Ascites in chickens : oxygen consumption and requirement related to its occurrence

摘要: The present thesis describes the etiology of heart failure syndrome (HFS) and ascites in broiler chickens. In Netherlands, ascites, as a cause mortality chickens, is increasing steadily. Rates flocks practice, related to HFS during growth period approximately six weeks, nowadays vary between 2 10 percent. This depends on genetically predisposition flock effects environmental factors which can differ different farms. occurrence at high altitudes its relation low oxygen pressure air well documented (chapter 1). Hypoxia (a tension inspired air) causes an increase pulmonary arterial humans animals. consensus all studies hypoxic pressor response that besides increased rate, vasoconstriction eminently important component control system matches ventilation perfusion preserves P 0 . A reduction stimulates recruitment reserve capillaries vascular bed previously were not perfused. Vasoconstriction arterioles main blood stream increases local resistance flow redistribution towards capillaries. total by use more small tubes distributing regions lungs (by vasoconstriction) distinctly work-load right ventricle Increased causing veins systemic circulation results edema parts body (lung edema, hydropericard ascites). Now same symptoms hypertrophy failure, known from altitudes, are found modern broiler-chicken breeds non hypobaric conditions sea level. Experimental obtained with species animals level showed both locations least partly initial responsible for development ascites. sense airways appears be directly response. More result hypoxia measured values (hypoxemia) affect arterioles. Hypoxemia leads tissue deprivation or anoxia influence oxidative phosphorylation induce chickens normoxic fast growing indicate cases hypoxemia initiating leading inhibited inducing subsequent including From this point view hypothesis was formulated changes metabolizable energy intake (MEi) partitioning affecting quantitatively thus requirements could accompaniment supply these pathophysiological processes Thyroid hormones stimulating therefore interfere those processes. Experiments populations combined described chapters 2, 3, 4, 5 6 carried out. aim explore impact MEi, together into deposited protein fat heat, consumption indices susceptibility Differences deposition (RE) heat production (HP) experiments using following experimental factors: 1 Different genetic groups differences selection rate feed conversion ratio (FCR) partitioning, efficiency (RE/MEi). 2. dietary compositions, density MEi nutrient composition (RE), (RIP), (RF), per weight gain (HP/BWG). 3. ambient temperatures mainly HP/BWG, (OXc/RP). 4. Supplementation exogenous thyroxine (T4) diets OXc followed responses HP RE. shown FCR exhibited HP/BWG OXc/RP RE/MEi susceptible relative other (chapters 5, 6). These indicated stocks, showing values, accretion achieved reduced ability convert chemical metabolic heat. HIP OXc, matched requirements, synthesis maintenance tissues, will lead hypoxemia, Fast birds less flexibility adaptation changed environment such content temperature. Especially temperature demand An demanding imbalance requirement birds. due inability above certain reduce transformation energy. stocks exhibiting FCR, if exposed temperature, lower venous stocks. respond sufficiently higher consumption, hypertension, again 3 4 support hypothyroidism reducing might one correlated FCR. Results chapter show supplementation have positive T4 resulted, only population haematocrits haemoglobin contents blood. High parameters added also adaptive birds, respect consumption. reveal thyroid hormone activity impaired unfavourable concluded procedures decreased gram (both them ratio)