Development Of Ascites Syndrome Research Articles

ANATOMICAL PARAMETERS OF CARDIOPULMONARY SYSTEM, VENOUS BLOOD PCO2 AND PO2 TENSIONS AND THE DEVELOPMENT OF ASCITES SYNDROME IN TWO GENETIC LINE CHICKENS THAT ARE DIFFERING IN THEIR GROWTH RATE

Summary The present study was designed to examine the anatomical parameters of the cardiopulmonary system, the function of venous blood gas parameters and the development of ascites incidence in two genetic line chickens. Three hundred forty day-old chickens from two pure broiler breeder lines, which were different in their growth rate and susceptibility to ascites syndrome were obtained. The relative heart and lung weights, the volumes of the heart, lung and thorax cavity, the incidence of ascites, and the venous blood gas parameters in these two genetic line chickens were followed. In the present study, the incidence of ascites and right ventricular hypertrophy was markedly higher in the fast-growing broiler chickens compared to the slow-growing chickens, as two genetic line chickens exhibited significant differences in their growth performance traits. The volumes of the thorax cavity, before and after removing the heart and lung tissues, were lower in fast-growing broiler chickens compared to the slow-growing chickens. The relative lung volume was significantly lower in the fast growth chickens than the slow growth chickens at the earlier age, but it did not differ at the later age. Additionally, a rise in carbon dioxide tension and a decline in oxygen pressure in the venous blood of rapid growth compared to the slow growth broiler chickens were observed. It could be concluded that there is an association between the insufficiencies of the cardiopulmonary system with the function of the venous blood gas parameters and the development of ascites syndrome in fast growing broiler chickens.

Effect of repetitive acute cold exposures during the last phase of broiler embryogenesis on cold resistance through the life span

The time just before hatch is critical, because the embryo shifts toward internal and external pipping. This study aimed to determine the beneficial effect of repeated acute reductions of the incubation temperature during the last phase of broiler embryogenesis on posthatch cold tolerance and on the development of ascites syndrome. Fertile eggs were incubated at 37.8°C and 56% RH. At 18 and 19 d of incubation, 3 treatments were conducted, comprising 2 or 3 exposures to 15°C for 30 or 60 min each. During these cold exposures, egg temperature was measured by infrared thermography to determine sensible heat loss from the eggs. At hatch, BW and body temperature were measured. At 3 and 14 d of age, chicks were challenged by cold exposure to 10°C for 3 h. From 14 d of age onward, three-quarters of the chicks were raised under ascites-inducing conditions (AIC) and the others were raised under regular conditions. The sensible heat loss from the eggs was 512 ± 66 cal and 718 ± 126 cal for 30 and 60 min of cold exposure, respectively. No effect of treatment on hatchability was observed, but body temperature and BW were greater to significantly greater in the treated chicks. Cold challenges at 3 and 14 d of age revealed a relative thermoregulatory advantage of embryos exposed to cold for 60 min. Under AIC, fewer treated chickens than controls developed ascites. At 38 d of age, BW and relative breast muscle weight were numerically to significantly greater in the treated chicks than in the control chicks when both were raised under regular conditions, whereas no differences were observed among the chicks raised under AIC. Repeated brief acute cold exposures during the last phase of embryogenesis appeared to improve the ability of growing broilers to withstand low ambient temperatures during their life span. Moreover, chickens treated during embryogenesis improved their performance under regular growth conditions.

