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PubMed1981

The in vivo effects of lymphokines on mitotic activity and keratinization in guinea pig epidermis.

Lymphokines may alter epidermal growth and differentiation contributing to changes such as acanthosis and hyperkeratosis. The main in vivo effects of lymphokines on epidermal mitotic activity were therefore investigated. Guinea pigs were injected intradermally with antigen-stimulated lymphocyte culture supernatants and a partially purified lymphokine preparation in phosphate buffered saline (PBS) 18, 24, 36 and 48 hr prior to biopsy. Control sites were injected with unstimulated supernatants and PBS respectively and the mitotic activity determined by use of a stathmokinetic agent. Both lymphokine injected areas and controls showed significantly increased mitotic indices compared to untreated skin which was apparent only at 24 hr. However mitotic activity in lymphokine lesions was significantly higher than in control lesions. There was no difference in the effect on mitotic activity between PBS and unstimulated culture supernatants. Lymphokine lesions at 24 hr also exhibited marked epidermal edema and acanthosis compared to minimal changes in controls. A variable patchy parakeratosis developed between 18 and 24 hr in areas injected with partially purified lymphokine but not in control sites or after injection with unpurified supernatants. The lymphokine-induced inflammatory infiltrate was mild and consisted mainly of neutrophils not differing significantly from that of the control lesions. This strongly suggests that lymphokines induce an alteration in epidermal kinetics and keratinization by a direct effect on keratinocytes and not indirectly via the dermal inflammatory infiltrate.

Animals↗
PubMed1982

Formation of UV-induced apoptosis relates to the cell cycle.

The relationship of the rate of epidermal proliferation to ultraviolet (UV)-induced cell death, namely sunburn cell (SC) formation, was investigated in vivo using the guinea-pig model. The number of SCs was correlated with (1) cellophane tape stripping which stimulates the proliferation rate and (2) treatment with antimitotic and antimetabolic agents which suppress the proliferation rate. The tape stripping performed 14 h before UV irradiation significantly increased the number of SCs counted 24 h after UV irradiation from a mean of 17.4 to 62.6 per section, and the tritiated thymidine (TdR-3H)-labelling index (LI) increased from a mean of 8.1 to 27.4%. SC counts and LI were markedly decreased by the intradermal injection of colchicine, methotrexate, hydroxyurea or 5-fluorouracil given once immediately after the tape stripping. The autoradiographic study showed that 23.2% of SCs were labelled when TdR-3H was given intradermally 1 h before UV exposure, while no SCs were labelled when TdR-3H was given immediately after UV exposure. The labelled SC count (23.2%) which presumably represents S phase cells at the time of UV exposure, was higher than the LI (mean 8.1%). These results suggest that proliferating cells, possibly S phase cells, may be responsible for SC formation.

Animals↗
PubMed2003

[Inhibiting scar formation in rat cutaneous wounds by blocking TGF-beta signaling].

OBJECTIVE: TGF-beta plays a key role in wound scarring. This study explored the possibility of using gene therapy to inhibit wound scarring by blocking TGF-beta signaling. METHODS: In vitro, human normal dermal fibroblasts were infected with recombinant adenoviruses of truncated TGF-beta receptor II (tTGF-betaRII, 100 pfu/cell) and beta-galactosidase (beta-gal, 100 pfu/cell), and their effects on regulating TGF-beta1 gene expression were analyzed by Northern blot. For gene therapy, beta-gal and tTGF-betaRII viruses (1 x 10(9) pfu)were injected intradermally at left and right side of dorsal skin of newborn Sprague-Dawley rats (n = 15) respectively. A full-thickness incisional wound (0.5 cm long) was created at the injection sites of each rat 2 days post-injection. An incisional wound was similarly created in the middle part of the dorsal skin of tTGF-betaRII transgenic mice (n = 5) and control mice (n = 5). Wound tissues of rats and mice were harvested at various time points post-wounding for histological and immunohistochemical analysis. Scar area in tissue section was measured by Image-Pro Plus software. RESULTS: Over-expression of tTGF-betaRII markedly reduced TGF-beta1 gene expression in dermal fibroblasts. Adenovirus mediated gene expression in skin reached a peak level 2 - 3 days post-injection, and decreased gradually at 5 - 7 days. Two weeks post-wounding, histology and quantitative analysis demonstrated that relative scar area in the wounds of transgenic mice and control mice were 136,969.8 +/- 66,339 and 474,641.6 +/- 227,396 respectively, the scar area of transgenic wounds was 29 percent of control area (P < 0.05). In all rats, wounds transfected with tTGF-betaRII gene healed with much less scarring (relative scar area 128,311.2 +/- 36,764.6) than control wounds (251,189.1 +/- 62,544.7) of the same rat, with a 45% reduction of scar area in average (P < 0.001). In addition, the tTGF-betaRII expression also decreased inflammation and TGF-beta1 production in treated wounds, and promoted the repair of panniculus muscle in treated wounds. CONCLUSIONS: Adenovirus mediated over-expression of tTGF-betaRII can block TGF-beta signaling and inhibit wound scarring, and thus can serve as a gene therapy strategy to control wound scarring.

