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PubMed1986

Luteinizing hormone and follicle-stimulating hormone responses to intransal gonadotropin-releasing hormone.

For determination of the dose-response relationships of plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to the intranasal administration of gonadotropin-releasing hormone (GnRH), normal adult men were administered doses of 100, 200, 400, and 800 micrograms of GnRH on separate days, and plasma LH and FSH were measured before and after nasal insufflation of GnRH. Plasma LH was increased after a minimum dose of 200 micrograms GnRH. Median peak plasma LH levels occurred 30 minutes after intranasal GnRH and followed a log-dose relationship. When compared with intravenous GnRH, the biopotency of intranasal GnRH at the 200-, 400-, and 800-microgram doses was 1.1%, 2.3%, and 6.2%, respectively. Plasma FSH levels rose significantly only after the highest (800-micrograms) intranasal GnRH dose. From these data, we conclude that in eugonadal adult men the minimal effective dose of intranasal GnRH to elicit a significant pituitary (LH) response is 200 micrograms and that the relative efficacy of intranasal GnRH increases with the dose. In spite of the apparently low biopotency for intranasal GnRH, this route of administration may be considered as an alternative to the parenteral mode of GnRH delivery, and the lower biopotency can be partly overcome by increasing the dose.

Adult↗

PubMed1994

Defective interfering type A equine influenza virus (H3N8) protects mice from morbidity and mortality caused by homologous and heterologous subtypes of influenza A virus.

Intranasal administration of defective interfering A/equine/Newmarket/7339/79 (H3N8) influenza virus (DI EQV) protected mice from otherwise lethal intranasal infection with homologous virus (EQV) or with the heterologous subtypes A/WSN (H1N1) or A/PR/8/34 (H1N1). Such protected mice showed little or no sign of clinical disease. Disease with only low mortality resulting from a 'low' dose of WSN was completely prevented with a 100-fold lower dose of DI EQV (4 haemagglutinating units/ml or 12 ng virus/mouse), indicating that there was a roughly proportional relationship between the protective dose of DI virus and the infecting inoculum. DI EQV-protected mice continued to gain weight at the normal rate, whereas those treated with inactivated DI EQV ceased putting on weight for about 7 days and were still underweight nearly 3 weeks later. Unlike DI WSN, DI EQV inhibited multiplication of infectious WSN in the lungs by 20 to 60-fold. Intranasal DI EQV on its own gave little protection to mice challenged 24 days later with EQV suggesting that it was only weakly immunogenic. DI EQV afforded significant protection when given up to 5 days before live virus challenge indicating that the DI genome remained active in the respiratory tract for this period of time.

Animals↗

PubMed2004

Macrophage participation in influenza-induced sleep enhancement in C57BL/6J mice.

Mice develop changes in sleep during the nonspecific immune response that occurs during the initial few days after inoculation with influenza virus. T lymphocytes, neutrophils, macrophages, and natural killer (NK) cells all participate in the early host response to influenza infection. All of these cell types are potential sources of endogenous substances that modulate sleep, but the contributory role of each cell type to the alteration of somnolence during infection has not been determined. To investigate which cell types contribute to the sleep enhancement that develops during influenza infection in mice, the sleep patterns of C57BL/6J mice with perturbations of particular facets of host immune response capabilities were assessed before and after influenza infection. Targeted mutation of the gene Ccl3 (macrophage inflammatory protein 1 alpha) prevented development of the dark phase sleep enhancement that is characteristic of C57BL/6J mice after influenza infection. Other experimental treatments that impair macrophage or monocyte function also produced significant (administration of pentoxifylline or CNI-1493) or marginally significant (deletion of the interferon-gamma gene or intranasal administration of carrageenan) changes in influenza-induced sleep enhancement in C57BL/6J mice. In contrast, functional impairments of NK cells, neutrophils, and T lymphocytes did not significantly influence sleep responses. These data therefore support a contributory role for macrophages, but not for NK cells, neutrophils, and T lymphocytes, in eliciting the sleep response typical of influenza-infected C57BL/6J mice.

