immunisation with pcDNA89 given by intradermal injection was compared with particle-mediated DNA delivery (PMDD) and contrasted with that induced by injection with the K181 MCMV strain and with temperature-sensitive mutants (tsm) derived from the K181 strain. Modest protection was afforded by pcDNA89 immunisation given by PMDD, but none was observed after intradermal injection. PMDD immunisation induced a frequency of 168YPHFMPTNL176-specific interferon-gamma (IFN-gamma)-secreting splenocytes, which was equivalent to that after K181 infection and significantly higher than tsm immunisation. Whereas tsm-immunised mice were completely protected from MCMV challenge, PMDD-immunised mice were only weakly protected. Tsm immunisation protected mice completely against challenge with natural isolates having sequence variation in the IE-1 nonapeptide, while PMDD-immunised mice were weakly protected from isolates encoding 168YPHFMPTNL176 and were not protected against isolates encoding 168YPHFMPPSL176 or 168YLDFMPPNL176. Thus, while IE-1-specific IFN-gamma-secreting splenocytes do contribute to immunity from MCMV challenge, their presence in isolation is insufficient to provide complete protection and they may not be involved in the protection observed against MCMV isolates having IE-1 sequence variation.

3T3 Cells↗

PubMed2001

Treatment of focal hyperhidrosis with botulinum toxin type A: long-term follow-up in 61 patients.

BACKGROUND: The blocking action of botulinum toxin type A (BTX-A) on cholinergically innervated sweat glands has been used successfully to treat patients with focal hyperhidrosis. OBJECTIVES: To investigate the long-term efficacy and safety of intradermal injections of BTX-A. METHODS: We performed an open-label study in 61 patients treated over a period of 3 years for axillary or palmar hyperhidrosis. A total dose of 400 mU BTX-A (Dysport) was injected into both axillae or 460 mU BTX-A (Dysport) into both palms. The injections were repeated after relapse. Objective quantification of sweat production was performed using digitized ninhydrin-stained sheets. RESULTS: Four weeks after BTX-A treatment the median reduction in sweat production was 71% compared with baseline (P < 0.001) in the axillary group and 42% (P = 0.005) in the palmar group. Subjective assessment of sweat production by the patients using a visual analogue scale (0, no sweating; 100, the most severe sweating) showed a significant reduction in both the axillary (P < 0.001) and palmar groups (P < 0.001). Secondary disturbances due to focal hyperhidrosis interfering with daily activities were markedly improved in both groups. The median time interval between the sets of injections was 34 weeks for axillary hyperhidrosis and 25 weeks for palmar hyperhidrosis. The treatment of palmar hyperhidrosis was complicated by transient but not disabling weakness of the small hand muscles in nine of 21 patients. CONCLUSIONS: Repeated intradermal injections of BTX-A in patients with axillary and palmar hyperhidrosis are as effective as first treatments.

Adult↗

PubMed1992

A naturally occurring opioid peptide from cow's milk, beta-casomorphine-7, is a direct histamine releaser in man.

beta-Casomorphine-7, a naturally occurring product of cow's milk with opiate-like activity, was studied for possible direct histamine liberation activities in humans. It was found to cause concentration-dependent in vitro histamine release from peripheral leukocytes of healthy adult volunteers. Intradermal injection of beta-casomorphine-7 induced a wheal and flare reaction in the skin similar to histamine or codeine. Oral pretreatment with the H1 antagonist terfenadine significantly inhibited the skin responses to beta-casomorphine-7. The intradermal injection of an opiate receptor antagonist, naloxone, inhibited in vitro histamine release and skin reactions only in a 100-fold excess over beta-casomorphine-7. These findings suggest that beta-casomorphine-7 can be regarded as a noncytotoxic, direct histamine releaser in humans. The clinical relevance of these findings deserves further studies.

Adult↗

PubMed1998

[Influence of infusion solution on the vascular permeability in rat skin].

In this study, we attempted to confirm the assessment system of incidence of angialgia and thrombophlebitis by evaluating the influence of test solutions on the vascular permeability by intradermal injection into rat skin, and following results were obtained: 1) Dimensions of dye leakage in the rat skin were not increased by injection of one commercially available preparation (solution 1), but increased significantly by injection of a preparation (solution 2) that had induced a high incidence of angialgia in a clinical study. 2) Dimensions of the dye leakage increased significantly by injection of glucose solutions with about four degrees of osmolality ratio. 3) In the injection of acetate buffers with different titratable acidity, dimensions of the dye leakage increased depending on titratable acidity. 4) Solution 1 was adjusted to pH 4.43 with L-lactate, acetic acid of HCl, and then these solutions were intradermally injected to rats. The influence on dimensions of the dye leakage was in the following order of strength: acetic acid >> L-lactate > HCl. These results suggest that the vascular permeability by injection into rat skin is influenced by osmolality, pH, titratable acidity and composition of test solutions. Therefore, this system using the vascular permeability reaction in rat skin may be useful for evaluation of angialgia and thrombophlebitis incidence.