Adenoviridae↗
PubMed1990

Effects of sedation on intradermal skin testing in flea-allergic dogs.

Effects of 4 commonly used sedatives on the wheal-and-flare response to histamine and flea antigen were evaluated in 8 flea-allergic Beagles. Skin testing was performed in 12 separate occasions, 3 to 4 days apart. Twelve intradermal injections were given during each skin test: 5 doubling dilutions of histamine phosphate, 6 doubling dilutions of flea antigen, and a phosphate-buffered saline solution (negative control). Of the 12 intradermal skin tests, 8 were control tests performed on nonsedated dogs. The remaining 4 tests were performed on dogs sedated with xylazine, ketamine and valium combination, acepromazine, or oxymorphone. Oxymorphone had the most profound effect on skin test results, significantly (P less than 0.05) decreasing skin responsiveness in 8 of 11 test sites (by objective evaluation) and in 5 of 11 test sites (by subjective evaluation). Xylazine sedation enhanced skin test results in 4 of 11 test sites (by objective evaluation) and in 1 of 11 test sites (by subjective evaluation). In non instance did xylazine significantly decrease skin responsiveness to histamine or flea antigen. Xylazine is the recommended sedative in dogs when sedation is necessary for intradermal skin testing.

Acepromazine↗
PubMed1998

Granulocyte/macrophage colony-stimulating factor increases wound-fluid interleukin 8 in normal subjects but does not accelerate wound healing.

Granulocyte/macrophage colony-stimulating factor (GM-CSF) is thought to play an important part under conditions of impaired wound healing. This is not confirmed and it is also unknown whether GM-CSF affects wound healing in healthy subjects. We conducted a randomized, double-blind, placebo-controlled pilot study in 10 healthy volunteers. Triplicate wounds (10 x 10 x 0.5 mm) on the right and left upper thigh were made by a razor blade and injected with GM-CSF or a solvent control. Four of the 10 volunteers were re-examined after 2 months by investigating the healing of a new set of triplicate wounds injected with solvent control alone (controls). Factors measured were wound healing time, wound-fluid cytokines by enzyme-linked immunosorbent assay, wound-fluid inflammatory cells and dermal thickness by ultrasonography. Intradermal injection with 20 micrograms GM-CSF per wound caused significantly higher wound-fluid GM-CSF and interleukin 8 (IL-8) levels than in controls, but did not affect the time needed for wound closure (mean 11 days in all groups), dermal thickness, wound-fluid inflammatory cells or other wound-fluid cytokines, e.g. vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF). Transforming growth factor (TGF) beta 1 and beta 2, epidermal growth factor (EGF), and beta-fibroblast growth factor (beta-FGF) were not measurable in any wound fluid. The lack of efficacy of exogenously delivered GM-CSF on wound healing in healthy subjects is probably based on the failure of GM-CSF to induce 'wound-healing cytokines' like PDGF, FGF, TGF, EGF or VEGF. However, GM-CSF increases IL-8 release, which is a potent chemotactic cytokine, indicating that GM-CSF might be of therapeutic value under conditions of impaired chemotaxis.

