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P Padrid

Publications and source records attributed to P Padrid.

14 recordsLinked to original sources
PubMed2000

Pulmonary diagnostics.

Respiratory medicine is an underdeveloped subspecialty in veterinary medicine, and there are relatively few sophisticated tests that are available to the clinician that actually diagnose specific pulmonary disorders. Instead, most of the commonly available tests are most helpful if used to point the veterinarian in the right direction and to rule out the presence of other potentially confounding disorders. This article reviews the diagnostic tests that are available to evaluate dogs and cats with signs of respiratory disease, including the advantages, disadvantages, and current controversies regarding many of the tests used to evaluate animals with signs of pulmonary impairment.

Animals↗
PubMed2000

Feline asthma. Diagnosis and treatment.

Human asthma is not a curable disease, although spontaneous resolution is common in adult asthmatics who developed asthma in childhood. We do not know if this is true or not for cats with asthma. We do know that some cats may be only mildly and intermittently symptomatic and that others may suffer life-threatening illness. An important new development in our understanding of this disease is the occurrence of airway inflammation even when patients are symptom-free. It is therefore crucial that we direct our therapeutic attention toward the underlying chronic inflammation that causes the acute clinical signs of cough, wheeze, and increased respiratory effort. Client education is also critical so that our clients develop realistic expectations of the effectiveness of these treatments for their pets. A great deal still needs to be learned regarding the pathogenesis of feline asthma and the optimal approach(es) to treating cats with this sometimes debilitating and potentially fatal respiratory syndrome. There is great hope and anticipation that ongoing research can bring new treatments for human and feline asthmatics alike.

Animals↗
PubMed2000

Canine and feline pleural disease.

Diseases of the pleural space are relatively common disorders in small animal clinical practice. The abnormal presence of air, fluid, or tissue within the pleural cavity does not generally reflect disease of the pleura per se; instead, it represents a disorder of the airways or lung parenchyma or the development of a primary systemic illness. This article discusses common causes of the most frequently seen pleural space disorders and outlines general treatment plans that can be used as guidelines when treating actual clinical cases.

Animals↗
PubMed1999

TRFK-5 reverses established airway eosinophilia but not established hyperresponsiveness in a murine model of chronic asthma.

We studied the effects of an anti-interleukin (IL)-5 monoclonal antibody (TRFK-5) or dexamethasone (DEX) to reverse already established airway hyperresponsiveness (AHR) and tissue eosinophilia in a Schistosoma mansoni antigen-sensitized and airway-challenged mouse model of chronic asthma. In this model at 4 d after antigen challenge there is dramatic bronchoalveolar lavage fluid (BAL) eosinophilia, AHR to intravenous methacholine (MCh), and histologic evidence of peribronchial eosinophilic infiltration and mucoid cell hyperplasia. These changes persist for up to 2 wk after antigen challenge. Treatment with DEX from Days 4 through 10 significantly reduced established airway eosinophilia compared with animals sham-treated with saline from Days 4 -10 (120 +/- 29 eosinophils/microl BAL for DEX-treated mice versus 382 +/- 60 eosinophils/microl BAL for sham-treated animals, p < 0.01). DEX-treated mice also had dramatically reduced mucoid cell hyperplasia, and airway responsiveness returned to normal. In contrast, TRFK-5 given during the same time period reduced airway eosinophilia (86 +/- 32 eosinophils/microl BAL versus 382 +/- 60 eosinophils/microl BAL, p < 0.01) but did not reduce goblet cell hyperplasia or reverse already established AHR. Treatment with DEX but not TRFK-5 also inhibited interferon gamma (IFN-gamma) content of BAL fluid (0.49 +/- 0.09 ng/ml BAL fluid for DEX versus 1.50 +/- 0.24 ng/ml BAL fluid and 1.36 +/- 0.13 ng/ml BAL fluid for TRFK-5 and sham-treated mice, respectively, both p < 0.001 versus DEX). Thus, treatment with DEX reduces established eosinophilic airway inflammation and AHR in S. mansoni-sensitized and airway-challenged mice but treatment with TRFK-5 reversed established eosinophilia without ameliorating established AHR. Together, these data suggest that once airway inflammation develops, neutralizing the effects of IL-5 or reducing eosinophilia alone may not result in inhibiting established AHR in atopic asthma.