Further evidence for the involvement of anatomical parameters of the cardiopulmonary system in the development of ascites syndrome in broiler chickens

Eggs from a broiler line were incubated at two different altitudes and hatched. Relative heart and lung weights, volumes of the heart, lung and thoracic cavity, incidence of right ventricular hypertrophy and ascites, and related physiological parameters were followed in the day-old chickens hatched from the above eggs. Lung and heart weights as a percentage of body weight, lung and heart volumes relative to the volume of the thoracic cavity after removing the heart and lungs were higher in chickens hatched at high altitude. Additionally, embryonic triiodothyronine (T3) and thyroxine (T4) levels relative to cardiopulmonary parameters were higher in day-old chickens that hatched at high altitude as compared with chickens hatched at low altitude. This was associated with a lower incidence of right ventricular hypertrophy and ascites in chickens hatched at high altitude. Our data indicate that chronic hypoxia interacting with the endogenous functions of embryos during embryonic development at high altitude, as adaptation mechanisms, changed the developmental trajectories of cardiopulmonary parameters in postnatal chickens. This important development facilitates an increase in the gas exchange area in broiler chickens, thus lowering their susceptibility to pulmonary hypertension and ascites.

Proliferation of Pulmonary Artery Smooth Muscle Cells in the Development of Ascites Syndrome in Broilers Induced by Low Ambient Temperature

Pulmonary vascular remodelling, mainly characterized by arterial medial thickening, is an important pathological feature of broiler ascites syndrome (AS). Since vascular smooth muscle cells (VSMC) form the major cellular component of arterial medial layer, we speculate that VSMC proliferation is one of the causes of pulmonary arterial medial thickening in ascitic broilers. Hence, the present study was designed to investigate the role of VSMC proliferation in pulmonary vascular remodelling in development of AS induced by low ambient temperature. Broilers in control group (22 +/- 1.5 degrees C) and low temperature group (11 +/- 2 degrees C) were sampled every week at 15-50 days of age. Proliferative indexes of VSMC in pulmonary arteries were assessed with proliferating cell nuclear antigen, and the relative medial thickness (RMT) and relative wall area (RWA), as indexes of pulmonary vascular remodelling, were examined by computer-image analysing system. The results showed that the high incidence (18.75%) of AS was induced by low temperature, and a significantly increased VSMC proliferation was observed in pulmonary arteries in the low temperature group at 22-50 days of age (P < 0.05). In addition, RMT and RWA in pulmonary arteries were significantly elevated in the low temperature group from 36 days of age (P < 0.05), indicating that pulmonary vascular remodelling occurred following VSMC proliferation in AS. Our data suggest that proliferation of VSMC may facilitate pulmonary vascular remodelling and have a pivotal role in AS induced by low ambient temperature.

Increased Calcium Deposits and Decreased Ca2+‐ATPase in Right Ventricular Myocardium of Ascitic Broiler Chickens

Right ventricular hypertrophy and failure is an important step in the development of ascites syndrome (AS) in broiler chickens. Cytoplasmic calcium concentration is a major regulator of cardiac contractile function and various physiological processes in cardiac muscle cells. The purpose of this study was to measure the right ventricular pressure and investigate the precise ultrastructural location of Ca(2+) and Ca(2+)-ATPase in the right ventricular myocardium of chickens with AS induced by low ambient temperature. The results showed that the right ventricular diastolic pressure of ascitic broilers was significantly higher than that of control broilers (P < 0.01), and the maximum change ratio of right intraventricular pressure (RV +/- dp/dt(max)) of ascitic broilers was significantly lower than that of the controls (P < 0.01). Extensively increased calcium deposits were observed in the right ventricular myocardium of ascitic broilers, whereas in the age-matched control broilers, calcium deposits were much less. The Ca(2+)-ATPase reactive products were obviously found on the sarcoplasmic reticulum and mitochondrial membrane of the control right ventricular myocardium, but rarely observed in the ascitic broilers. The data suggest that in ascitic broilers there is the right ventricular diastolic dysfunction, in which the overload of intracellular calcium and the decreased Ca(2+)-ATPase activity might be the important factors.

Erythropoiesis regulation during the development of ascites syndrome in broiler chickens: a possible role of corticosterone.