Adult↗
PubMed1981

Pathogenic effects of bullous pemphigoid autoantibodies on rabbit corneal epithelium.

Bullous pemphigoid (BP) is associated with circulating autoantibodies reactive with an antigen(s) of the basement membrane zone (BMZ) of skin and mucosae. The pathogenicity of these autoantibodies, although suspected, is unconfirmed. We have investigated the effects of BP autoantibodies on a closely related tissue, the corneal epithelium of the rabbit. IgG fractions from the sera of seven patients with BP were purified by (a) ammonium sulfate precipitation, (b) ion exchange chromatography, or (c) gel filtration. Control IgG was prepared by ion exchange chromatography of pooled normal human gamma globulins. 32 rabbits received corneal intrastromal injections of BP IgG fractions (50 microliter, 0.95-2.05 mg total dose) in one eye, and control IgG (50 microliter, 1.8 mg) in the contralateral cornea. 28 of 32 BP IgG injections produced corneal inflammatory lesions, 10 of which developed visible blisters. Histologically, lesions showed polymorphonuclear cells clustering along the BMZ, and subepithelial blister formation. Immunofluorescence showed in vivo bound IgG and C3 at the BMZ. The intensity of inflammation was dose dependent and correlated often with in vitro complement fixation titers of the fractions. None of 32 corneas injected with control IgG became inflamed. BP IgG fractions injected intradermally into the ear skin of rabbits failed to produce inflammation. This may be due to slow clearance of IgG in the cornea, and optimal binding by the corneal epithelium. The intracorneal injections of BP IgG reproduce the clinical, histological, and immunological features of BP. This study provides evidence that BP autoantibodies are pathogenic.

Animals↗
PubMed2000

[Preoperative lymphoscintigraphy guided sentinel lymph node biopsy in malignant melanoma]

The authors present preliminary experience with preoperative sentinel lymph node biopsy carried out with lymphoscintigraphy in patients with malignant melanoma. PATIENTS AND METHODS: In the present study patients operated for primary cutaneous malignant melanoma of moderate and high severity were included. On the day of surgery isotope labelled colloid was injected intradermally around the tumor to indicate the lymphatics and to obtain basic information about the localization of the sentinel lymph node(s).During surgery the lymph node(s) previously visualized by the injection of patent-blue staining were detected with the aid of a gamma probe. Simultaneously, the excision of the primary tumor was extended. Histologically verified metastasis in the surgically removed lymph node(s) necessitated block dissection possibly within two weeks. RESULTS: The distribution of patients (19) according to tumor localisation: 2 - upper extremities; 9 - lower extremities; 2 - sacral region; 6 - trunk. Tumor thickness ranged from <1.5 mm (6 patients) to 1.5-3 mm (5 patients) and to >3 mm (8 patients). In two cases the identification of the lymph node has failed. Positive sentinel ymph nodes were detected in two patients. It is noteworthy that with one patient the sentinel lymph node was not regional but intransit. This study was aimed at the development of a suitable method. Further on we wish to try it in prospective randomized studies.

Journal Article↗
PubMed2002

A validation trial of subdermal injection compared with intraparenchymal injection for sentinel lymph node biopsy in breast cancer.

