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At least 649 records · Page 36Linked to original sources
PubMed1987

Leukotriene B4 and prostaglandin E2 mediate the inflammatory response of rabbit skin to intradermal arachidonic acid.

1. Acute inflammation was induced in rabbit skin by intradermal injection of arachidonic acid. 2. Inflammation was assessed by the local accumulation of intravenously-injected 125I-serum albumin (plasma extravasation) and histologically (polymorphonuclear leucocyte, PMNL infiltration). 3. Leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) were extracted from skin and fractionated using C18 mini-columns. They were quantitated by specific radioimmunoassays and authenticated by reversed-phase high performance liquid chromatography analysis. 4. Maximally elevated levels of LTB4 and PGE2 were detected in skin 5 min after arachidonic acid injection. At subsequent times the eicosanoid content of the skin decreased. 5. The decrease in the eicosanoid content of the skin was due to rapid clearance (t 1/2 approximately 5 min) via the microvasculature and not a consequence of metabolism. 6. The concentration of LTB4 and PGE2 measured in inflamed skin was sufficient to account for the plasma extravasation and PMNL infiltration induced by arachidonic acid. The model therefore is useful for evaluating the anti-inflammatory efficacy of inhibitors of arachidonic acid metabolism including 5-lipoxygenase inhibitors. 7. The consequences of the rapid clearance of LTB4 from inflammatory sites are discussed with respect to its measurement in inflammatory disease and its role as an acute inflammatory mediator.

Animals↗
PubMed1990

Neutralized lidocaine with epinephrine for local anesthesia--II.

The pain usually associated with intradermal injection of lidocaine and epinephrine is significantly attenuated by the addition of either sodium bicarbonate or sodium hydroxide to 1% lidocaine with epinephrine. This suggests that sodium bicarbonate attenuates pain by increasing the pH of the anesthetic solution. The clinical effects of a solution of lidocaine (1%) with epinephrine (1:100,000) and sodium bicarbonate (80 meq/L) were assessed after infiltration in skin. Anesthetic stored for 1 week caused nearly equal areas of anesthesia and vasoconstriction as an identical solution prepared on the day of use.

Anesthesia, Local↗
PubMed1998

Botulinum A neurotoxin for axillary hyperhidrosis. No sweat Botox.

BACKGROUND: Axillary hyperhidrosis causes considerable emotional stress and is associated with extraordinary costs and limitations in clothing. Existing topical and surgical therapies are either ineffective or associated with unacceptable morbidity and sequelae. Botulinum A neurotoxin (Botox) has been shown to decrease sweating in normal skin and in palmar hyperhidrosis. OBJECTIVE: The current study was undertaken to demonstrate the utility of using Botox in the treatment of axillary hyperhidrosis. METHODS: Twelve patient with axillary hyperhidrosis underwent intradermal injection with 50 units of Botox in the axillary skin bilaterally. RESULTS: All patients enjoyed relatively complete anhidrosis of the axillary skin in periods ranging from 4 to 7 months. Repeat injections produced similar results. CONCLUSION: Botulinum A neurotoxin (Botox) is an elegant and simple treatment for axillary hyperhidrosis.

Adult↗
PubMed1995

Infiltration pain and local anesthetic effects of buffered vs plain 1% diphenhydramine.

OBJECTIVE: To compare the levels of infiltration pain and local anesthetic effects of plain and buffered 1% diphenhydramine. METHODS: A prospective, randomized, double-blind, paired study was performed using 30 adult volunteers. Intradermal injections (0.5 mL) of plain and buffered 1% diphenhydramine were made in the subjects' forearms, one in the left and the other in the right. The pain of infiltration was recorded on a previously validated 10-cm visual analog scale (VAS). The volunteers also were asked which injection was less painful. Sequential measurements of the diameter of anesthesia to pinprick were made at 1, 2, 5, 10, 15, 20, 25, and 30 minutes. The VAS scores and anesthetic diameters were compared for plain and buffered diphenhydramine using a paired Wilcoxon rank sum test. RESULTS: There was no statistically significant difference between buffered diphenhydramine and plain diphenhydramine for pain of injection (23.5 +/- 19.2 mm vs 28.2 +/- 18.7 mm, p = 0.24). Repeated-measures analysis of variance for anesthetic diameters demonstrated no significant difference between buffered diphenhydramine and plain diphenhydramine (p = 0.87). At no single measurement period were the anesthetic diameters different. CONCLUSIONS: In a study with a sample size large enough to detect an 11-mm difference in VAS scores (power = 80%), no difference was found in pain of infiltration and anesthetic effects when plain 1% diphenhydramine was compared with buffered 1% diphenhydramine. Buffering of diphenhydramine does not appear to result in a clinically significant reduction in the pain of infiltration.