The ascites syndrome in broiler chickens is attributed to metabolic burdening, which results from intensive genetic selection for rapid growth coupled with exposure to extreme environmental conditions, such as low ambient temperature. These conditions impose on the broilers difficulties in fulfilling tissue demands for oxygen, and the birds exhibit a decrease in blood oxygen saturation and high hematocrit values. It is unknown whether the increase in hematocrit results from alteration in erythropoiesis or from fluid exudation out of the blood system to the abdominal cavity. The present study was conducted to examine the association between abnormal stress response and erythropoiesis process in ascitic broilers. Ascitic chickens revealed a uniquely continuous stress response: expressing an increase (P < or = 0.05) in plasma corticosterone concentration 2 to 3 wk before death. At 5 wk of age, ascitic broilers exhibited an increase (P < 0.05) in hematocrit, blood cell count, and packed cells and blood volumes, with no significant change in plasma volume. These results confirm an accelerated erythropoiesis process in ascitic birds. Increased blood cell production in ascitic birds was matched by an increase (P < 0.05) in the proportion of immature red blood cells (23%) in comparison with broilers that remained healthy (7%), and by decreased (P < 0.05) hemoglobin content relative to red blood cells. We conclude that continually increased corticosterone concentrations, as an inducer of erythropoiesis proliferation and differentiation arrest, in ascitic chickens, resulted in increased production of red blood cells (partially immature) with decreased hemoglobin content; this decrease in hemoglobin might have contributed to enhanced development of hypoxemia and to aggravation of the syndrome.

Hyper- or hypothyroidism: its association with the development of ascites syndrome in fast-growing chickens

The ascites syndrome in broiler chickens is attributed to the progress in genetic selection for rapid growth, coupled with the metabolic burden imposed by exposure to a relatively low-ambient temperature ( T a). The syndrome is mainly characterized by hematocrit elevation, decline in blood oxygen saturation, accumulation of fluid in the abdominal cavity, and finally, death. Ascitic chickens have demonstrated hypothyroidism coupled with a marked stress response (high corticosterone concentration) and reduction in the hemoglobin content. The objective of the present study was to examine the role of thyroid and corticosterone hormones in the development of the syndrome. Ascites was induced by exposure to a gradually declining T a and supplementation of a pellet-form diet. Exogenous thyroxin (T 4) and propylthiouracil (PTU) (in Experiments 1 and 2, respectively) were supplemented in drinking water to induce hyper- or hypothyroidism, respectively. Ascites syndrome was developed in 21.5% and 23% of the birds exposed to ascites-induced conditions (Exps. 1 and 2, respectively). Excess T 4 (Exp. 1) significantly reduced the percentage of ascites (down to 7%), whereas PTU (Exp. 2) significantly increased the appearance of the syndrome (35%). In the T 4-treated chickens, although the T 4 concentration reached pharmacological levels, the triiodothyronine (T 3) concentration remained within physiological levels, whereas T 3 in the ascitic birds exhibited a reduction pattern similar to that observed in the ascitic non-supplemented ones. In the PTU-treated chickens, however, both ascitic and non-ascitic birds demonstrated significant reductions in both T 4 and T 3 concentrations. In both experiments, ascitic chickens exhibited a considerable stress response, characterized by a significant and persisted elevation in plasma corticosterone concentration, which was in accordance with a similar elevation of hematocrit, and the PTU-treated non-ascitic birds exhibited a similar stress response. At 5 weeks of age, ascitic birds and the PTU-treated non-ascitic ones exhibited significant reductions in the hemoglobin content of their red blood cells. It may be concluded that deficiency in the thyroid hormones and elevated corticosterone may play a key deleterious role in the development of the ascites syndrome.

