53 research outputs found
Haemodynamic changes during propofol induction in dogs: New findings and approach of monitoring
Abstract Background Propofol is one of the most widely used injectable anaesthetic agents in veterinary practice. Cardiovascular effects related to propofol use in dogs remain less well defined. The main objective of this study was to evaluate the haemodynamic changes during induction of general anaesthesia with propofol in healthy dogs, by a beat-to-beat continuous monitoring. All dogs were premedicated with intramuscular acepromazine (0.015Â mg/kg) and methadone (0.15Â mg/kg). Transthoracic echocardiography was used to measure the velocity time integral (VTI) of the left ventricular outflow tract. A syringe driver, programmed to deliver propofol 5Â mg/kg over 30Â s followed by a continuous infusion of 25Â mg/kg/h, was used to induce and maintain anaesthesia. From the initiation of propofol administration, heart rate (HR) and mean invasive arterial blood pressure (MAP) were recorded every 5Â s for 300Â s, while aortic blood flow was continuously recorded and stored for 300Â S. maximum cardiovascular depression was defined the lowest MAP (MAP_Tpeak) recorded during the monitored interval. VTI and VTI*HR were calculated at 0, 30, 90, 120, 150 and 300Â s post administration of propofol, and at MAP_Tpeak. Haemodynamic effects of propofol in relation to plasma and biophase concentrations were also evaluated by pharmacokinetics simulation. Results The median (range) HR was significantly higher (pâ=â0.006) at the moment of maximum hemodynamic depression (Tpeak) [105(70â148) bpm] compared with pre-induction values (T0) [65(50â120) bpm]. The median (range) MAP was significantly lower (pâ<â0.001) at Tpeak [61(51â69) mmHg] compared with T0 [88(72â97) mmHg]. The median (range) VTI and VTI*HR were similar at the two time points [11.9(8.1â17.3) vs 13,3(9,4-16,5) cm, and 1172(806â1554) vs 1002(630â1159) cm*bpm, respectively]. Conclusions Induction of anaesthesia with propofol causes a drop of arterial pressure in healthy dogs, however cardiac output is well maintained by compensatory chronotropic response. The magnitude of MAP_Tpeak may be strictly related with propofol plasma concentration
A Novel Mutation in the Upstream Open Reading Frame of the CDKN1B Gene Causes a MEN4 Phenotype
PubMed ID: 23555276This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Evaluation of benazepril in cats with heart disease in a prospective, randomized, blinded, placebo-controlled clinical trial
© 2019 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. Background: Heart disease is an important cause of morbidity and mortality in cats, but there is limited evidence of the benefit of any medication. Hypothesis: The angiotensin-converting enzyme inhibitor benazepril would delay the time to treatment failure in cats with heart disease of various etiologies. Animals: One hundred fifty-one client-owned cats. Methods: Cats with heart disease, confirmed by echocardiography, with or without clinical signs of congestive heart failure, were recruited between 2002 and 2005 and randomized to benazepril or placebo in a prospective, multicenter, parallel-group, blinded clinical trial. Benazepril (0.5-1.0 mg/kg) or placebo was administered PO once daily for up to 2 years. The primary endpoint was treatment failure. Analyses were conducted separately for all-cause treatment failure (main analysis) and heart disease-related treatment failure (supportive analysis). Results: No benefit of benazepril versus placebo was detected for time to all-cause treatment failure (P =.42) or time to treatment failure related to heart disease (P =.21). Hazard ratios (95% confidence interval [CI]) from multivariate analysis for benazepril compared with placebo were 1.00 (0.57-1.74) for all-cause failure, and 0.99 (0.50-1.94) for forward selection and 0.93 (0.48-1.81) for bidirectional selection models for heart disease-related failure. There were no significant differences between groups over time after administration of the test articles in left atrium diameter, left ventricle wall thickness, quality of life scores, adverse events, or plasma biochemistry or hematology variables. Conclusions and Clinical Relevance: Benazepril was tolerated well in cats with heart disease, but no evidence of benefit was detected
Supraventricular tachycardia in 23 cats; comparison with 21 cats with atrial fibrillation (2004-2014)
Supraventricular tachycardia (SVT) has not been well-described in cats. The aim of this study was to describe the signalment, clinical findings and outcome for cats with SVT versus cats with atrial fibrillation (AF)
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