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PubMed1997

RANTES is a pro-inflammatory chemokine and chemoattracts basophil cells to extravascular sites.

RANTES (regulated upon activation normal T expressed and secreted) is another member of the intercrine beta subfamily which acts as a selective chemoattractant for human monocytes and CD4-positive lymphocytes and increases the adherence of monocytes to endothelial cells. In this work, the effect of RANTES was studied on rat skin injection sites. Rats were intradermally injected with 50 microliters of RANTES, at different concentrations, fMet-Leu-Phe (FMLP), or LPS (positive controls) or PBS vehicle (negative control). The animals were then injected with 0.6 ml of Evans' blue in the tail vein in order to obtain a blue colour in the areas where the compounds were injected. After 4 h the rats were killed and the maximum diameter of the blue extravasation area was measured. The coloured areas were then excised and optical and electron microscopic studies were performed. In addition, in some of the excised tissue, a Northern blot analysis for histidine decarboxylase (HDC) mRNA was performed along with an estimation of the amount of histamine generated in the tissue injection sites. In these studies it was found that intradermal injections of 5, 2.5, and 1.25 x 10(-5) M RANTES produced a strong inflammatory response with the accumulation of a great number of basophil cells compared with the PBS (50 microliters) negative control, or FMLP (10(-6) M/50 microliters) or LPS (10 ng/50 microliters) positive control, after 4 h. Moreover, 5, 2.5, 1.25 x 10(-5) M RANTES produced a dose-response stimulation of HDC mRNA in the tissues of skin injection sites. The increasing number of basophils in the RANTES inflamed tissues led to augmentation of histamine content, compared with the PBS control. In conclusion, the pro-inflammatory chemokine RANTES stimulates the generation of HDC mRNA in skin injection sites.

Animals↗
PubMed1976

Vascular permeability induced by pancreatic exudate formed during acute pancreatitis in dogs.

Acute pancreatitis was produced in five dogs by injecting bile into the pancreatic duct. The capillary permeability effects of the exudate formed within the peritoneal cavity were studied by injecting the exudate intradermally into puppies. The amount of radioactively labeled albumin escaping from the circulation and appearing at the intradermal injection site was used as a measure of capillary permeability. It was observed that the peritoneal exudate, especially that produced in the early stage of bile induced pancreatitis, contains one or more substances which result in an increased capillary permeability when injected intradermally into puppies.

Amylases↗
PubMed1974

Immunological studies of Brown recluse spider venom.

Polyacrylamide gel electrophoresis of Loxosceles reclusa venom demonstrated that only one of seven or eight major (plus three or four minor) protein components caused necrosis in guinea pig skin. Sephadex gel filtration separated the venom into three major peaks, the second peak of which contained the dermonecrotic activity. Hyperimmunization of rabbits with increasing doses of venom from L. reclusa produced potent precipitating antisera, and the rabbits became resistant to lesion development. Ouchterlony-type immunodiffusion and immunoelectrophoretic studies revealed six to seven distinct precipitation lines, one of which stained intensely for esterase activity. Immunohistochemical techniques failed to detect any protease, lipase, catalase, acid phosphatase, alkaline phosphatase, or amylase activity in the venom. The spreading activity of recluse spider venom in guinea pig skin was inhibited as much as 71% by antivenom. Venom preincubated with antivenom was unable to incite lesions in guinea pig skin. Passive immunization of guinea pigs 18 h before an injection of venom conferred venom resistance upon the animals. Local injections of antivenom immediately after intradermal injections of venom markedly reduced the dermal lesion. Heparin reduced the local and systemic effects of venom when preincubated with whole venom or when administered systemically before an intradermal injection of venom. Treatment of whole venom with the chelating agent ethylenediaminetetraacetate did not inhibit its necrotic activity. Transfer studies from a 24-h lesion indicated that the necrotic activity was localized and remained active in tissue for at least 24 h but not for 5 days. No lesions developed when high concentrations of venom were intradermally injected into the skin of sacrificed guinea pigs, indicating that an interaction of body constituents and venom is essential for the development of a lesion.

Acid Phosphatase↗
PubMedDate not supplied

Evaluation of acellular dermal graft in sheet (AlloDerm) and injectable (micronized AlloDerm) forms for soft tissue augmentation. Clinical observations and histological analysis.