Analysis of Variance↗

PubMed2000

Possible role of prostaglandins in pathogenesis of nocturnal enuresis in children.

OBJECTIVE: To compare excretion of ions and prostaglandins by the kidney in children with noctural enuresis. MATERIAL AND METHODS: Thirty-two children with primary nocturnal enuresis and 23 normal children were examined. Osmolality and sodium and potassium concentrations were measured in their urine and blood serum. Prostaglandins E2, E1, and F2alpha were determined using kits for immunoenzyme analysis. Luminal and contraluminal prostaglandin secretions were studied in frog urinary bladder. RESULTS: Children with nocturnal enuresis have increased nocturnal diuresis and renal sodium excretion, but no increase was found in excretion of prostaglandins E2, E1, and F2alpha. Administration of sodium diclofenac before bed-time eliminated episodes of nocturnal enuresis in 37% of children; intranasal administration of Adiuretin SD had a positive effect in 69% of enuretics. In children with nocturnal enuresis there is a correlation between renal excretion of PGE2 and sodium ions; this correlation is absent in the control group children, and disappears in enuretics treated with desmopressin. To evaluate the representativeness of the data on prostaglandin secretions to urine as compared with their release to extracellular fluid, experiments on frog urinary bladder were performed: a correlation was found between prostaglandin secretion to the urinary bladder lumen and to the extracellular fluid. CONCLUSIONS: The results of the study suggest that changes in renal function are due not to a higher secretion of prostaglandins in nocturnal enuresis but to the relative dominance of their effect as compared with other physiologically active substances that simultaneously act on renal tubular cells.

Adolescent↗

PubMed2003

Transforming growth factor (TGF)-beta1-producing regulatory T cells induce Smad-mediated interleukin 10 secretion that facilitates coordinated immunoregulatory activity and amelioration of TGF-beta1-mediated fibrosis.

Interleukin (IL)-10 and transforming growth factor (TGF)-beta1 are suppressor cytokines that frequently occur together during a regulatory T cell response. Here we used a one gene doxycycline (Dox)-inducible plasmid encoding TGF-beta1 to analyze this association and test its utility. In initial studies, we showed that intranasal administration of this plasmid (along with Dox) led to the appearance of TGF-beta1-producing cells (in spleen and lamina propria) and the almost concomitant appearance of IL-10-producing cells. Moreover, we showed that these cells exert Dox-regulated suppression of the T helper cell (Th)1-mediated inflammation in trinitrobenzene sulfonic acid colitis. In subsequent in vitro studies using retroviral TGF-beta1 expression, we established that IL-10 production by Th1 cells occurs after exposure to TGF-beta1 from either an endogenous or exogenous source. In addition, using a self-inactivating retrovirus luciferase reporter construct we showed that TGF-beta1 induces Smad4, which then binds to and activates the IL-10 promoter. Furthermore, intranasal TGF-beta1 plasmid administration ameliorates bleomycin-induced fibrosis in wild-type but not IL-10-deficient mice, strongly suggesting that the amelioration is IL-10 dependent and that IL-10 protects mice from TGF-beta1-mediated fibrosis. Taken together, these findings suggest that the induction of IL-10 by TGF-beta1 is not fortuitous, but instead fulfills important requirements of TGF-beta1 function after its secretion by regulatory T cells.

Animals↗

PubMed2006

Lipopolysaccharide-induced lung inflammation is inhibited by neutralization of GM-CSF.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) plays an important role in the pathogenesis of acute and chronic lung disease as a major regulator governing the functions of granulocyte and macrophage lineage populations. Chronic obstructive pulmonary disease (COPD) is a disease characterized by lung inflammation with accumulation of neutrophils and increased levels of pro-inflammatory cytokines including GM-CSF in the patient's lungs. We used intranasal administration of lipopolysaccharide (LPS) to mice to induce a disease that resembles COPD with pulmonary inflammation, neutrophil recruitment and release of pro-inflammatory mediators in the bronchoalveolar lavage fluid of the diseased mice. 2 h prior to LPS administration, mice were systemically treated with the murine GM-CSF neutralizing antibody mAb 22E9 per intraperitoneal injection. Intranasal challenge with LPS-induced an increase of total cell number and of neutrophils in the bronchoalveolar lavage fluid. Elevated levels of tumor necrosis factor alpha (TNF-alpha), keratinocyte cytokine and macrophage inflammatory protein-2 (MIP-2) were also observed at this time point. GM-CSF was no longer detectable in bronchoalveolar lavage fluid at 24 h due to its early expression with a peak reached 6 h after LPS challenge. Pretreatment of mice with GM-CSF neutralizing antibody dose-dependently inhibited the accumulation of neutrophils and reduced TNF-alpha and MIP-2 protein levels in bronchoalveolar lavage fluid. These data suggest that neutralization of GM-CSF may represent a novel treatment modality for lung inflammation and in particular for COPD.