Adult↗
PubMed1980

Cumulative irritancy in the guinea pig from low grade irritant vehicles and the angry skin syndrome.

A 4-week open cumulative irritancy test in guinea pigs discriminated between two low grade irritant vehicles, nonionic base (anhydrous) and hydrophilic ointment. The procedure might be useful as a predictive test for low grade irritants. The angry skin syndrome was established in the guinea pigs by one Freunds complete adjuvant intradermal injection on day 0, or by daily open applications of 10% sodium lauryl sulfate in petrolatum to the neck area of the animals.

Animals↗
PubMed1982

Release of nickel into fluid stored in the reservoir of Dermo-Jets.

Release of nickel into triamcinolone acetonide suspensions stored in the reservoir of a Dermo-Jet was demonstrated by electrothermal atomic absorption spectrometry. Increased urinary nickel excretion was found for three days following intradermal injections (with the Dermo-Jet) of triamcinolone acetonide in patients suffering from alopecia areata. The dimethylglyoxime test showed that the internal rod of the reservoir as well as metallic internal parts of the nozzle leached appreciable amounts of nickel, even before any clinical use.

Alopecia Areata↗
PubMed1997

Induction of psoriasiform inflammation by a bacterial superantigen in the SCID-hu xenogeneic transplantation model.

Psoriasis is a chronic skin disease affecting about 2% of the Caucasian population, characterized by co-existing inflammation and epidermal hyperproliferation. A T-lymphocyte-mediated autoimmune reaction induced by bacterial superantigens might be central in its pathogenesis. To model psoriasiform inflammation, we transplanted clinically uninvolved skin from psoriatic patients onto SCID mice. Repetitive intradermal injections with a bacterial superantigen and simultaneous intraperitoneal injections with the patients superantigen-stimulated peripheral mononuclear blood cells resulted in an inflammatory reaction exhibiting some of the hallmarks of psoriasis, e.g. epidermal hyperproliferation, papillomatosis, focal neo-expression of ICAMI, and an exocytotic T-lymphocytic infiltrate characterized by the expression of the cutaneous lymphocyte-associated antigen. These observations document the potential of superantigens to trigger psoriasiform dermatitis and provide a model to study lymphocyte homing.

Animals↗
PubMed1984

The influence of mechanical vibratory stimulation and transcutaneous electrical nerve stimulation on experimental pruritus induced by histamine.

The effect of conditioning mechanical vibratory stimulation and transcutaneous electrical nerve stimulation (TENS) on experimentally induced pruritus was studied on 12 healthy subjects. Pruritus was provoked by intradermal injection of histamine on the upper arm. Vibration at 10, 100 and 200 Hz and TENS at 2 and 100 Hz were applied (i) over or (ii) proximal (in the same dermatome) to the pruritic area for a period of 5 min following itch elicitation. In addition the influence of a 5 min pre-stimulatory regimen of the injection area was investigated (iii). The results obtained were compared with unconditioned values and with those obtained following a placebo conditioning procedure (i, ii). It was found that vibratory as well as electrical stimulation, for all frequencies used, reduced subjective itch intensity. Vibration at 100 Hz was the most effective mode of stimulation especially when applied directly to the pruritic area. Conditioning with 100 Hz vibration was also the most effective mode for reducing the duration of the itch response as well as the total experience of pruritus (estimated as a total itch index). Induction time to partial and maximal itch alleviation was shortest for 100 Hz vibration. The results indicate that treatment of pruritic conditions with conditioning stimulation, especially vibration, may be of therapeutic interest.

Adult↗
PubMed1992

Effects of selective histamine receptor antagonists on skin responses to intradermal bradykinin in healthy volunteers.

The effects of chlorpheniramine and cimetidine on the cutaneous responses to intradermal injections of bradykinin were investigated in a randomized, double-blind, placebo-controlled, cross-over study. Chlorpheniramine significantly attenuated the increase in cutaneous blood flow and erythema induced by bradykinin but not the weal response. Cimetidine was without influence on these parameters and the effects of the combined therapy of chlorpheniramine and cimetidine were not significantly different from those due to chlorpheniramine alone. These results suggest that the cutaneous vasodilator effect of bradykinin is in part due to histamine release acting on histamine H1-receptors.

