Use of esmolol for control of tachycardia in 28 dogs and cats (2003-2020).

OBJECTIVE: To describe the indications and clinical response for dogs and cats treated with esmolol. DESIGN: Retrospective case series from 2003 to 2020. SETTING: Single university veterinary teaching hospital. ANIMALS: Twenty-two dogs and 6 cats. INTERVENTIONS: Animals received either a bolus or bolus and continuous rate infusion of the ultrashort-acting beta receptor antagonist, esmolol. MEASUREMENTS AND MAIN RESULTS: Twenty-two animals were treated for either a supraventricular or sinus tachycardia, 5 were treated for a ventricular tachycardia, and 1 was treated for atrial fibrillation. Esmolol was most frequently used in dogs (N = 9) who had ingested a toxin such as albuterol, amphetamine, or chocolate. Esmolol was administered at median bolus dose of 330 µg/kg (range 10-1000 µg/kg) and continued as a continuous rate infusion in 15 animals at a median dose of 50 µg/kg/min. Defining success as a reduction in heart rate of 20% or greater, esmolol therapy was considered successful in 13 of 28 animals (46%). Animals treated for a toxicosis were more likely to have a successful rate reduction than those treated for other causes (P = 0.006). Nineteen animals survived to discharge. Both treatment success (P = 0.046) and treatment for a toxicosis (P = 0.003) were associated with survival. CONCLUSIONS: Esmolol administration was well tolerated by dogs and cats with tachycardia due to intoxication. Heart rate reduction by at least 20% was achieved in 46% of cases. Animals with toxin ingestion were more likely to be discharged from the hospital.

Treatment of naturally occurring asthma with inhaled fluticasone or oral prednisolone: A randomized pilot trial.

The objective of this study was to compare inhaled glucocorticoids with oral glucocorticoids for treatment of naturally occurring feline asthma. Secondary goals were to evaluate serum allergy testing results in cats and to quantify the effect of an inhaled glucocorticoid (fluticasone) on glucose homeostasis. Nine cats with asthma were enrolled on the basis of clinical signs, thoracic radiographic findings, and airway eosinophilia. Cats were randomized and 4 cats were treated with oral glucocorticoids and 5 cats with inhaled glucocorticoids, with a 7-day course of oral glucocorticoids overlapping at the start of therapy. Cats were evaluated at baseline and at 8 wk with thoracic radiographs, bronchoalveolar lavage, lung function testing, and fructosamine levels. Serum allergen panels were evaluated. All cats were clinically normal after treatment and had significantly improved airway eosinophilia and decreased nucleated cell count. No improvement was seen in radiographic changes after treatment with either therapy. Oral, but not inhaled glucocorticoids, caused a decrease in airway resistance, although cats in the inhaled group had a higher baseline resistance than those in the oral group. Fructosamine levels did not change with treatment. Fifty percent of cats tested positive for immunoglobulin E (IgE) antibodies. Asthma is a heterogeneous condition; individual cats responded well to both oral and inhaled glucocorticoids. Ongoing evaluation of the potential underlying causes and therapeutic options is warranted with a larger group of cats.

L'objectif de l'étude était de comparer le traitement de l'asthme félin avec des glucocorticoïdes inhalés et administrés par voie entérale. Les objectifs secondaires étaient d'évaluer les résultats de tests d'allergies de chats atteints d'asthme félin et de quantifier l'effet d'un glucocorticoïde inhalé (fluticasone) sur l'homéostasie du glucose. Neuf chats atteints d'asthme félin ont été recrutés selon les signes cliniques, les trouvailles radiographiques et les évaluations cytologiques des voies aériennes (éosinophilie). Les chats ont été randomisés. Quatre chats ont été traités avec des glucocorticoïdes par voie entérale et cinq chats avec des glucocorticoïdes inhalés dont les 7 premiers jours ont été associés à l'administration de glucocorticoïdes par voie orale. Les chats ont initialement été évalués au moment du recrutement et puis à huit semaines avec des radiographies thoraciques, lavage bronchoalvéolaire, tests de fonction pulmonaire et dosage de la fructosamine. Des tests sériques d'allergènes ont également été évalués. Tous les chats ont eu une résolution des signes cliniques après le traitement et avaient une amélioration significative du compte éosinophilique du LBA. Aucune amélioration des lésions radiographiques suivant le traitement soit inhalé ou entéral n'a été observée. Seuls les glucocorticoïdes entéraux ont causés une diminution de la résistance des voies respiratoires. Toutefois les chats du groupe de traitement de glucocorticoïdes inhalés avaient, avant l'initiation du traitement, une résistance pulmonaire plus importante. Les niveaux de fructosamine n'ont pas changé significativement, et ce dans les deux groupes de traitement. 50 % des chats ont testé positif pour des anticorps IgE contre des allergènes inhalés communs. L'asthme est une entité clinique hétérogène; les chats ont individuellement bien répondu autant au traitement inhalé qu'au traitement entéral. L'étude des potentielles causes sous-jacente et des différentes options thérapeutiques sont recommandées dans une population plus grande de chats.(Traduit par les auteurs).

Phosphine substitution reactions of (η5-cyclopentadienyl)ruthenium bis(triarylphosphine) chloride, CpRu(PAr3)2Cl {PAr3 = PPh3, P(p-CH3C6H4)3, P(p-FC6H4)3, P(p-CH3OC6H4)3, and PPh2(p-CH3C6H4)}: a tale of two mechanisms.

The kinetics of phosphine substitution in CpRu(PAr3)2Cl by PMePh2 under pseudo-first order conditions in CDCl3 have been measured for PAr3 = PPh3, 1a, PPh2(p-tol), 1b, P(p-tol)3, 1c, P(p-CH3OC6H4)3, 1d, and P(p-FC6H4)3), 1e. Activation parameters characteristic of a dissociative pathway (ΔH(†) = 110-124 ± 2 kJ mol(-1), ΔS(†) = 16-44 ± 5-12 J mol(-1) K(-1)) are observed for all five compounds. The rate of substitution in CpRu(PAr3)2Cl (1a) and CpRu[P(p-FC6H4)3]2Cl (1e) is independent of added chloride ion and decreases in the presence of excess PAr3, however, the rate of substitution in CpRu[P(p-CH3OC6H4)3]2Cl (1d) is first order in added chloride ion and is less dependent on added PAr3. A mechanism involving [CpRu(PAr3)2(PMePh2)](+)[Cl](-) intermediates contributes to the substitution in 1b-d.