OBJECTIVES: To evaluate the histological and clinical properties of (1) subdermally implanted acellular dermal graft (AlloDerm) sheets vs intradermal bovine collagen and (2) subdermally or intradermally injected micronized AlloDerm vs type I bovine collagen cross-linked with glutaraldehyde (Zyplast). PATIENTS: Twenty-five adult patients testing nonallergic to bovine collagen. METHODS: (1) Stacked disks of AlloDerm were implanted subdermally behind one ear, and bovine collagen was injected intradermally behind the other. The soft tissue augmentation caused by the implants was measured by digital photography at 1, 4, and 12 weeks, and biopsy specimens of each implant type were examined at 3 months after implantation. (2) Micronized AlloDerm was injected intradermally and subdermally in 2 different locations behind one ear, and bovine collagen was injected in the same manner behind the other. The soft tissue augmentation caused by the implants was measured by digital photography at the time of implantation and at 1 and 4 weeks after implantation. All implants were examined 1 month after implantation. RESULTS: All patients tolerated both implants well. (1) AlloDerm implants retained a higher percentage of the original implant volume than Zyplast at 1 and 3 months after implantation. Histologically, AlloDerm implants were extensively invaded by host fibroblasts without any foreign body reaction. (2) Intradermally injected micronized AlloDerm implants retained a higher percentage of the original implant volume at 1 month after implantation than intradermal Zyplast. Histologically, micronized AlloDerm implants were extensively invaded by host fibroblasts without any foreign body reaction. No significant differences were noted between subdermally injected micronized AlloDerm and Zyplast. CONCLUSIONS: The macroscopic and microscopic behavior of subdermally implanted AlloDerm sheets and subdermally and intradermally injected micronized AlloDerm was compared with intradermally injected Zyplast. AlloDerm sheet volume persisted to a significantly (P < .001) greater degree than bovine collagen during the first 3 months after placement. Clinically, intradermally injected micronized AlloDerm volume persisted to a significantly (P = .01, .04, and .01, respectively) greater degree than intradermal Zyplast or subdermal micronized AlloDerm or Zyplast. Histologically, micronized AlloDerm and AlloDerm are well tolerated at 1 and 3 months, respectively. Host tissue incorporation with fibroblast in-growth and collagen deposition is seen in both materials. AlloDerm and micronized AlloDerm hold promise for use in facial soft tissue augmentation.

Adult↗
PubMed1988

Lymphocyte recruitment in delayed-type hypersensitivity. The role of IFN-gamma.

Lymphocytes are recruited out of the blood into delayed-type hypersensitivity (DTH) reactions, but the factors controlling their migration are poorly understood. Our previous studies have shown that IFN-alpha/beta, its inducers, and T cell lymphokines can induce lymphocyte migration into the skin after intradermal injection. The present studies were designed to determine the effect of rIFN-gamma, IL-1, and anti-IFN-gamma on lymphocyte recruitment into DTH. Small peritoneal exudate lymphocytes, which preferentially migrate to inflammatory sites, were labelled with 111In and injected i.v. into rats. The intradermal injection of IFN-gamma stimulated the migration of these lymphocytes into the skin. IL-1 induced very little migration by itself, but enhanced the effect of IFN-gamma. Kinetic analysis demonstrated that the migration of lymphocytes to IFN-gamma was rapid, with a peak at 6 h, whereas migration into a DTH reaction was minimal for the first 8 h and reached a peak 24 h after intradermal injection. Polyclonal rabbit anti-IFN-gamma anti-serum, and a Mab to IFN-gamma, DB-2, could almost completely block lymphocyte migration induced by IFN-gamma. Furthermore, DB-2 inhibited lymphocyte recruitment into DTH reactions by 50 to 90%. This Mab did not affect migration in response to IFN-alpha/beta, although it partially inhibited the response to polyI:C. The effect of IFN-gamma on lymphocyte recruitment was not specific for small peritoneal exudate lymphocytes, because both spleen T cells and lymph node cells migrated in response to IFN-gamma and DB-2 inhibited the recruitment of splenic T cells to DTH. Thus, IFN-gamma is a potent stimulator of lymphocyte migration into the skin and a major mediator of lymphocyte recruitment into DTH.

Animals↗
PubMed1986

Interleukin 1: a common endogenous mediator of inflammation and the local Shwartzman reaction.