Animals↗

PubMed2005

A murine model of invasive aspergillosis: variable benefit of interferon-gamma administration under in vitro and in vivo conditions.

BACKGROUND: Interferon-gamma modulates host defense in a number of infectious diseases. Previous studies have shown that systemic administration of interferon-gamma (IFN-gamma) can enhance survival in experimental invasive aspergillosis (IA). METHODS: Using a novel model of murine IA that is characterized by primary pulmonary infection, we investigated the role of IFN-gamma in the phagocytosis and killing of Aspergillus fumigatus by murine neutrophils and pulmonary alveolar macrophages in vitro and the impact of systemic and regional administration of IFN-gamma on the course of IA in glucocorticoid-treated mice. RESULTS: In vitro, IFN-gamma significantly enhanced phagocytosis and killing function of both neutrophils and alveolar macrophages from normal animals, but not cortisone-treated animals. In vivo, intravenous administration of IFN-gamma did not improve phagocyte recruitment, in vivo killing, or mortality from IA. Regional (intranasal) administration of IFN-gamma to the lungs enhanced recruitment of phagocytic cells to the lungs and improved in vivo killing, but did not alter (and actually worsened) mortality from IA. CONCLUSIONS: The in vitro and in vivo effects of IFN-gamma in IA are contingent on many variables, including the route of administration and the specific pathogenesis of infection.

Animals↗

PubMed2003

Mucosal and systemic antibody responses against an acellular pertussis vaccine in mice after intranasal co-administration with recombinant cholera toxin B subunit as an adjuvant.

To investigate the possibility of intranasal immunization with an acellular pertussis vaccine, groups of mice were administered intranasally with aluminium-non-adsorbed pertussis toxoid (PTd; 0.5 or 5 microg) and formalin-treated filamentous hemagglutinin (fFHA; 5 microg) with and without recombinant cholera toxin B subunit (rCTB; 10 microg) as a mucosal adjuvant. At a low concentration of PTd, the following things became clear: (1) earlier and higher elevation of serum anti-PTd and anti-FHA IgG antibody titres in the presence of rCTB than in its absence, (2) higher serum anti-PTd and anti-FHA IgG antibody titres than 200 and 100 ELISA units ml(-1) (EU ml(-1)) in all mice, respectively, in the presence of rCTB, which were obtained by calibration against a reference anti-pertussis mouse serum, and (3) in an intranasal challenge experiment with Bordetella pertussis, slightly more rapid elimination of the bacteria from the lungs of mice intranasally immunized in the presence of rCTB, suggesting the effectiveness of rCTB as a mucosal adjuvant. However, irrespective of rCTB and dose of PTd, mice which were immunized four times and sacrificed on day 35 developed high levels of anti-PTd serum IgG antibodies, high or moderate levels of anti-FHA serum IgG antibodies and mucosal anti-PTd IgA antibodies in the lungs; only a slight or no increase of anti-FHA mucosal IgA antibodies was observed in the lung. These facts suggested the immunogenicity and mucosal adjuvanticity of PTd, and therefore, the mucosal adjuvanticity of rCTB seemed to be inconspicuous. Moreover, the addition of rCTB induced higher anti-PTd serum IgE antibody responses than no addition of it depending on dose of PTd. These results show that dose of PTd included in an acellular pertussis vaccine had better be low as possible and the addition of rCTB may not be always necessary in case of this nasal vaccine alone unlike tetanus and diphtheria toxoids and hepatitis B virus vaccine reported before.