Sentinel lymph node (SLN) biopsy is increasingly being used as an accurate and less morbid surrogate for axillary dissection. However, a standardized technique in the biopsy of SLNs is not used. Some authors propose subdermal injection to be as accurate as peritumoral intraparenchymal injection (IPI). Our objective is to determine whether the SLNs identified by subdermal injection truly represent SLNs and match those found with IPI. Specific end points of the study were 1) successful localization of the SLN by the IPI of isosulfan blue or the radiocolloid intradermal injection, 2) successful uptake of radiocolloid and isosulfan blue on individual SLN, and 3) determination of the frequency with which the radiocolloid injection detected the "gold standard" blue SLN. SLNs were found in 71 of 73 cases (success rate = 97%). Blue SLNs were identified in 64 patients (88%). SLNs in 61 patients (84%) were radioactive. A total of 112 SLNs were identified in 71 patients (1.6 nodes/patient). Seventy-six of 87 SLNs found with IPI were also radioactive (concordance of 87%). All SLNs harboring metastatic cancer (16 patients) were found by both techniques, being both blue and radioactive. Our results support the concept of shared lymphatic pathways in the breast with a high degree of communication between the subdermal lymphatics and the intraparenchymal lymphatics. The success in identification of the SLN is made simpler and improved by the addition of subdermal radiocolloid injection.

Adult↗
PubMed2006

Use of local anesthesia for arterial punctures.

BACKGROUND: Except for intravenous therapy, arterial access is the most common invasive procedure performed on critically ill patients. Arterial puncture is a source of pain and discomfort. Intradermal injection of lidocaine around the puncture site decreases the incidence and severity of localized pain when used before arterial puncture. OBJECTIVE: To review the recommendations and studies related to the use of intradermal lidocaine to decrease pain during arterial punctures. METHODS: Articles were identified by doing a systematic computerized search of MEDLINE (1980 to January 2006) to evaluate articles and reference lists of articles and a manual search of the references listed in original and review articles. English-language articles that evaluated any aspect of pain related to arterial puncture and cannulation, pain related to and methods of introducing lidocaine subcutaneously, and perceptions and use of local anesthesia for arterial or intravenous punctures were reviewed. RESULTS: Except among anesthesia providers, the use of a local anesthetic before arterial puncture is not universal, contrary to the standard of practice. A number of false perceptions may prevent wider use of such anesthetics. CONCLUSION: Before a plan for behavior modification or policy change is recommended for use of local anesthesia to decrease pain associated with arterial puncture, further research must be done to determine nurses' perceptions of use, actual practice, and currently established local policies.

Anesthetics, Local↗
PubMed1981

Allergy to aminophylline: lack of predictability by skin testing.

Problems with determining hypersensitivity to aminophylline, ethylenediamine, and theophylline with intradermal skin tests and patch tests are reported in three patients. Three patients were tested with intradermal injections of 0.9% sodium chloride, 1% aminophylline, 1% ethylenediamine, and 0.5% theophylline following apparent allergic reactions to aminophylline. Patch testing using hydrophilic ointment base, 1% aminophylline, 1% ethylenediamine, and 0.5% theophylline was also done. All three patients had no reaction to intradermal sodium chloride or theophylline; all patch tests were negative. The first patient reacted to ethylenediamine strongly and to aminophylline more weakly; punch biopsy of the ethylenediamine reaction site showed a direct toxic effect with no allergic component. Punch biopsy of the aminophylline site showed a typical hypersensitivity reaction. Two concentrations (0.5% and 1.0%) of ethylenediamine injection were used to test the second patient, and he reacted to both concentrations but not to any other injections. His positive reactions contained blisters rather than the typical wheal-and-flare reaction of hypersensitivity. The third patient had similar responses including reactions to 0.5% and 0.1% ethylenediamine (he was not tested with 1% ethylenediamine). Skin testing may be of value in predicting aminophylline or ethylenediamine allergy, but the nonspecific toxic effect of ethylenediamine makes interpretation difficult.

Aged↗
PubMed1999

Use of subatmospheric pressure to prevent doxorubicin extravasation ulcers in a swine model.