In this study we investigated the role of interleukin 1 (IL 1) in the induction of inflammatory lesions and in the preparation and provocation of the local Shwartzman reaction. Both of these phenomena can be induced with a variety of agents. This suggested to us that a common endogenous mediator may be crucial to the development of these two lesions. When IL 1 was injected intradermally into shaved rabbit backs, 51Cr-labeled neutrophils accumulated at the injection site. Neutrophils began to accumulate less than 1 hr after injection, and the maximum rate of accumulation was observed by 4 hr. This activity was dose dependent. It was calculated that in all animals, 10(-14) mol of IL 1 induced significant neutrophil accumulation, whereas in many animals, as little as 10(-15) mol of IL 1 sufficed. When 4.2 X 10(-9) mol of E. coli 0111:B4 lipopolysaccharide W was injected i.v. 24 hr after an intradermal injection of IL 1 (2.9 X 10(-13) mol), a local Shwartzman reaction was seen 4 hr later at the intradermal injection site. IL 1 injected i.v. 24 hr after an intradermal injection of either IL 1 or lipopolysaccharide also produced a local Shwartzman reaction. These data indicate that IL 1 may be the common endogenous mediator of the inflammatory response, and IL 1 may serve in the same role for the preparation and provocation of the local Shwartzman reaction.

Animals↗
PubMed1997

No release of histamine and substance P in capsaicin-induced neurogenic inflammation in intact human skin in vivo: a microdialysis study.

BACKGROUND: Studies in rodents' skin have indicated substance P to be the main inflammatory mediator involved in neurogenic inflammation, acting partly by release of histamine from skin mast cells. The mediators released in neurogenic inflammation in human skin remain to be determined. OBJECTIVES: To determine the effects of intradermally injected and topically applied capsaicin on the release of histamine and substance P and skin responses in intact human skin in vivo. METHODS: Extracellular skin levels of histamine and substance P were measured by microdialysis technique and assayed by enzyme and radio immunoassays. Two kinds of dialysis fibres (210 microm, 2 kDa, and 500 microm, 20 kDa) were inserted intradermally into forearm skin for studies of histamine release to topically administered capsaicin and intradermally injected capsaicin and substance P. RESULTS: Baseline histamine skin levels were 8.0 +/- 0.7 nM. Intradermally injected capsaicin (0.3-30 microM, 7.5-750 pmol) caused significantly and dose-related flare and pain reactions, but no significant histamine release or weals. Intradermally injected substance P (1 and 3 microM, 25 and 75 pmol) released significant amounts of histamine (peak levels being 90 and 475 nM), evoked weal-and-flare reactions, but did not cause pain. Capsaicin 2% ointment, applied on the skin for 2.5 h, increased skin blood flow by 300-400% as measured by laser Doppler flowmetry, elicited a longstanding burning sensation, but did not release histamine. Substance P-like immunoreactivity (SP-LI) was below the 1.8 pM detection limit following insertion of 20 kDa dialysis fibre and after intradermal injection of capsaicin 3 microM. Intradermal injection of injection of 1 microM of substance P increased SP-LI levels to values greater than 4500 pM, confirming the ability of the dialysis fibre to recover this peptide. CONCLUSIONS: Capsaicin-induced neurogenic activation does not involve the release of histamine from mast cells or detectable amounts of substance P release from sensory nerves in normal human skin in vivo.

Administration, Topical↗
PubMed1969

Smallpox vaccination by intradermal jet injection. 3. Evaluation in a well-vaccinated population.

Smallpox vaccinations were performed in a well-vaccinated prison population by multiple-pressure technique and by intradermal jet injection using serial dilutions of vaccine. A total of 140 subjects were divided into groups, and each group was vaccinated by the multiple-pressure technique or by jet injection using 1 of 3 vaccine dilutions with the following calculated titres: ID-Jet 1 = 10(7.0) TCID(50)/ml, ID-Jet 1a = 10(6.3) TCID(50)/ml, ID-Jet 2 = 10(6.0) TCID(50)/ml. Clinical observations were made at intervals during the first week after vaccination. Prevaccination and post-vaccination serum samples were obtained immediately before and 30 days after the vaccination. Results based on clinical and serological evaluations indicated that smallpox vaccination by jet injection with the ID-Jet 1 vaccine was at least as efficacious as vaccination by the standard multiple-pressure technique.

Adult↗
PubMed1994

Antioxidant inhibition of skin inflammation induced by reactive oxidants: evaluation of the redox couple dihydrolipoate/lipoate.