Adult↗
PubMed1994

Pharmacokinetic and pharmacodynamic studies of the histamine H1-receptor antagonist ebastine in dogs.

The pharmacokinetics and pharmacodynamics of ebastine at single oral doses of 10 and 20 mg were studied in six healthy beagle dogs. Plasma concentrations of the active metabolite of ebastine were measured at predetermined times after the dose. At these times an intradermal injection of 0.01 mL of a 0.2 mg mL-1 histamine diphosphate solution was given, and wheal areas were computed. The plasma elimination half-life of ebastine was 4.38 +/- 1.01 h after 10 mg ebastine and 4.09 +/- 0.74 h after 20 mg ebastine; the distribution volume was 3.99 +/- 0.88 and 3.65 +/- 0.75 L kg-1 after 10 and 20 mg of ebastine, respectively; the clearance after the 10 mg dose of ebastine was 0.67 +/- 0.24 L h-1 kg-1 and after 20 mg ebastine was 0.63 +/- 0.17 L h-1 kg-1. The mean histamine-induced wheal areas were significantly suppressed from 1 to 25 h after the 10 mg dose ebastine and from 1 to 32 h after the 20 mg dose ebastine, compared with the mean predose wheal areas (P < 0.001). Maximum suppression of the wheals was 75 and 82% from 10 and 20 mg ebastine, respectively. A combined pharmacokinetic-pharmacodynamic model was used to analyse the relationship between inhibition of wheal skin reaction and changes in the active metabolite of plasma concentration after ebastine administration. A significant delay of 3-4 h was present between the maximum effect and the peak plasma concentration. Calculated from mean data, the rate constant for equilibration of the drug between plasma and effect site was 0.17 and 0.22 h-1 after 10 and 20 mg ebastine with a half-life of 4.13 and 3.56 h, respectively, and the steady-state plasma concentration resulting in 50% of maximal effect was 18.9 +/- 4.8 ng mL-1 after 10 mg and 18.2 +/- 5.7 ng mL-1 after 20 mg ebastine.

Administration, Oral↗
PubMed1967

Responses of skin blood vessels to bradykinin, histamine and 5-hydroxytryptamine.

1. The responses of human cutaneous blood vessels to intradermal injection of bradykinin, histamine and 5-hydroxytryptamine (serotonin) are studied in order to evaluate the ability of these agents to mediate the vascular changes of sustained acute inflammation in the skin.2. Bradykinin produces erythema, owing to a direct effect on blood vessels, and wealing. Dose-response studies indicate that bradykinin is more potent than serotonin or histamine in respect of wealing.3. The response to serotonin differs qualitatively as well as quantitatively according to dose. High doses cause wealing and erythema with the characteristics of an axon reflex flare, but low doses produce erythema by a local effect without wealing.4. Using the technique of arterial occlusion, the occurrence of tachyphylaxis in respect of wealing was demonstrated with histamine and serotonin, but not with bradykinin. This evidence suggests that of the three agents, only bradykinin can mediate increased vascular permeability in sustained acute inflammation.5. The specificity of tachyphylaxis and the failure of anti-histamine to antagonize bradykinin wealing suggest that bradykinin and histamine act on separate blood vessel receptors.6. Corticosteroids do not inhibit wealing due to a wide range of doses of bradykinin. The anti-inflammatory activity of corticosteroids may therefore be due to reduced formation of kinins.

Adult↗
PubMed1969

The response of the sweat glands of the newborn baby to thermal stimuli and to intradermal acetylcholine.