Allergens↗
PubMed1999

CD28 interactions with either CD80 or CD86 are sufficient to induce allergic airway inflammation in mice.

Previous studies have shown that the pan CD28/cytotoxic T lymphocyte antigen (CTL)A-4 antagonist CTLA4 immunoglobulin (Ig) inhibits eosinophilic airway inflammation in Schistosoma mansoni-sensitized and airway-challenged mice. In the present study, the importance of CD28 as well as the individual roles of CD80 and CD86 were examined in this system using wild-type and CD28 knockout (KO) mice. Unlike wild-type controls, CD28KO mice did not produce systemic IgE or eosinophilic airway inflammation after antigen challenge. However, a lymphocytic infiltrate and continued production of interferon-gamma was observed in these animals. Thus, CD28 is not essential for the initial recruitment of lymphocytes into antigen-challenged airways but critically regulates the allergic T-helper 2 phenotype. We next determined by polymerase chain reaction and flow cytometry that CD80 and CD86 molecules are constitutively expressed in the naive murine lung and on eosinophils in the allergic lung, suggesting a potential important role for both ligands in the development of asthma. Combined anti-CD80/anti-CD86 treatment throughout the antigen challenge period fully blocked the development of allergic airways, whereas a partial reduction was observed in mice treated with either anti-CD80 or anti-CD86 antibody alone. However, only anti-CD86 blocked systemic IgE production. Therefore, signaling through either CD80 or CD86 is sufficient to generate a partial local allergic response, whereas CD86 costimulation is essential to induce systemic allergic (IgE) reactions. Finally, combined anti-B7 monoclonal antibody treatment after sensitization reduced airway eosinophilia and interleukin (IL)-4/IL-5 cytokine secretion consistent with an ongoing role for CD28/B7 interactions in the effector phase of the disease. These results emphasize the importance of differential B7 expression on different cells and in different organs on subsequent CD28/B7-mediated immune events, including the potential for CD28/B7 blockade in the treatment of atopic airway disease in people.

Animals↗
PubMed1995

Bioactivity of recombinant feline interleukin-2 on human and feline leukocytes.

Interleukin (IL)-2 is a 16,000 Da protein product of T lymphocytes which is the principle cytokine responsible for clonal expansion of T lymphocytes as a response to antigen exposure. Deficiency of functional IL-2 plays a pivotal role in the pathogenesis of human immunodeficiency syndrome and may be important in the pathogenesis of feline immunodeficiency syndrome as well. Additionally, IL-2 may enhance secretion of interleukin-5 from the TH2 subset of CD4+ T cells, promote peripheral and systemic eosinophilia, and contribute to the eosinophilia which characterizes the inflamed airways of human beings and cats with asthma. We recently reported the sequence of feline IL-2 and the synthesis of recombinant feline IL-2. The purpose of the present study was to evaluate the bioactivity of recombinant feline IL-2 on human and feline leukocytes. We established dose-response relationships between recombinant feline IL-2 and radiolabeled proliferating human and feline leukocytes using thymidine incorporation as a marker of bioactivity. We found that recombinant human IL-2 promotes proliferation of both human and feline leukocytes. However, recombinant feline IL-2 promotes proliferation of feline cells, but not human cells.

Animals↗
PubMed1995

Persistent airway hyperresponsiveness and histologic alterations after chronic antigen challenge in cats.