Reactive oxygen species play an important role in mediating skin inflammation, and antioxidants may provide protection. We investigated the anti-inflammatory activity of natural antioxidants, such as superoxide dismutase, catalase, trolox (a water-soluble tocopherol analog) and the redox couple dihydrolipoate/lipoate in skin. Furthermore we compared the anti-inflammatory potency of natural R and racemic dihydrolipoate, as well as R and S lipoate. Skin inflammation in hairless mice was induced by intradermal injection of the hydrogen peroxide producing enzyme glucose oxidase (GOD) or by topical application of the prooxidant drug anthralin. Intradermal injection of the antioxidants inhibited skin inflammation caused by GOD (catalase, dihydrolipoate) and anthralin (trolox, superoxide dismutase, dihydrolipoate). There was no statistically significant difference between the anti-inflammatory activity of the natural R and racemic dihydrolipoate. R or S lipoate did not inhibit skin inflammation when injected intradermally. In feeding experiments, however, R lipoate significantly inhibited GOD-mediated skin inflammation, while S lipoate was only marginally protective. We conclude that (1) several natural antioxidants such as catalase, superoxide dismutase and dihydrolipoate have anti-inflammatory properties in dermatitis induced by reactive oxidants, (2) lipoate (oxidized dihydrolipoate) has skin anti-inflammatory activity when administered orally and (3) naturally occurring R lipoate is a more potent anti-inflammatory agent than the non-physiological S lipoate.

Animals↗
PubMed2003

Nitric oxide enhances substance P-induced itch-associated responses in mice.

1 Substance P (SP) elicits itch and itch-associated responses in humans and mice, respectively. In mice, NK(1) tachykinin receptors are involved in SP-induced itch-associated responses, scratching, and mast cells do not play a critical role. The present study was conducted to elucidate the role of nitric oxide (NO) on SP-induced scratching in mice. 2 An intradermal injection of SP (100 nmol site(-1)) elicited scratching in mice, and it was suppressed by an intravenous injection of the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), but not by its inactive enantiomer D-NAME. Intradermal injections of L-NAME (100 nmol site(-1)), another NOS inhibitor 7-nitroindazole (10 nmol site(-1)) and the NO scavenger haemoglobin (0.01-10 nmol site(-1)) also inhibited SP-induced scratching. 3 L-NAME (100 nmol site(-1)) did not affect scratching induced by an intradermal injection of 5-hydroxytryptamine (100 nmol site(-1)). 4 Intradermal injections of L-arginine (300 nmol site(-1)) and the NO donor (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (NOR3; 100 nmol site(-1)) increased scratching induced by SP. Intradermal injections of L-arginine (1-1000 nmol site(-1)) or NOR3 (1-100 nmol site(-1)) alone were without effects on scratching. 5 Intradermal injections of SP (10-100 nmol site(-1)) increased the intradermal concentration of NO in a dose-dependent manner in mice. An increase in NO levels induced by SP was inhibited by L-NAME and the NK(1) tachykinin receptor antagonist L-668,169, but not by the NK(2) tachykinin receptor antagonist L-659,877. 6 SP (1-10 micro M) elicited NO production in cultured human keratinocytes and the SP-induced NO production was inhibited by L-NAME and L-668,169. 7 We conclude that intradermal SP increases NO in the skin, possibly through the action on NK(1) tachykinin receptors on the epidermal keratinocytes and that NO enhances SP-induced itch-associated responses.

Adult↗
PubMed2000

Aluminium-induced granulomas after inaccurate intradermal hyposensitization injections of aluminium-adsorbed depot preparations.

BACKGROUND: The development of persistent subcutaneous nodules at the injection sites of aluminium-adsorbed hyposensitization solutions is rare. These nodules have been interpreted as a delayed, granulomatous hypersensitivity reaction to aluminium. We report for the first time a case of persistent intradermal granulomas that developed at the sites of inaccurate intradermal, instead of subcutaneous, hyposensitization injections. METHODS: An intradermal nodule was excised and processed for histopathology, scanning electron microscopy, and X-ray microanalysis. Intradermal and patch tests with aluminium hydroxide were performed. RESULTS: Histologically, the nodule presented a pattern of granulomatous inflammatory reaction surrounding foci of necrotic tissue. Scanning electron microscopy and X-ray microanalysis revealed deposits of aluminium within the granulomas. Patch tests with aluminium hydroxide were negative, and intradermal tests caused persistent intradermal granulomas. Subsequent hyposensitization therapy in our department with the usual subcutaneous injections of aluminium-adsorbed allergen extracts was well tolerated by the patient. CONCLUSIONS: Local toxic effects of aluminium may be crucial in the development of persistent intradermal injection-site granulomas. Such intradermal nodules may develop even if the subcutaneous route is well tolerated. We conclude that inaccurate intradermal injections of aluminium-containing solutions have to be strictly avoided.