Adhesins, Bacterial↗

PubMed1978

Prevention of death in Semliki Forest virus-infected mice by administration of defective-interfering Semliki Forest virus.

Adult mice inoculated with Semliki Forest virus (SFV) were protected from a lethal infection of the central nervous system by intranasal administration of defective-interfering (DI) SFV. DI SFV was prepared by eight passages at high m.o.i. in BHK 21 cells. Mice were treated with unpurified, unconcentrated tissue culture fluid which had been u.v.-irradiated to inactivate the infective virus present. Prevention of death was maximal when the DI virus was administered simultaneously with the infecting inoculum, and under the same conditions multiplication of infective virus in the brains of treated mice was reduced by 10(5)-fold. It was shown that DI SFV was propagated in mouse brains followed intranasal inoculation and it was concluded that protection was brought about through the intrinsic interfering capacity of the DI virus.

Animals↗

PubMed1999

Protective immunity against murine hepatitis virus (MHV) induced by intranasal or subcutaneous administration of hybrids of tobacco mosaic virus that carries an MHV epitope.

Hybrids of tobacco mosaic virus (TMV) were constructed with the use of fusion to the coat protein peptides of 10 or 15 amino acids, containing the 5B19 epitope from the spike protein of murine hepatitis virus (MHV) and giving rise to TMV-5B19 and TMV-5B19L, respectively. The TMV hybrids were propagated in tobacco plants, and the virus particles were purified. Immunogold labeling, with the use of the monoclonal MAb5B19 antibody, showed specific decoration of hybrid TMV particles, confirming the expression and display of the MHV epitope on the surface of the TMV. Mice were immunized with purified hybrid viruses after several regimens of immunization. Mice that received TMV-5B19L intranasally developed serum IgG and IgA specific for the 5B19 epitope and for the TMV coat protein. Hybrid TMV-5B19, administered by subcutaneous injections, elicited high titers of serum IgG that was specific for the 5B19 epitope and for coat protein, but IgA that was specific against 5B19 was not observed. Mice that were immunized with hybrid virus by subcutaneous or intranasal routes of administration survived challenge with a lethal dose (10 x LD50) of MHV strain JHM, whereas mice administered wild-type TMV died 10 d post challenge. Furthermore, there was a positive correlation between the dose of administered immunogen and protection against MHV infection. These studies show that TMV can be an effective vaccine delivery vehicle for parenteral and mucosal immunization and for protection from challenge with viral infection.

Administration, Intranasal↗

PubMed1996

Pulmonary pharmacology.

This article reviews the basic principles of pharmacodynamics and pharmacokinetics, with a special emphasis on the pharmacologic considerations that must be taken into account when treating the patient with respiratory disease who is also pregnant or nursing the neonate. A description of the four classes of therapeutic agents used for COPD is given with a discussion of the scientific evidence for their safety during pregnancy. The understanding of asthma suggests that bronchodilators relieve the symptoms, while antiinflammatories suppress the disease. Direct administration to the target tissue by inhalation of the bronchodilators (beta-adrenoreceptor agonists and anticholinergics) and immunosuppressors (corticosteroids and cromolyn) leads to low systemic levels of these drugs, which reduces fetal drug exposure. Oral administration of beta-adrenoreceptor agonists, corticosteroids, and theophylline may be necessary to obtain sufficient maternal lung function and ensure adequate oxygenation of the fetus. This must be carefully weighed against the potential fetal and maternal risks involved with increased systemic levels of these drugs. A brief description of classes of drugs used for upper respiratory diseases (antihistamines, alpha-adrenergic agonists, corticosteroids, antitussives, and expectorants) and their safety during pregnancy is also given. There is concern that most alpha-adrenergic agonists increase blood pressure at therapeutic doses needed to relieve nasal congestion. Therefore, for pregnant patients requiring decongestants, opinion favors administration of pseudoephedrine, which has the most favorable therapeutic index, to reduce potential cardiovascular adverse reactions in the fetus. Intranasal administration of the newer corticosteroids, which have limited absorption, is useful for suppression of allergic rhinitis, while minimizing the risk of adverse reactions. The purpose of this article has been to provide pharmacologic/toxicologic information about commonly used respiratory drugs. This will to enable the clinician to make an educated decision regarding the choice of therapy for respiratory disorders to ensure that fetal and maternal outcomes are optimal.