UNLABELLED: Application of subatmospheric pressure to sites injected with doxorubicin prevented ulcer formation in treated sites (0 ulcers/16 sites) compared to control wounds (10 ulcers/16 sites) in a pig model. BACKGROUND AND OBJECTIVES: Extravasation of doxorubicin hydrochloride (Adriamycin) frequently causes chronic ulcers, which usually progress and expose underlying structures such as tendons and bone. The exact mechanism of action that causes cell death and the chronic ulcers is unknown. METHODS: Eight sites were injected intradermally with doxorubicin on each of 4 pigs. Four sites on each animal served as untreated controls. The remaining four sites were exposed to 125 mm Hg subatmospheric pressure applied 1 h after injection. The sites were observed on a three times per week schedule. Sites that did not develop ulcers were re-injected up to a total of four injections. The animals were observed for 5 weeks. RESULTS: Ten of sixteen control sites developed ulcers. No subatmospheric pressure treated sites developed ulcers. The incidence of ulcer formation was significantly less for treated wounds compared to control wounds at P < 0.001 by Fisher's exact test. CONCLUSIONS: This physical modality appears to successfully prevent ulcer formation after doxorubicin injection.

Animals↗
PubMed1988

Altered leukocyte delivery to specific and nonspecific inflammatory skin lesions following burn injury.

This study assessed the effect of burn trauma on the in vivo leukocyte cell delivery during the first 24 hr of the delayed type hypersensitivity (DTH) skin test reaction and a bacterial skin abscess. Inbred male Lewis rats sensitized to keyhole limpet hemocyanin (KLH) were given a 30% scald burn or sham burn. Three days later the animals were injected intradermally, at different sites, with 0.3 mg of KLH, 10(8) organisms of S. aureus 502A, and 0.1 cc of saline, at 2 to 24 hr. Leukocytes labelled with Indium111 oxine(leu111) were injected intravenously. In sham rats the peak leu111 influx in the DTH reaction occurred at 2-4 hr while in the abscess it was biphasic with peaks at 3 hr and 6-8 hr. In burn trauma rats there was a markedly increased leu111 peak at 2 hr in both the DTH and abscess reactions followed by a significantly lower than normal leu111 delivery in the late (6-24) hours. This marked early leukocyte influx in burned rats was paralleled by a reduced DTH skin test lesion (8.2 +/- 1.1 mm to 4.2 +/- 1.1 mm) and an increased bacterial abscess (5.1 +/- 1.1 mm to 8.1 +/- 0.9 mm) post burn. There was a direct correlation between leukocyte cell delivery to a DTH reaction and a bacterial abscess (r8 = 0.69, Spearman rank; p less than 0.001). We conclude that burn trauma results in altered leukocyte delivery to inflammatory lesions and the DTH response can be used to assess the ability of a burn trauma host to recruit leukocytes at a site of infection.

Abscess↗
PubMed1984

Labeling of peripheral blood polymorphonuclear leukocytes with indium-111: a new method for the quantitation of in-vivo accumulation of PMNLs in rabbit skin.

A precise method for quantitation of polymorphonuclear leukocyte (PMNL) accumulation in skin in vivo, has been developed so that the proinflammatory effects of various agents can be compared. This method can also be used to evaluate the effect of therapeutic agents on PMNL accumulation in vivo. Rabbit PMNLs were purified from heparinized blood by dextran sedimentation, hypotonic lysis, and separation on Ficoll-Hypaque. The PMNLs were labeled with 3-5 microCi per 10(6) cells of 111In oxine and reinfused coincidentally with different concentrations of different chemotactic and proinflammatory materials injected intradermally into the back. In some experiments, varying concentrations of acetic acid were applied topically. Four to 18 hours later, the rabbits were sacrificed. Eight-millimeter punch biopsies were obtained from the injection sites and counted in a gamma counter. The number of PMNLs infiltrating the dermis was also quantitated in histologic sections. A significant correlation was found between the percent increase in radioactivity and the percent increase in PMNL accumulation morphologically. Dose-response curves were generated using such proinflammatory materials as formyl-methionyl-leucyl-phenylalanine, lipopolysaccharide, activated serum, trypsin, glycogen, and acetic acid. These curves were highly reproducible from animal to animal. Using this assay, we found that as little as 1 microgram of trypsin induced detectable PMNL accumulation. This is 2-3 logs more sensitive than injecting mice intraperitoneally with trypsin. Diisopropyl fluorophosphate-inactivation of trypsin inhibited PMNL accumulation. This sensitive and quantitative bioassay of PMNL accumulation permits evaluation of multiple agents in the same animal, which decreases animal to animal variation.