Aluminum Hydroxide↗
PubMed1976

Effect of needle puncture and intradermal fluid injection on epidermal cell kinetics of albino guinea-pig skin.

The flanks of male albino guinea pigs were used to study the effect of needle puncture with or without intradermal (id) injection of 0.1 ml fluid. The center of the raised bleb was marked and biopsies taken 1,4,8,24,50 and 72 hrs after needle puncture and 1 hr after intraperitoneal (ip) injection of tritiated thymidine (3H-TdR). There were no significant differences in labeling index (LI) or mitotic index (MI) 1 hr after id, ip, or subcutaneous (sc) injection nor in percent labeled mitoses, 7 hrs after id or ip injection. The earliest increase in LI (180% above control) occurred 12 hrs after needle puncture, peaked at 24 hrs (ca. 3X control), and returned to control level by 50 hrs. The area affected had a radius of about 5 mm from the point of needle entry or center of the bleb. Within 12 hrs after needle puncture, there was an increase in labeled cells primarily at the periphery of the bleb area, about 4 mm from the point of needle entry. By 24 hrs, the distribution of labeled cells had moved toward the bleb center (LI = 65%). The first increase in mitoses (MI = 2.5%) was seen 24 hrs after needle puncture. It is concluded that id injection introduces no significant error in LI or MI to 8 hrs after needle puncture. It does, however, trigger many noncycling basal cells into DNA synthesis after 8 hrs, and this may increase the rate of transit of these cells to the granular layer.

Animals↗
PubMed1999

Attenuation of experimental pruritus and mechanically evoked dysesthesiae in an area of cutaneous allodynia.

We investigated the effects of tactile allodynia on the itch and mechanically evoked dysesthesiae produced by an intradermal injection of histamine in human volunteers. After an intradermal injection of capsaicin into the volar surface of one forearm, there developed an area of tactile allodynia to stroking and hyperalgesia to pricking the skin. Histamine was then injected simultaneously into the area of allodynia (experimental arm) and into the opposite forearm (control arm). Magnitude estimates of itch were obtained every 15 s for 5 min, and the areas of cutaneous hyperalgesia (pricking-evoked pain), alloknesis (stroking-evoked itch), hyperknesis (pricking-evoked itch) and wheal and flare were measured. The areas of wheal and flare were not significantly different on the two arms. The magnitude of itch and the areas of hyperknesis and alloknesis developed normally on the control arm but were absent or greatly reduced on the experimental arm. Thus, both the itch and the alloknesis and hyperknesis normally induced by histamine were absent or greatly reduced when histamine was injected in an area of capsaicin-induced allodynia. These results are compatible with the hypothesis that activity in capsaicin-sensitive, nociceptive primary afferent neurons evokes a central neuronal inhibitory process that prevents or reduces the itch and mechanically evoked dysesthesiae normally produced by an intradermal injection of histamine.

Adult↗
PubMed2003

Intradermal radioisotope injection optimises sentinel lymph node identification in breast cancer.

AIM: Currently there is no consensus on the optimal technique for sentinel lymph node (SLN) identification in patients with breast cancer. The aim was to compare the efficacy of intraparenchymal and intradermal isotope injection in sentinel lymph node mapping for breast cancer. METHODS: One hundred and twenty-five patients with histologically confirmed invasive breast cancer underwent SLN mapping using radioisotope and isosulphan blue dye followed by a back-up axillary dissection. The first 80 patients had intraparenchymal (IP) injection of radioisotope given in four portions around the tumor. The remaining 45 patients had an intradermal (ID) injection given at a single site over the tumour. Both groups had isosulphan blue dye injected around the tumour. Sentinel node(s) were identified using a combination of lymphoscintigraphy, blue dye and an intra-operative hand held gamma probe. RESULTS: The preoperative lymphoscintigram (LSG) demonstrated a SLN significantly more often in the ID isotope group compared to the IP isotope group (P=0.002). A combination of blue dye and isotope successfully located the SLN in 96% of the intraparenchymal group and 100% of the intradermal group. CONCLUSION: Our results suggest that intradermal isotope injection in combination with intraparenchymal blue dye optimises the localization of the sentinel lymph node in breast cancer.

Axilla↗
PubMed2006

Comparison of bacteriostatic normal saline and lidocaine used as intradermal anesthesia for the placement of intravenous lines.