1. Measurements of evaporative sweat loss were made on fifty-six premature and full-term babies 1-67 days after birth with an infra-red analyser and a ventilated capsule placed on the thigh. Measurements were also made of total evaporative water loss while in a closed metabolic chamber and of the regional distribution of sweating with starch-iodine paper.2. No sweating to thermal stimuli could be detected in infants of less than 210 days post-conceptual age, even when rectal temperature rose as high as 37.8 degrees C. In older infants sweat was detected first on the forehead and temple, later on the chest, and usually by 240-260 days post-conceptual age on the legs (term approximately 268 days). Generalized sweating on the limbs appeared at an earlier post-conceptual age in the more prematurely born infants.3. The response of sweat glands on the thigh to an intradermal injection of 2 mug acetylcholine (ACh) was tested. No sweat response was detected in infants under 225 days post-conceptual age, while all infants born within 2 weeks of term responded. The response was often augmented after 2-5 tests at 5-10 min intervals; all the eight infants born within 2 weeks of term who were examined twice in the first 2 weeks of life showed a greater response on the second occasion.4. An average of 414 active sweat glands/cm(2) were detected on the thigh in eight babies 7-10 days old born within 2 weeks of term. This was 6(1/2) times the number found in adults. The mean peak sweat rate to chemical stimulation was however only 2.4 nl./gland.min, which was 3 times lower than the maximum rate recorded in adults.5. In five infants with congenital defects of the brain and complete absence of temperature control there was no sweat response to thermal or direct chemical stimulation of the glands.6. Functional maturation appears to depend on intact central innervation and is marginally hastened by post-natal factors. Immaturity of the sweat glands can account for the lack of any response to thermal stimuli in premature babies, but not for the modest thermal response obtained in babies at term.

Acetylcholine↗
PubMed1966

Biological properties of streptococcal cell-wall particles. 3. Dermonecrotic reaction to cell-wall mucopeptides.

Abdulla, Essa M. (University of North Carolina School of Medicine, Chapel Hill), and John H. Schwab. Biological properties of streptococcal cell-wall particles. III. Dermonecrotic reaction to cell-wall mucopeptides. J. Bacteriol. 91:374-383. 1966.-Intradermal injection of rabbits and guinea pigs with mucopeptide suspensions produced an acute necrotic lesion which reached maximal severity within 24 hr and gradually subsided with scar formation. Necrosis was evident within 4 hr after injection of 100 mug, and an indurated area (10 x 10 mm) was produced with as little as 5.0 mug. Mucopeptides from six bacterial strains were studied. Comparison of cell walls and derived mucopeptides showed that the acute necrotic lesion tended to be more severe as the residual polysaccharide was decreased. Hyperimmunization with mucopeptide reduced the acute reaction, with evidence of immunological specificity. Incubation with lysozyme also modified the reaction in relation to extent of digestion. Toxicity was related to particle size, since extended sonic vibration decreased activity. Histological sections showed intense accumulations of polymorphonuclear leukocytes, along with altered collagen. A chronic nodular lesion appeared about 7 days after injection of the intact cell-wall fragments. In contrast to the acute necrotic reaction, this lesion was rarely produced by the mucopeptide separated from polysaccharide.

Animals↗
PubMed1999

A replication-incompetent adenovirus vector with the preterminal protein gene deleted efficiently transduces mouse ears.

Adenoviruses offer great potential as gene therapy agents but are limited by the strong inflammatory response that occurs in response to the recombinant virus. Since the degree of inflammation correlates in part with the potential of the viral vector for replication, we constructed a preterminal protein (pTP) deletion mutant adenovirus type 5 vector, Ad5dl308DeltapTPbeta-gal, that is replication incompetent due to deletion of the pTP gene and that has the E1 genes replaced by the Escherichia coli lacZ reporter gene under the control of the cytomegalovirus major immediate-early promoter. This virus was compared with a first-generation, replication-defective adenovirus vector, Ad5dl308beta-gal, that is isogenic except that it contains a wild-type pTP gene. To examine transduction efficiency and induction of inflammation, we developed a novel system involving intradermal injection of BALB/c mouse ears. Mouse ears can be accurately measured to determine the degree of edema as an indirect measurement of inflammation. Edema and inflammation were induced in a dose- and time-dependent manner by both viruses and correlated well. LacZ activity correlated inversely with edema and inflammation. The pTP-defective vector Ad5dl308DeltapTPbeta-gal transduced mouse ears much more efficiently and induced edema and inflammatory cell infiltration approximately 10-fold less efficiently than the first-generation vector Ad5dl308beta-gal. The diminished inflammatory response and increased efficiency of transduction observed with Ad5dl308DeltapTPbeta-gal indicate its promise as a gene therapy agent for other tissues. The results also demonstrate that the mouse ear model offers potential for the study of adenovirus-induced inflammation because of the ready access of the ears, the relative ease of continuous measurement, and the sensitivity to adenovirus transducing vectors.