Asthma↗

PubMed2006

Inhibition of chronic airway inflammation and remodeling by galectin-3 gene therapy in a murine model.

We previously demonstrated that treatment of acute asthmatic rats with gene therapy using plasmid-encoding Galectin-3 (Gal-3) resulted in an improvement of cellular and functional respiratory parameters. The next question that we wanted to clarify was if in a chronic situation where the treated animal continues to inhale the Ag, does this procedure prevent the chronicity and the remodeling? Chronic inflammation was induced by intranasal administration of OVA over a period of 12 wk. In the treated group, the Gal-3 gene was introduced by intranasal instillation in 50 mul of plasmid-encoding Gal-3. Noninvasive airway responsiveness to methacholine was tested at different times. Cells were obtained by bronchoalveolar lavage and used for RNA extraction and cytometric studies. Eosinophils were counted in blood and bronchoalveolar lavage fluid. Real-time PCR was used to measure Gal-3 and cytokine mRNA expression in lung. Lungs were paraffined and histologic analyses were performed (H&E, periodic acid-Schiff, and Masson Trichrome stain). Our results showed that 12 wk after the first intranasal Ag instillation in chronically asthmatic mice, treatment with the Gal-3 gene led to an improvement in the eosinophil count and the normalization of hyperresponsiveness to methacholine. Concomitantly, this treatment resulted in an improvement in mucus secretion and subepithelial fibrosis in the chronically asthmatic mice, with a quantitatively measured reduction in lung collagen, a prominent feature of airway remodeling. Plasmid-encoding Gal-3 acts as a novel treatment for chronic asthma in mice producing nearly complete blockade of Ag responses with respect to eosinophil airway accumulation, airway hyperresponsiveness, and remodeling.

Animals↗

PubMed2001

Beclomethasone dipropionate: absolute bioavailability, pharmacokinetics and metabolism following intravenous, oral, intranasal and inhaled administration in man.

AIMS: To assess the absolute bioavailability, pharmacokinetics and metabolism of beclomethasone dipropionate (BDP) in man following intravenous, oral, intranasal and inhaled administration. METHODS: Twelve healthy subjects participated in this seven-way cross-over study where BDP was administered via the following routes: intravenous infusion (1000 microg), oral (4000 microg, aqueous suspension), intranasal (1344 microg, aqueous nasal spray) and inhaled (1000 microg ex-valve, metered dose inhaler). The contribution of the lung, nose and gut to the systemic exposure was assessed by repeating the inhaled, intranasal and oral dosing arms together with activated charcoal, to block oral absorption. Blood samples were collected for 24 h postdose for the measurement of BDP, beclomethasone-17-monopropionate (B-17-MP) and beclomethasone (BOH) in plasma by liquid chromatography tandem mass spectrometry. RESULTS: Intravenous administration of BDP (mean CL 150 l h-1, Vss 20 l, t(1/2) 0.5 h) was associated with rapid conversion to B-17-MP which was eliminated more slowly (t1/2 2.7 h). In estimating the parameters for B-17-MP (mean CL 120 l h-1, Vss 424 l) complete conversion of BDP to B-17-MP was assumed. The resultant plasma concentrations of BOH were low and transient. BDP was not detected in plasma following oral or intranasal dosing. The mean absolute bioavailability (%F, 90% CI; nominal doses) of inhaled BDP was 2% (1-4%) and not reduced by coadministration of charcoal. The mean percentage F of the active metabolite B-17-MP was 41% (31-54%), 44% (34-58%) and 62% (47-82%) for oral, intranasal and inhaled dosing without charcoal, respectively. The corresponding estimates of nasal and lung absorption, based on the coadministration of charcoal, were < 1% and 36% (27-47%), respectively. CONCLUSIONS: Unchanged BDP has negligible oral and intranasal bioavailability with limited absorption following inhaled dosing due to extensive (95%) presystemic conversion of BDP to B-17-MP in the lung. The oral and intranasal bioavailabilities of the active metabolite B-17-MP were high and similar, but direct absorption in the nose was insignificant. The total inhaled bioavailability of B-17-MP (lung + oral) was also high (62%) and approximately 36% of this was due to pulmonary absorption. Estimates of oral bioavailability and pulmonary deposition based on total BOH were approximately half those found for B-17-MP.