We studied the effect of chronic immune sensitization on the airway reactivity and associated cytologic and histologic alterations in initially nonatopic cats, a species that spontaneously develops idiopathic asthma. Seven cats were sensitized by intramuscular injection of Ascaris suum antigen (AA) for 4 wk, and four other cats served as sham controls. Airway sensitization was demonstrated by an increased response to nebulized AA in sensitized animals (RL = 45.9 +/- 6.1 cm H2O/L/s, versus a baseline response of 24.7 +/- 1.5 cm H2O/L/s, p < 0.01), and hyperresponsiveness was demonstrated by an increased response to acetylcholine (ACh)-challenge 24 h after AA (approximately 1.0 log decrease in PD200, p < 0.01). The number of eosinophils in the sensitized animals' bronchoalveolar lavage (BAL) fluid increased 12-fold (p < 0.01 versus control) in response to AA challenge; 32 +/- 5% of the BAL eosinophils had a specific density < 1.050, versus 8 +/- 2% prior to AA challenge (p < 0.05). There was no change in airway reactivity, eosinophil recovery, or density in the control group 24 h after sham challenge with saline. The same seven sensitized cats further received nebulized AA three times weekly for 4 to 6 wk, after which BAL samples were again obtained and ACh dose-response curves generated 72 h after the final administration of nebulized AA. Airway hyperresponsiveness increased (approximately 1.5 log decrease in PD200, p < 0.001) and the number of eosinophils recovered in BAL fluid was increased 11-fold (p < 0.05). Necropsy specimens demonstrated bronchoconstriction in AA-challenged animals but not controls; luminal narrowing was accompanied by: (1) a 29.0 +/- 0.34% increase in smooth-muscle thickness (p < 0.05); (2) goblet-cell and submucosal-gland hypertrophy and hyperplasia; and (3) epithelial erosion and eosinophilic infiltration. We demonstrate in nonhuman species persistent airway hyperreactivity associated with a complete constellation of histologic changes in epithelium, smooth muscle, and mucus glands, and cytologic changes in BAL fluid, all induced by immune sensitization. Our data suggest that chronic immune sensitization per se could be a salient factor in causing many of the changes associated with chronic bronchial asthma.

Acetylcholine↗
PubMed1993

Identification and propagation of a putative immunosuppressive orphan parvovirus in cloned T cells.

A putative parvovirus related to minute virus of mice (MVM), but distinct from MVM-prototype and MVM-immunosuppressive, was identified, using serologic techniques and Southern blot analysis, in maintenance cultures of established T cell clones. This putative viral agent resulted in a lytic infection of cloned L3 cytotoxic T cells but was unable to produce a productive infection in BHK.21 or EL-4(G) cells. Moreover, maintenance cultures of several distinct subsets of cloned T cells apparently contaminated with this putative viral agent contained poorly growing cells and erythrocyte aggregates. The aggregation of mouse erythrocytes appeared to be a reliable indicator of infection with this putative virus and may be related to the ability of this agent to agglutinate mouse erythrocytes. This putative virus also was found to inhibit the proliferative response of certain cloned T cells to IL-2 and Ag. Viremic mice and secondary MLC supernatant were identified as two potential sources of contamination and represent ways of propagating this agent in vitro. The finding that this agent interferes with the ability of T cell clones to thrive and, therefore has the potential to alter immune responses, emphasizes the importance of identifying and excluding parvoviral infections in cultures of murine T lymphocytes.

Animals↗
PubMed1993

Augmented muscarinic responsiveness caused by 5-lipoxygenase products secreted from alveolar macrophages in isolated-perfused rat lung.