Acetates↗
PubMed1990

Cutaneous dermal Ia+ cells are capable of initiating delayed type hypersensitivity responses.

The presence of Langerhans cells (LC) within the epidermis has been shown to be critical for inducing T-cell-mediated immune responses in the skin. The purpose of this study was to assess whether cells in the dermis can initiate T-cell-mediated delayed-type hypersensitivity responses in vivo. Initially, back skins from C3H mice were trypsinized to remove the epidermis. The dermis was enzymatically dispersed and filtered to obtain a cell suspension. However, dermal cells exposed to trypsin were contaminated with numerous disaggregated hair follicles. These hair follicles contained Ia+ cells (presumably LC), and upon haptenation in vitro with trinitrophenyl, initiated contact hypersensitivity reactions in vivo. We therefore used dispase in place of trypsin to prevent follicular disaggregation and to allow preparation of dermal cell suspensions free of hair follicles. These hair follicle-free dermal cells were haptenated with trinitrophenyl and injected intradermally. Elicitation of contact hypersensitivity by epicutaneous painting 6 d later revealed the mean +/- SEM incremental ear-swelling response to be 53 +/- 8 mm X 10(-3). In contrast, mice sensitized by injection with dermal cells depleted of Ia+ cells demonstrated only 10 +/- 1 mm X 10(-3) of ear swelling. Thus, like dendritic LC of the epidermis, perivascular dendritic Ia+ cells of the dermis are capable of initiating T-cell-mediated contact hypersensitivity in vivo and may be highly relevant for presentation of antigen to T cells trafficking through the dermis.

Animals↗
PubMedDate not supplied

Complete regression of a guinea pig hepatocarcinoma by immunotherapy with "tumor-immune" RNA or antibody to fibrin fragment E.

Two novel immunotherapeutic regimens were developed for a uniformly lethal, intradermally growing transplantable ascites variant (line 10) of a diethylnitrosamine-induced hepatoma in strain 2 guinea pigs. In an apparently tumor-specific immunotherapy model, 32 guinea pigs were cured by the injection into the tumor area, five or seven days after tumor challenge, of syngeneic or xenogeneic RNA extracts obtained from lymphoid tissues of line 10-immune strain 2 guinea pigs or rhesus monkeys, as part of a total regimen which included syngeneic nonsensitive peritoneal exudate cells injected prior to, and tumor-specific antigen injected after, the RNA. In another immunotherapy model, not tumor-specific, 18 strain 2 guinea pigs were cured by the injection into the tumor area, 6 and 16 days after tumor challenge, of antibody specific for fibrin fragment E (FFE), an essential component in the formation of a fibrin matrix considered to be important in tumor development. When therapy was delayed to 12 days in the RNA test system, or to 16 days in the anti-FFE test system, complete abrogation of the tumors did not occur. The long-term survival of the 50 successfully treated animals and their immunity to further tumor challenge indicated that both immunotherapeutic procedures had systemic effects. To test this further, line 10 cells were injected intradermally simultaneously at two sites and only one site was treated. When the one tumor location was treated with anti-FFE, complete regression of the treated tumor and a 30% retardation in the development of the untreated tumor were observed. When this tumor location was treated with the RNA regimen, complete regression of the tumors occurred at both the treated and the untreated sites. Optimal conditions for both immunotherapeutic models and their combination have yet to be establshed. Nonetheless, both immunotherapeutic regimens were more effective than any other immunotherapy thus far reported for this tumor, including the use of BCG or its derivatives.

Animals↗
PubMed1975

[Effect of injection of a phosphorylcholine-containing compound from Nippostrongylus brasiliensis on the infestation of the rat by this parasite].

Rats were injected intradermally with the purified phosphorycholine bearing component of the nematode Nippostrongylus brasiliensis. Eight days later they were experimentally infected with 1 X 10(3) infective larvae of the parasite. Compared to the non injected controls we showed a significant decrease in the number of adult worms able to be established in the small intestine. This protective effect seems to be due at least partly to a phenomenom being located between the skin and the lungs of the rats.