Pain with intravenous (IV) insertion is a common fear for preoperative patients. As perianesthesia nurses, we take the necessary measures to minimize the discomfort and anxiety of our patients. Several research studies have found the use of bacteriostatic normal saline (BNS) to produce a less painful, yet equally effective, safer, and less expensive alternative method for intradermal anesthesia. The purpose of this study was to determine whether a difference existed in pain with intradermal injection and pain with venipuncture when intradermal anesthesia was used. Using an experimental design, 221 participants were randomly assigned by lottery convenience sampling into three groups: lidocaine, BNS, and no local anesthesia. Patients were asked to quantify their pain/discomfort level after the intradermal injection and IV insertion using a modified visual analog scale. Significant findings (P = < .05) indicated that BNS was less painful on injection, and both BNS and lidocaine were effective as local anesthetics for IV insertion. This study helped perianesthesia nurses and patients in determining which method of IV insertion is more effective and reasonably acceptable to ensure patient comfort, satisfaction, and positive outcomes.

Adult↗
PubMed1991

Role of lipooligosaccharides in experimental dermal lesions caused by Haemophilus ducreyi.

The mouse and rabbit intradermal injection models have been used to define factors that may be important in Haemophilus ducreyi pathogenesis. We used H. ducreyi strains with diverse geographic origins and phenotypic characteristics to evaluate the experimental models. Injection of live and heat-killed bacteria caused skin abscesses in both models. Semiquantitative cultures of skin injected with live bacteria showed that H. ducreyi failed to replicate in animal tissue. These data suggested that the experimental lesions were caused by a heat-stable substance such as lipooligosaccharide (LOS). In mice, injection of H. ducreyi and Haemophilus influenzae LOS and Escherichia coli lipopolysaccharide caused mild to moderate inflammation. In rabbits, injection of H. ducreyi LOS caused intradermal abscesses that were histologically similar to those caused by live and heat-killed bacteria. H. ducreyi and Neisseria gonorrhoeae LOS caused significantly larger lesions than equivalent amounts of H. influenzae LOS and E. coli lipopolysaccharide in the rabbit model. We conclude that the intradermal injection models are not valid models to study the growth of H. ducreyi in vivo. However, these data indicate that H. ducreyi LOS may play an important role in the pathogenesis of chancroid and that the rabbit model should be useful in studying H. ducreyi LOS toxicity at the cellular level.

Animals↗
PubMed1995

Role of tryptase in immediate cutaneous responses in allergic sheep.

In this study, we used a specific tryptase inhibitor, APC-366 [N-(1-hydroxy-2-napthoyl)-L-arginyl-L- prolinamide hydrochloride] to investigate the effect of intradermally administered tryptase and tryptase released by antigen challenge on the immediate cutaneous reaction (ICR) in allergic sheep. The surface areas of cutaneous wheals produced by intradermal injections (0.05 ml) of 1 and 10 ng tryptase alone, tryptase combined with 3 U heparin (tryptase-heparin), or Ascaris suum antigen (10(-5) dilution) with or without pretreatment with APC-366 (1 mg/ml) were measured at 20 and 60 min after challenge. Intradermal injections of 1 and 10 ng tryptase alone (n = 7) produced an ICR of < or = 20% of that obtained after injection of histamine (5% wt/vol). Intradermal injection of tryptase-heparin (n = 7), however, resulted in 50 (1 ng) and 82% (10 ng) of the ICR to histamine (both, P < 0.05 vs. tryptase alone). APC-366 inhibited (P < 0.05) the ICR to 1 and 10 ng tryptase-heparin by > or = 70% at all times (n = 8) but had no effect on the histamine-induced ICR (n = 3). A combination of the histamine H1 antagonist chlorpheniramine (2 mg/kg iv) and the H2 antagonist metiamide (3 mg/kg iv) given 40 min before challenge (n = 8) inhibited the response to 1 and 10 ng tryptase-heparin by 42 and 62% at 20 min and by 96 and 86% at 60 min, respectively (all, P < 0.05). APC-366 also blocked the ICR to A. suum antigen by 68% (P < 0.05) in nine sheep. These results indicate that intradermal injection of tryptase-heparin can induce an ICR. This ICR can be inhibited by APC-366 or a combination of the histamine H1 and H2 antagonists, suggesting that the tryptase response is mediated by histamine. APC-366 also blocks the mast cell-mediated ICR to intradermally injected A. suum antigen. Collectively, these results suggest that tryptase may modulate mast cell histamine release.

Animals↗