Fritz' Feline Asthma Site http://groups.yahoo.com/group/felineasthma/
Feline asthma group at yahoo
Great overview discussion of feline asthma with details on treatment and inhalers and other medications such as prednisone. Discusses how cat asthma and human asthma may have different dynamics or that the jury is still out.
NEW TREATMENTS BEING CONSIDERED FOR FELINE ASTHMA
Article mentions Accolate."It reduces inflammation in the air passages, which helps prevent asthma attacks"
Aerokat from the manufacturer
"Feline asthma mimics the human form of asthma and responds well to the pharmacological agents used with humans2. However, because typical inhalers propel a dose at speeds of over 60 miles per hour (100 Kph)3, effective delivery of the medications to domestic cats without a delivery system is extremely difficult.
The AeroKat* FAC is a system that aids the formation of an aerosol cloud and helps to separate the large particles from the small (breathable) particles in the metered dose. Inhalation through the AeroKat* FAC facilitates aerosol delivery to the lungs. Initial experience indicates that the cat willingly takes the chamber in most cases
Medications that aerokat writes used for asthma
and it gives the doses
Inhaled medications for feline asthma by VIN
a feline aerosol chamber
feline asthma -update by Dr.Susan Little
"Feline asthma has been called by many other names, including chronic bronchitis, bronchial asthma, and allergic bronchitis"
Yahoo's group for inhaled meds for asthmafeline asthma =website devoted to feline asthma
Glucocorticosteroids (Corticosteroids, Steroids)
J Allergy Clin Immunol. 2003 May;111(5):938-46. :
Early exposure to allergen: is this the cat's meow, or are we barking up the wrong tree?
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pennsylvania, Philadelphia 19104, USA.
Several recent studies have suggested that exposure to cat and dog allergen in infancy is protective against the subsequent risk of allergic sensitization and asthma. The methodologic problems to be overcome in clinical research addressing these hypotheses are complex. Appreciation of these studies requires an assessment of the design and adequacy of variables measuring exposures, outcomes, and confounders. It includes understanding the role of effect modification. This article discusses some of the epidemiologic issues in interpreting these studies. Review of relevant epidemiology demonstrates that much research remains to be performed before these interesting hypotheses are proved or disproved.
Curr Opin Allergy Clin Immunol. 2003 Feb;3(1):7-14. :
Early pet exposure: friend or foe?
Simpson A, Custovic A.
North West Lung Center, Wythenshawe Hospital, Manchester, UK.
PURPOSE OF REVIEW: Sensitization to pets is a risk factor for asthma and it was assumed that pet ownership was a risk factor for sensitization. Epidemiological studies failed to confirm this, some even suggesting that keeping pets decreased the risk of sensitization and asthma. In the last year, 10 studies have been published which have, at least in part, attempted to address the question. The results, however, are heterogeneous and it is still not clear how we should advise our patients on this issue of pet ownership. RECENT FINDINGS: Results of studies of the association between exposure to cat or cat allergen and the development of sensitization are such that almost any view on the relationship could be supported by evidence from the literature. For dogs, there are fewer data, but there is little to suggest that keeping a dog increases the risk of sensitization to dog. The majority of studies reviewed find either no association or a reduced risk of asthma amongst pet owners, but only one of these selectively excludes those who deliberately avoid pets from the analysis. There is evidence to suggest that amongst non-pet owners, the risk of sensitization and of asthma increases in areas with a high proportion of pet owners. There is evidence emerging that the effect of exposure to pets may be different in different relative risk groups, based on parental allergy. There is also evidence that asthma is more severe amongst pet sensitized pet owners. SUMMARY: There are several large birth cohort studies being conducted around the world designed to measure the development of asthma and allergies in children with prospective and objective measures of environmental exposures. The results of such studies are required before the association between pets and asthma can be determined
Am J Respir Crit Care Med. 2001 Sep 1;164(5):785-9. :
Repeated hyperventilation causes peripheral airways inflammation, hyperreactivity, and impaired bronchodilation in dogs.
Davis MS, Freed AN.
Division of Physiology, Department of Environmental Health Sciences, The Johns Hopkins School of Public Health, Baltimore, Maryland, USA.
