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Acta Physiologica 2009; Volume 196, Supplement 671
Scandinavian Physiological Society’s Annual Meeting
8/14/2009-8/16/2009
Uppsala, Sweden
CARDIOVASCULAR RESEARCH BASED ON STUDIES OF PRIVATE DOGS WITH OR WITHOUT SPONTANEOUS CARDIAC DISEASE.
Abstract number: L26
Kvart1 C
1Department of Anatomy, Physiology and Biochemistry, Faculty of veterinary medicine and animal husbandry, University of Agricultural Science, Uppsala, Sweden. [email protected]
Cardiovascular research has a long history of animal experiments more or less invasive as a necessary procedure to gain scientific knowledge. Dogs have often been used for research on different aspects of heart failure. Thus heart failure has usually been induced experimentally i.e. by invasive procedures as surgical cutting of chordae tendinae or rapid pacing with implanted pacemaker or cardio toxic drugs. A high incidence of spontaneous heart disease was reported 1985 from UK, in a common companion dog, the cavalier King Charles spaniel. Investigations of prevalence in the population of cavaliers showed the same result in other countries as Sweden and USA. Heart murmurs, easily detected by cardiac auscultation could be found in 50% of the breed at an age of 67 years. Time from onset of murmur to heart failure is usually 35 years meaning that over 50% of the breed will dye or be euthanized because of heart failure from chronic valvular insufficiency. This situation opened a unique opportunity to study the pathophysiology of spontaneously and slowly developing heart failure without the use of experimental animals. At the same time as the owner of a dog got professional help with diagnosis, prognosis and advice for handling of the dog interesting research data could be collected by examination with, history, physical examination, ECG, phonocardiogram, chest X-ray, echocardiography, blood samples and post mortem examination. Examples of interesting findings are: The renin angiotensin aldosteron system (RAAS) is not activated before and at onset of heart failure with pulmonary edema but instead an increased release of the atrial natriuretic peptides (ANP) could be found (Häggström et al 1996). Prophylactic therapy with angiotensin converting enzyme inhibitors (ACEI) did not at all abolish or postponed the onset of heart failure (Kvart et al 2002). Häggström J., K. Hansson, B.E. Karlberg C. Kvart, A. Madej,and K. O
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Acta Physiologica 2009; Volume 196, Supplement 671 :L26