Association Between Weight Gain, Blood Parameters, and Thyroid Hormones and the Development of Ascites Syndrome in Broiler Chickens

The present study examined the association between thyroid hormones and the development of ascites on one hand and the ability to predict ascites from growth rate and hematocrit on the other hand. Ascites syndrome was induced in broiler chickens in two trials by exposing the chicks to low ambient temperature (Ta) and by supplying a pellet form of diet. Weight gain, hematocrit, hemoglobin, and plasma thyroxin (T4) and triiodothyronine (T3) concentrations were measured weekly for each bird, and comparisons were made between birds that eventually died from ascites and those that did not. Mortality from ascites amounted to 24.3 and 24.2% in Trials 1 and 2, respectively. Weight gain did not differ between ascitic and healthy chickens up to approximately 2 wk before death but was significantly lower in the ascitic broilers 1 to 2 wk before death. Hematocrit was significantly higher in broilers with ascites with the exception of ascitic broilers that died at the age of 7 wk (Trial 1). In ascitic broilers, T4 and T3 concentrations declined significantly during the week of death. The present findings raise the question of whether the association between low levels of thyroid hormones and the development of ascites is one of the physiological responses in the syndrome cascade, or whether the failure to maintain thyroid hormones concentration is one of the triggers of the syndrome initiation. This question requires further investigation. It can be concluded that a high rate of weight gain is not always a good predictor of ascites development. Hematocrit and thyroid hormones can provide a good indication but only during the last week of life, and not in all cases. None of these parameters, however, can predict the development of ascites at an early age.

Experimental Reduction of Eggshell Conductance during Incubation. I. Effect on the Susceptibility to Ascites Syndrome

Two hundred-four fertile broiler chicken eggs were obtained from a commercial source and divided into three equal groups. On day 1 of incubation, 68 eggs were selected randomly and four strips of vinyl tape were applied to the shell below the air cell (tape-day 1) to reduce eggshell conductance. This procedure was repeated with an additional group of 68 eggs on day 14 (tape-day 14). Sixty-eight eggs were incubated without treatment, as controls. One week after hatch, 20 chickens from each treatment group and control group were placed into a hypobaric chamber (simulated altitude of 2500 m) for 5 weeks. The remaining chickens in each group were maintained under normobaric conditions. The hematocrit and the mean frontal resultant electrical vector (MRV) of the heart were measured following 1 week, 3 weeks, and 5 weeks of hypobaric or normobaric exposure. Surviving chickens were euthanized at the end of 5 weeks. The weight ratio of right ventricle to left ventricle plus septum (the hypertrophy index [HI]) and the cardiac index, the HI divided by body weight, were determined. All mortality during the study was subjectively scored for the presence of ascites syndrome lesions. The percentage of chickens dying during, or exhibiting ascites syndrome at the completion of, the 5-week hypobaric exposure was 16.7%, 66.7%, and 58% for control, tape-day 1, and tape-day 14 treatments, respectively. MRV values of birds following hypobaric exposure were significantly different between treatment and control groups of the hypobaric exposure and between the two tape treatments. These results suggest that reducing conductance of the eggshell during incubation significantly potentiates the development of ascites syndrome in the broiler chicken.

Changes in Hematological, Blood Gas, and Serum Biochemical Variables in Broilers during Exposure to Simulated High Altitude

One-day-old broilers were reared until 35 days of age at both natural low (100 m) and simulated high altitude (2133 m) to assess the incidence and development of ascites syndrome. Clinical measurements were conducted at 7, 14, 21, 28, and 35 days of age. Birds reared at 2133 meters exhibited significantly (P less than or equal to 0.05) reduced body weights at 7 through 28 days of age. Total serum calcium and biochemical enzyme activities were found to be altered at 35 days of age. In addition, the high-altitude group had significantly (P less than or equal to 0.05) higher erythrocyte counts, hematocrits, and hemoglobin at 14, 21, 28, and 35 days of age and higher serum inorganic phosphorus at each weekly sample time than birds at the low altitude. Total mortality was 20.3% at 2133 meters and 4.6% at 100 meters. The incidence of ascites syndrome in the high-altitude group ranged from 16.6% to 61.1% during the 5-week experimental period.