<br/>The present thesis describes the etiology of heart failure syndrome (HFS) and ascites in broiler chickens.<p>In The Netherlands, ascites, as a cause of mortality in broiler chickens, is increasing steadily. Rates of mortality in broiler flocks in practice, related to HFS and ascites, during a growth period of approximately six weeks, nowadays vary between 2 and 10 percent. This depends on a genetically predisposition of the flock and on effects of environmental factors which can differ between different farms.<p>The occurrence of ascites at high altitudes and its relation to the low oxygen pressure in the air is well documented (chapter 1). Hypoxia (a low oxygen tension in the inspired air) causes an increase in pulmonary arterial pressure in humans and in animals. The consensus of all studies on hypoxic pulmonary pressor response is that besides an increased heart rate, pulmonary vasoconstriction is an eminently important component in a control system that matches ventilation and perfusion and that preserves arterial P <sub>0<font size="-2">2</font></sub> . A reduction of the oxygen tension in the air stimulates a recruitment of reserve capillaries in the pulmonary vascular bed which previously were not perfused. Vasoconstriction of arterioles in the main pulmonary blood stream increases the local resistance to flow and causes a redistribution of blood towards reserve capillaries.<p>The increased total resistance to flow by the use of more small tubes distributing the blood to all regions of the lungs (by vasoconstriction) increases distinctly the work-load of the right ventricle of the heart (chapter 1). Increased blood pressure in the lungs and failure of the right heart ventricle causing an increased blood pressure in the veins of the systemic circulation results in edema in different parts of the body (lung edema, hydropericard and ascites).<p>Now the same symptoms of edema and right ventricle hypertrophy and failure, known from high altitudes, are found in modern broiler-chicken breeds in non hypobaric conditions at sea level.<p>Experimental results obtained with different species of animals at high altitudes and at sea level showed that at both locations at least partly the same initial conditions are responsible for the development of HFS and ascites.<p>Hypoxia in the sense of a low oxygen tension in the airways appears not to be directly responsible for the pulmonary pressure response. More important is the result of hypoxia which can be measured as low values for oxygen tension in the blood (hypoxemia) and which directly can affect pulmonary arterioles. Hypoxemia leads to tissue oxygen deprivation or anoxia which directly can influence oxidative phosphorylation and which can induce vasoconstriction of pulmonary arterioles.<p>Experimental results obtained with hypoxic chickens at high altitudes and with normoxic fast growing chickens at sea level indicate that in both cases hypoxemia and anoxia can be the initiating factors leading to an inhibited oxidative phosphorylation inducing vasoconstriction of pulmonary arterioles. The subsequent increased pulmonary blood pressure results in hypertrophy and failure of the right heart ventricle and in edema including ascites. From this point of view a hypothesis was formulated that changes in metabolizable energy intake (MEi) and in energy partitioning in the body affecting oxidative phosphorylation quantitatively and thus oxygen requirements could be initial factors in the development of ascites. In accompaniment with changes in oxygen supply these factors could be responsible for pathophysiological processes in the body inducing HFS and ascites. Thyroid hormones initiating and stimulating oxidative phosphorylation therefore could interfere in those pathophysiological processes.<p>Experiments with different populations of broiler chickens combined with effects of different environmental factors described in chapters 2, 3, 4, 5 and 6 were carried out. The aim was to explore the impact of changes in MEi, together with changes in energy partitioning into deposited protein and fat and into heat, and of changes in oxygen consumption on indices of susceptibility for ascites in chickens. Differences in MEi, in deposition of energy (RE) and in heat production (HP) between populations of chickens in experiments were obtained by using following experimental factors:<br/>1 . Different genetic groups of chickens obtained by differences in selection pressure on a fast growth rate and on a low feed conversion ratio (FCR) affecting MEi, energy partitioning, and energy efficiency for growth (RE/MEi).<br/>2. Different dietary compositions, differences in energy density affecting MEi and nutrient composition affecting deposition of energy (RE), deposition of protein (RIP), deposition of fat (RF), and heat production per body weight gain (HP/BWG).<br/>3. Different ambient temperatures affecting mainly MEi, HP/BWG, and oxygen consumption per deposition of protein (OXc/RP).<br/>4. Supplementation of exogenous thyroxine (T4) in diets affecting MEi, and directly OXc followed by responses of HP and RE.<p>In the experiments was shown that populations which combined a low FCR with a fast growth rate exhibited low values for HP/BWG and OXc/RP and high values for RE/MEi and were more susceptible to ascites relative to other populations (chapters 2, 3, 4, 5, and 6). These results indicated that in fast growing stocks, showing low FCR values as a result of high RE/MEi values, a fast protein accretion was achieved together with a reduced ability to convert chemical energy to metabolic heat. A low rate of HIP and thus of OXc, which is not matched to high oxygen requirements, for synthesis and maintenance of protein in tissues, will lead to hypoxemia, heart failure and ascites.<p>Fast growing birds with a low FCR showed less flexibility in metabolic adaptation to a changed environment such as a high fat content in diets and a low ambient temperature. Especially a low ambient temperature will demand a high rate of HP and OXc (chapter 2, 3, 4, and 6). An environment demanding a high level of OXc can induce an imbalance between oxygen supply and requirement in birds. A low FCR can be due to an inability to increase OXc above a certain level. This can reduce the transformation of dietary energy in heat energy.<p>The same fast growing stocks exhibiting a low FCR, if exposed to a low temperature, showed distinctly lower oxygen tension values in venous blood relative to other stocks. The metabolic inability of birds to respond sufficiently to a low temperature by a higher rate of oxygen consumption, inducing hypoxemia and pulmonary hypertension, again can be responsible for the development of ascites. Experimental results described in chapters 3 and 4 support the hypothesis that hypothyroidism reducing HIP and OXc might be one of correlated responses to a selection for a low FCR.<p>Results described in chapter 5 show that supplementation of exogenous thyroxine (T4) to chickens susceptible for ascites can have positive effects on initial conditions responsible for the development of ascites in birds. Supplementation of T4 resulted, only in a population which was susceptible for ascites, in lower haematocrits and haemoglobin contents in blood. High values of both blood parameters are indices of susceptibility for ascites. T4 added to diets also increased adaptive responses of birds, which were susceptible for ascites, to a low ambient temperature, with respect to oxygen consumption. The experimental results reveal that a low thyroid hormone activity might cause impaired adaptive responses of birds to an unfavourable environment which can induce ascites.<p>From the results is concluded that selection procedures and environmental factors which result in decreased values for heat production per gram of body weight gain and in decreased values for oxygen consumption per gram of deposited protein (both of them are related to a decreased feed conversion ratio) will increase the susceptibility for ascites in populations of broiler chickens.
|Qualification||Doctor of Philosophy|
|Award date||24 May 1996|
|Place of Publication||S.L.|
|Publication status||Published - 1996|