Ancylostomatoidea↗
PubMed2000

Nociceptive neuroendocrine negative feedback control of neurogenic inflammation activated by capsaicin in the rat paw: role of the adrenal medulla.

Recently we have found that inhibition of bradykinin-induced synovial plasma extravasation by transcutaneous electrical stimulation at strengths which excite unmyelinated afferent axons is mediated by the hypothalamo-pituitary-adrenal axis. Here we tested whether stimulation of nociceptors in the rat paw by intradermally injected capsaicin inhibits bradykinin-induced synovial plasma extravasation and whether this inhibition is mediated by the hypothalamo-pituitary-adrenal or sympatho-adrenal axis. Furthermore, we tested whether inhibition of bradykinin-induced plasma extravasation generated by intraperitoneally injected capsaicin, which preferentially excites visceral afferents, is mediated by the hypothalamo-pituitary-adrenal or sympatho-adrenal axis. We used normal rats, subdiaphragmatically vagotomized rats, rats with denervated adrenal medullae and rats with acutely transected spinal cords at the segmental levels T1/T2 or T12/L1. Injection of capsaicin into the plantar or palmar surface of the paws produced a depression of bradykinin-induced plasma extravasation. The inhibition elicited from the forepaw was larger than that from the hindpaw. The inhibition of bradykinin-induced plasma extravasation elicited from both paws was potentiated by subdiaphragmatic vagotomy. Denervation of the adrenal medullae abolished the inhibitory effect of intradermal capsaicin in vagus-intact and in vagotomized animals. After spinalization at the segmental level T1/T2, capsaicin injected into the forepaw did not depress bradykinin-induced plasma extravasation either in vagus-intact or in vagotomized animals. Capsaicin injected into the hindpaw in these spinalized animals produced a small depression. After spinalization at the segmental level T12/L1 no depression was produced by capsaicin injected into the hindpaw. Depression of bradykinin-induced plasma extravasation generated by intraperitoneal injection of capsaicin in vagus-intact and in vagotomized animals was also abolished or attenuated after denervation of the adrenal medullae. This shows that this depression was also largely dependent on the activation of the sympatho-adrenal system. We conclude that depression of bradykinin-induced plasma extravasation during stimulation of nociceptors by capsaicin is mediated predominantly by the sympathoadrenal pathway. This finding differs from the inhibitory mechanism of depression of bradykinin-induced plasma extravasation generated by cutaneous electrical stimulation, which is mediated by the hypothalamo-pituitary-adrenal axis.

Adrenal Medulla↗
PubMed1999

Inhibitory effect of oral administration of Lactobacillus casei on 3-methylcholanthrene-induced carcinogenesis in mice.

The present study was designed to determine whether tumor induction by 3-methylcholanthrene (MC), a carcinogenic hydrocarbon, can be inhibited by oral administration of Lactobacillus casei strain Shirota (LC). C3H/HeN mice were divided into four groups and assigned to the following treatments: treated with MC and given control or LC-containing diet; treated with vehicle only and given control or LC-containing diet. MC (1 mg) was injected intradermally at 7 weeks of age and the tumor incidence was monitored; LC was mixed into a diet at a concentration of 0.05% (w/w) and the diet was fed from the day of MC injection throughout the study. Spleen cells were analyzed for the immune parameters at 12 and 16 weeks after the MC injection. Oral feeding of mice with LC reduced tumor incidence (P < 0.05). MC treatment lowered the in vitro response to concanavalin A (Con A) of spleen cells, the secretion of interleukin-2 in spleen cell culture after stimulation of the cells with Con A and the proportions of CD3+ CD4+ and CD8 + splenic cells. However, the analysis of the spleen cells obtained from the mice treated with MC and given the LC-containing diet revealed that these disrupted host immune parameters were maintained at the level of normal controls. These results suggest that oral feeding of mice with LC inhibits MC-induced tumorigenesis by modulating the disrupted host immune responses during MC carcinogenesis.

Animals↗