Adenoviruses, Human↗
PubMed2004

A randomised placebo controlled trial of delipidated, deglycolipidated Mycobacterium vaccae as immunotherapy for psoriatic arthritis.

OBJECTIVES: To test the hypothesis that PVAC, delipidated, deglycolipidated heat killed Mycobacterium vaccae, is an effective and safe treatment for psoriatic arthritis (PsA). This treatment has shown promising results in psoriasis. METHODS: 36 patients with PsA in two centres were studied in this double blind, placebo controlled, randomised trial. Patients were randomised to receive two intradermal injections of 50 micro g PVAC or placebo and were followed up for 24 weeks. The primary end point was the Psoriatic Arthritis Response Criteria (PsARC), a composite measure based on changes in joint tenderness and swelling scores and physician and patient global assessments. RESULTS: The PsARC response at either 12 or 24 weeks was achieved by 9/18 (50%) placebo and 9/18 (50%) PVAC patients (p = 1.0). No significant differences in the Psoriasis Activity and Severity Index (PASI), patient or physician global assessments, CRP, or Health Assessment Questionnaire score over time were found between the two groups. However, changes in the pain visual analogue scale over time did differ between the two groups (p = 0.006): at 24 weeks the mean score in the PVAC group had declined by 19.2 mm and in the placebo group had increased by 4.8 mm. PVAC was well tolerated with no increased incidence of adverse events compared with placebo. CONCLUSIONS: PVAC was not shown to be as effective as immunotherapy for PsA. The striking response to placebo in this study reinforces the importance of adequately controlling therapeutic trials in PsA.

Adult↗
PubMed1992

Absence of potentiation of the skin response to intradermal bradykinin by a long-acting angiotensin converting enzyme inhibitor, trandolapril, at conventional antihypertensive dosage in human volunteers: a double-blind, randomized, cross-over, placebo-controlled trial.

A double-blind, randomized, cross-over, placebo-controlled study was carried out to determine the extent and duration of potentiation of the action of bradykinin introduced intradermally by a long-acting novel angiotensin converting enzyme (ACE) inhibitor, trandolapril. The investigations were performed in a temperature and humidity-controlled laboratory. Intradermal injections of 1 microgram, 2.5 micrograms and 5 micrograms of bradykinin and normal saline (as control) were made into the forearm skin of eight healthy normotensive male volunteers aged 21-33 years (mean 28 years) at baseline, 2, 4, 8, 24, 48, 72 and 96 hours after either 2 mg trandolapril or placebo given orally. Skin blood flow outside the induced weal was monitored by laser Doppler flowmetry (mean of recordings at four sites adjacent to the weal within the flare area). Flare area and weal volume were also measured. Trandolapril reduced the mean arterial pressure. However, there was no evidence that this activity was associated with a potentiation of the cutaneous action of bradykinin. In conclusion, it would appear that potentiation of the action of bradykinin may not be an important contributing factor to the fall in total peripheral vascular resistance associated with ACE inhibition in humans in the control of hypertension.

Administration, Oral↗
PubMed1999

Use of NK(1) knockout mice to analyze substance P-induced edema formation.

The mechanisms involved in tachykinin-induced neurokinin-1 (NK(1)) receptor-mediated edema formation have been studied in anesthetized wild-type and NK(1) knockout mice. Intradermally injected substance P (30-300 pmol), NK(1) agonists septide (3-30 pmol) and GR-73632 (3-30 pmol), and the mast cell-degranulating agent, compound 48/80 induced dose-dependent edema in wild-type skin, measured by the accumulation of intravenously injected (125)I-labeled albumin. Septide was 3-10x more potent than substance P. The tachykinins were inactive in knockout mice, but compound 48/80 induced a significantly greater edema (P < 0.05) than that observed in paired wild-type mice. Capsaicin (which releases endogenous neuropeptides) and exogenous tachykinins induced edema formation, which was reduced by the mast cell amine histamine H(1) antagonist mepyramine (P < 0.05). These findings confirm that tachykinins mediate edema formation via the NK(1) receptor and provide direct evidence that the septide-sensitive binding site is on the NK(1) receptor. Furthermore, results suggest that edema induced by the tachykinins, although totally dependent on NK(1) receptor-mediated mechanism, contains a mast cell-dependent component. The evidence is in keeping with an NK(1) receptor on mast cells.

Animals↗