Acetic Acid↗

PubMed2003

[Efficacy of botulinum toxin A in the treatment of axillary and palmar hyperhidrosis: 10 cases].

UNLABELLED: Axilliary and palmar hyperhidrosis can become a considerable social and psychological handicap. Local treatments are not always effective and endoscopic thoracic sympathectomy is not without side effects. The efficacy of botulinum toxin has recently been demonstrated in axillary and palmar hyperhidrosis. Between June 2001 and June 2002, we treated all the patients presenting with axillary and palmar hyperhidrosis, resistant to classical treatments, with intradermal injections of botulinum toxin A (Dysport). The aim was to assess the interest of this technique at moderate doses, in a prospective, open, controlled study. PATIENTS AND METHODS: The hyperhidrotic areas, revealed by Minor's test, were treated with intradermal injections of 100 U of Dysport in the axilliary form and 250 U in the palmar form. Patients were seen after 1 month and 6 months and underwent a Minor's test, photographic control and they filled-in a questionnaire to measure their satisfaction. RESULTS: Ten patients: 9 women and 1 man aged 19 to 63, were included. Three of them consulted for palmar hyperhidrosis and 7 for auxiliary hyperhidrosis. Within 2 to 7 days, treatment was successful in all patients. The follow-up was of 3 to 12 months. The satisfaction index was comprised between 7/10 and 9/10. The relapse-free interval was of 2 to 9 months. Three patients were given a second injection, which doubled the relapse-free period. Side effects included pain with the palmar injections and moderate headaches. DISCUSSION: This French study confirms the efficacy of botulinum toxin A in the treatment of axillary and palmar hyperhidrosis with relatively low doses (100 U of Dysport per armpit and 250 U per palm). This is an easily reproducible, well tolerated, method without major side effects.

Adult↗

PubMed1995

An investigation into the mechanism of capsaicin-induced oedema in rabbit skin.

1. Oedema formation induced by intradermal capsaicin has been studied in rabbit skin. The effect of the anti-inflammatory steroid dexamethasone and also of a range of known inhibitors of oedema formation have been investigated in order to elucidate mechanisms involved in capsaicin-induced oedema formation. 2. Oedema formation, in response to intradermally-injected test agents, was measured by the local extravascular accumulation of intravenously injected 125I-labelled albumin. In separate experiments skin blood flow was assessed by the clearance of intradermally-injected 133xenon. 3. Oedema formation induced by intradermal histamine (3 nmol) and bradykinin (1 nmol), when in the presence of vasodilator doses of calcitonin gene-related peptide (CGRP) (3 pmol) or prostaglandin E1, (PGE1) (10 pmol), was significantly inhibited (P < 0.01) in rabbits pretreated with intravenous dexamethasone (3 mg kg-1, -4 h). In contrast dexamethasone had no effect on capsaicin (3 mumol)-induced oedema formation or, on capsaicin (30-100 nmol)-induced blood flow. 4. Oedema formation observed in response to intradermal capsaicin (3 mumol) was significantly inhibited (P < 0.01) when the selective capsaicin antagonist, ruthenium red (3 nmol) was co-injected. This suggests that the mechanism of capsaicin-induced oedema involves activation of sensory nerves. However, oedema was not inhibited when capsaicin was co-injected with the neurokinin NK1 receptor antagonist, RP67580 (10 nmol), the NK2 antagonist SR48960 (10 nmol) or the CGRP antagonist CGRP8-37 (300 pmol). 5. Oedema formation induced by capsaicin was not inhibited when co-injected with the histamine HI receptor antagonist, mepyramine (3 nmol), the PAF antagonist, WEB 2086 (100 nmol), the bradykinin B2 receptor antagonist, Hoel4O (1 nmol), or the cyclo-oxygenase inhibitor, indomethacin (10 nmol),suggesting that these mediators do not play a major role in the capsaicin-induced response.6. Histological analysis of capsaicin-treated skin sites revealed undamaged, intact microvessels and lack of haemorrhage. Further, co-injection of capsaicin with the hydrogen peroxide remover, catalase(2,200 u), had no effect on oedema formation. This suggests that capsaicin does not induce oedema formation secondary to free radical-induced damage.7. These results indicate that capsaicin-induced oedema in rabbit skin involves activation of sensory nerves. However, the oedema is not inhibited by pretreatment with the anti-inflammatory steroid,dexamethasone. Further the mechanisms which lead to the oedema formation observed after intradermal capsaicin remain unknown.

Alprostadil↗