We examined the effect of activated alveolar macrophages (AM) on airway responsiveness to muscarinic stimulation in 33 adult Sprague-Dawley rats. An isolated-perfused lung preparation was used to ensure precise and uniform delivery of cells into peripheral airways. The bronchoconstrictor response to acetylcholine (ACh) delivered into the pulmonary arterial circulation was augmented in 8 rats after infusion of 3 x 10(6) AM activated with 10(-6) M f-met-leu-phe and 5 micrograms/ml of cytochalasin B. Lung resistance (RL) caused by 10(-6) mol ACh increased 2.5-fold from 0.10 +/- 0.004 cm H2O/ml/s before infusion of activated AM to 0.35 +/- 0.05 cm H2O/ml/s after infusion of activated AM (N = 8; p < 0.05); the response to ACh was not augmented after infusion of nonactivated AM (N = 7) or vehicle control (N = 6). Baseline RL before ACh was similar in all three groups (p NS). Perfusion with activated AM also significantly increased the wet/dry (W/D) lung weight ratios (7.1 +/- 0.5) compared with nonactivated AM (5.2 +/- 0.1) or vehicle control (5.5 +/- 0.3) (p < 0.05 versus either nonactivated AM or vehicle control). A63162, a 5-lipoxygenase inhibitor, but not indomethacin, a cyclooxygenase inhibitor, completely inhibited augmentation of bronchoconstrictor responses to ACh caused by activated AM and also completely attenuated the increase in W/D lung weight ratios. A highly significant (p < 0.01) correlation (R = 0.76) between W/D lung weight ratios and RL was observed after 10(-6) mol ACh (the greatest dose of ACh administered). Baseline RL was equivalent for all groups before and after infusion of cells or vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Chronic tracheobronchial disease in the dog.

Tracheobronchial collapse and chronic bronchitis (CB) are the two most common forms of chronic tracheobronchial disease in dogs. These conditions may exist independently of one another, although CB and some degree of tracheobronchial collapse often co-exist in the same patient. Diagnosis of CB can be established on clinical grounds alone, whereas radiographic or bronchoscopic evidence is required to confirm the diagnosis of tracheobronchial collapse. Although glucocorticoid drug therapy remains one of the most effective methods for managing CB, surgical implantation of a prosthetic airway device may be of great benefit for some dogs with a focal area of collapsing trachea. With early diagnosis and aggressive medical and surgical management, the prognosis for many dogs with chronic tracheobronchial disease is good for reasonable quality of life.

Animals↗
PubMed1992

Chronic lower airway disease in the dog and cat.

The most common form of lower airway disease (LAD) in dogs is chronic bronchitis, whereas in cats a syndrome resembling chronic bronchial asthma in humans is commonly reported. In most cases, the cause(s) of LAD remains unproven. The primary symptom of LAD in dogs and cats is chronic cough, although many cats are free of symptoms between episodes of acute, life-threatening bronchoconstriction. Diagnosis is based on a careful history, physical examination, and diagnostic tests designed to rule out other causes of cough and dyspnea such as pneumonia, heartworm infestation, and congestive heart failure. More sophisticated tests, such as bronchoscopy, flow volume loops, and radioisotope ventilation scans are available to define the extent of the disease process better. Glucocorticoids remain the mainstay of chronic therapy for most dogs and cats with LAD. Bronchodilators are indicated for most cats with symptoms of acute bronchoconstriction, whereas a smaller number of dogs may respond to bronchodilator administration and demonstrate an increase in exercise capacity and a decrease in cough frequency. LAD in dogs and cats is a progressive disorder, and prognosis is guarded. Nevertheless, with aggressive medical management many of these animals can live relatively symptom-free lives.

Animals↗
PubMed1988

Bizarre lymphoid cells in serous effusion of a dog with mediastinal lymphoma.

An 8-year-old collie dog was examined because of dyspnoea. Thoracocentesis revealed a modified transudate containing a predominance of large (10 to 15 microns diameter) unusual-appearing mononuclear cells showing cloverleaf-shaped nuclei. These cells were categorized as lymphoid in origin on the basis of ultrastructural and cytochemical methods. Subsequent necropsy examination revealed lymphoma, localized primarily to the cranial mediastinum, but also infiltrating tissues surrounding the thyroid, parathyroid and adrenal glands.

Animals↗