Winter athletes have an increased incidence of asthma, suggesting that repetitive hyperventilation with cold air may predispose individuals to airways disease. We used a canine model of exercise-induced hyperpnea to examine the effects of repeated hyperventilation with cool, dry air (i.e., dry air challenge [DAC]) on peripheral airway resistance (Rp), reactivity, and inflammation. Specific bronchi were exposed to a single DAC on five consecutive days. Rp and Delta Rp to aerosolized histamine, intravenous histamine, or hypocapnia were measured daily. Bronchoalveolar lavage fluid (BALF) was obtained on the fifth day. Rp increased from 0.70 +/- 0.08 to 1.13 +/- 0.22 cm H(2)O/ml/s (n = 25) 24 h after the first DAC, rose to 1.49 +/- 0.24 cm H(2)O/ml/s by Day 3, and remained elevated throughout the remainder of the protocol. Repeated DAC increased reactivity to hypocapnia and intravenous histamine. Intravenous salbutamol failed to reduce Rp as effectively in challenged airways (111% of Day 1 baseline) as in naive airways (54% of baseline). Repeated DAC caused increased BALF neutrophils, eosinophils, and sulfidopeptide leukotrienes. We conclude that repeated DAC causes peripheral airways inflammation, obstruction, hyperreactivity, and impaired beta-agonist-induced relaxation. This suggests that other mechanisms in addition to increased smooth muscle tone may contribute to the development of repetitive hyperventilation-induced bronchial obstruction and hyperreactivity.
Anesth Analg. 2001 Jul;93(1):230-3. :
A comparison of the relaxant effects of olprinone and aminophylline on methacholine-induced bronchoconstriction in dogs.
Hirota K, Yoshioka H, Kabara S, Kudo T, Ishihara H, Matsuki A.
Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan.
IV aminophylline, a nonselective phosphodiesterase (PDE) inhibitor, is often used to treat an asthma attack during anesthesia. However, in some instances, aminophylline-resistant attacks are observed. Selective PDE3 inhibitors are now clinically available and have been reported to produce bronchodilation. Thus, we compared the relaxant effects of olprinone, a novel PDE3 inhibitor, and aminophylline on methacholine-induced bronchoconstriction. Dogs were anesthetized with pentobarbital. Bronchoconstriction was elicited with methacholine (0.5 microg/kg + 5.0 microg. kg(-1). min(-1)) and assessed as percentage of changes in the bronchial cross-sectional area (BCA; basal = 100%) monitored by bronchoscope. Initially, the relaxant effects of olprinone (n = 8; 0-1000 microg/kg) and aminophylline (n = 8; 0-50 mg/kg) were compared. The bronchial cross-sectional areas were assessed before and 30 min after methacholine infusion began and 5 min after each dose of olprinone or aminophylline. We then determined whether propranolol (0.4 mg/kg) reversed the relaxation induced by olprinone (1000 microg/kg) and aminophylline (50 mg/kg). Olprinone and aminophylline dose-dependently antagonized bronchoconstriction by 56.2% +/- 21.3% (SD) and 68.0% +/- 30.3% with -log 50% effective dose (mean) of 4.80 +/- 0.38 (15.8) microg/kg and 1.96 +/- 0.42 (10.9) mg/kg, respectively. Aminophylline 50 mg/kg significantly increased plasma epinephrine, whereas olprinone did not. In addition, propranolol significantly reduced aminophylline-induced relaxation, but not olprinone-induced relaxation. Therefore, the relaxant effects of olprinone are independent of plasma epinephrine, whereas aminophylline effects may partially result from increased circulating concentrations of epinephrine. Implications: We compared the relaxant effects of olprinone and aminophylline on methacholine-induced bronchoconstriction in dogs. The relaxant effects of olprinone are independent of plasma epinephrine, whereas the aminophylline effects may be partly caused by an increase in plasma epinephrine.
Am J Physiol Lung Cell Mol Physiol. 2001 May;280(5):L930-7. :
Responsiveness of canine bronchial vasculature to excitatory stimuli and to cooling.
Janssen LJ, Lu-Chao H, Netherton S.
Asthma Research Group, Firestone Institute for Respiratory Health, St. Joseph's Hospital and Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5.
Changes in bronchial vascular tone, in part due to cooling during ventilation, may contribute to altered control of airflow during airway inflammation, asthma, and exercise-induced bronchoconstriction. We investigated the responses of canine bronchial vasculature to excitatory stimuli and cooling. Electrical stimulation evoked contractions in only some (8 of 88) tissues; these were phentolamine sensitive and augmented by N(omega)-nitro-L-arginine. However, sustained contractions were evoked in all tissues by phenylephrine [concentration evoking a half-maximal response (EC(50)) approximately 2 microM] or the thromboxane A(2) mimetic U-46619 (EC(50) approximately 5 nM) and less so by beta,gamma-methylene-ATP or histamine. Cooling to room temperature markedly suppressed ( approximately 75%) adrenergic responses but had no significant effect against U-46619 responses. Adrenergic responses, but not those to U-46619, were accompanied by an increase in intracellular Ca(2+) concentration. Chelerythrine (protein kinase C antagonist) markedly antagonized adrenergic responses (mean maxima reduced 39% in artery and 86% in vein) but had no significant effect against U-46619, whereas genistein (a nonspecific tyrosine kinase inhibitor) essentially abolished responses to both agonists. We conclude that cooling of the airway wall dramatically interferes with adrenergic control of bronchial perfusion but has little effect on thromboxane-mediated vasoconstriction.
Bronchial asthma in Cats by Dr.Gloria Dodd, alternative treatment