Administration, Inhalation↗

PubMed1995

Treatment of cluster headache and its variants.

In cluster headache, subcutaneous administration of sumatriptan has been established as an efficient, safe and well tolerated treatment for acute attacks. For prophylactic treatment, capsaicin (intranasal administration) and leuprolide (a synthetic slow-release gonadotrophin-releasing hormone) seem to be promising. Hyperbaric oxygen therapy seems to be effective in acute attacks, but it is of interest mostly because of its apparent interruption of the cluster period in some patients. In chronic paroxysmal hemicrania, which clinically resembles cluster headache, indomethacin is still necessary for diagnosis, and it is the treatment of choice in most patients. However, because of its potential side effects, alternative treatments should be sought.

Cluster Headache↗

PubMed2002

Clinical pharmacokinetics of intranasal sumatriptan.

A substantial proportion of migraine patients have gastric stasis and suffer severe nausea and/or vomiting during their migraine attack. This may lead to erratic absorption from the gastrointestinal tract and make oral treatment unsatisfactory. For such patients, an intranasal formulation may be advantageous. Sumatriptan is a potent serotonin 5HT(1B/1D) agonist widely used in the treatment of migraine; the effectiveness of the intranasal formulation (20mg) has been well established in several clinical studies. This article reviews the pharmacokinetics of intranasal sumatriptan and includes comparisons with oral and subcutaneous administration. After intranasal administration, sumatriptan is directly and rapidly absorbed, with 60% of the maximum plasma concentration (C(max)) occurring at 30 minutes after administration of a single 20mg dose. Following intranasal administration, approximately 10% more sumatriptan is absorbed probably via the nasal mucosa when compared with oral administration. Mean C(max) after a 20mg intranasal dose is approximately 13.1 to 14.4 ng/mL, with median time to C(max) approximately 1 to 1.75 hours. When given as a single dose, intranasal sumatriptan displays dose proportionality in its extent of absorption and C(max) over the dose range 5 to 10mg, but not between 5 and 20mg for C(max). The elimination phase half-life is approximately 2 hours, consistent with administration by other routes. Sumatriptan is metabolised by monoamine oxidase (MAO; predominantly the A isozyme, MAO-A) to an inactive metabolite. Coadministration with a MAO-A inhibitor, moclobemide, leads to a significant increase in sumatriptan plasma concentrations and is contraindicated. Single-dose pharmacokinetics in paediatric and adolescent patients following intranasal sumatriptan were studied to determine the effect of changes in nasal morphology during growth, and of body size, on pharmacokinetic parameters. The pharmacokinetic profile observed in adults was maintained in the adolescent population; generally, factors such as age, bodyweight or height did not significantly affect the pharmacokinetics. In children below 12 years, C(max) is comparable to that seen in adolescents and adults, but total exposure (area under the concentration-time curve from zero to infinity) was lower in children compared with older patients, especially in younger children treated with 5mg. Clinical experience suggests that intranasal sumatriptan has some advantages over the tablet (more rapid onset of effect and use in patients with gastrointestinal complaints) or subcutaneous (noninvasive and fewer adverse events) formulations.

Administration, Intranasal↗

PubMed2003

Studies on the toxicity of Punica granatum L. (Punicaceae) whole fruit extracts.

Current investigation focuses on the toxicity evaluation of whole fruit hydroalcoholic extract of Punica granatum L. (Punicaceae), used in Cuban traditional medicine a.o. for the treatment of respiratory diseases. Previous findings on the anti-influenza activity of Punica granatum extracts has given support to the ethnopharmacological application. In our study, in chick embryo model, it was found that doses of the extract of less than 0.1 mg per embryo are not toxic. The LD50 of the extract, determined in OF-1 mice of both sexes after intraperitoneal administration, was 731 mg/kg. Confidence limits were 565-945 mg/kg. At the doses of 0.4 and 1.2 mg/kg of extract, the repeated intranasal administration to Wistar rats produced no toxic effects in terms of food intake, weight gain, behavioural or biochemical parameters, or results of histopathological studies. We conclude that toxic effects of Punica granatum fruit extract occurred at higher doses than those effective in the models where the anti-viral activity has been studied or than those doses used in Cuban folk medicine.

Abnormalities, Drug-Induced↗

PubMedDate not supplied

Experimental Escherichia coli respiratory infection in broilers.

This study determined optimal conditions for experimental reproduction of colibacillosis by aerosol administration of avian pathogenic Escherichia coli to 2-to-4-wk-old broiler chickens. The basic model for reproducing disease was intranasal administration of approximately 10(4) mean embryo infectious dose of infectious bronchitis virus (IBV) followed by aerosol administration of an 02 or an 078 strain of E. coli in a Horsfall unit (100 ml of a suspension of 10(9) colony-forming units/ml over 40 min). Scores were assigned to groups of infected chickens on the basis of deaths; frequency and severity of lesions in the air sacs, liver and heart; and recovery of the challenge E. coli 6 days post-E. coli infection. An interval of 4 days between the IBV and E. coli challenges was best whether the chickens received the IBV at 8 or 20 days of age. Typically, 50%-80% of the chickens developed airsacculitis and 0 to 29% of the chickens developed pericarditis or perihepatitis, with little or no mortality. Escherichia coli alone resulted in no deaths and 0 to 20% airsacculitis, but these percentages increased to 0 to 5% and 52%-60% when the E. coli aerosol was administered through a cone-shaped chamber. Administration of IBV alone failed to induce lesions. Recovery of the challenge E. coli from chickens did not correlate well with lesions. On the basis of these data, administration of IBV to 20-day-old chickens followed 4 days later by exposure to an avian pathogenic E. coli reproduces avian colibacillosis with the low mortality, high percentage of airsacculitis, and low percentage of septicemic lesions characteristic of the conditions seen in the natural disease.

Animals↗

PubMed1994

Efficacy of the intranasal route for administration of anesthetic agents to adult rabbits.

Anesthetic agents were administered to adult rabbits by using the intranasal route. Six sedative or anesthetic protocols were studied as follows: group 1 (n = 12), 2.0 mg midazolam/kg body weight (BW); group 2 (n = 8), 25.0 mg ketamine/kg BW; group 3 (n = 8), 10 mg of combination of tiletamine and zolazepam/kg BW; group 4 (n = 10), 3 mg xylazine/kg BW and 10 mg ketamine/kg BW; group 5 (n = 8), 1.0 mg midazolam/kg BW and 25 mg ketamine/kg BW; and group 6 (n = 6), 0.3 ml of a combination of fentanyl and droperidol/kg BW. All drugs were diluted to a final volume of 0.4 ml/kg BW and an equal volume was administered with a catheter-tipped syringe into each nostril. Time to onset and duration of sedation or anesthesia were recorded. Muscle relaxation was graded as poor, fair, or excellent on the basis of flexibility of limbs. Presence or absence of a toe pinch response was recorded. Heart rate, respiratory rate, and hemoglobin saturation were measured before and at 5-min intervals after drug administration. The mean onset times for groups 1, 2, 3, 4, and 5 were 3.0, 1.2, 2.5, 2.0, and 0.8 min, respectively. The mean duration of action was 24.6, 36.7, 44.4, 35.2, and 52.5 min for midazolam, ketamine, tiletamine/zolazepam, xylazine/ketamine, and midazolam/ketamine, respectively. All protocols resulted in a significant decrease in respiratory rate. Hemoglobin saturation decreased in all groups except group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