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This study examined the putative role of blood vessel pathology in the development of ascites in broilers. Major blood vessels (aorta, brachiocephalic arteries, pulmonary arteries, and vena cava) from normal commercial male broiler chickens, and broilers that developed congestive heart failure (CHF) with or without ascites were subjected to gross and microscopic examination. On cross-section, grossly, the arteries from normal broilers and those showing dilated cardiomyopathy without ascites appeared circular, with firm wall tone characteristic of the normal artery. In contrast, the arteries from ascitic broilers appeared flaccid and lacked elasticity, which was evidenced by collapsing, ellipsoid cross-sectional arterial lumen owing to the structural weakness of the arterial walls. Microscopically, ascitic broilers showed thinning or occasionally total loss of elastic elements in the arterial wall, and reduced network density of the structural matrix of the vascular wall, as well as increased thickness of fibers in vena cava. The structural changes seen in the major arteries from ascitic broilers are maladaptive, and as such would definitively impose an increased hemodynamic burden on the already failing heart pump. The changes in veins are indicative of pathological remodeling conducive to increased permeability of the vascular wall, particularly in the situation when a poorly distensible structure is further subjected to wall stress associated with increased pressure and volume overload. Taken together, increased hemodynamic burden and reduced structural density of the venous wall constitute conditions conducive for seepage and accumulation of ascitic fluid.

In order to explain the biochemical mechanisms associated with deteriorating heart function in broiler chickens, this study compared myocardial high energy phosphate substrates in leghorns, feed restricted (Broilers-Res) broilers, ad libitum fed broilers (Broilers-AL), and in broilers that developed heart failure and ascites. The profile of adenine nucleotide content in the heart tissue did not differ between leghorns and Broilers-Res, but there were significant differences among Broilers-Res, Broilers-AL, and broilers with ascites. During intensive growth periods, leghorns and Broilers-Res showed increasing trends in heart ATP levels, whereas in fast growing broilers the heart ATP declined (p<0.021). ATP:ADP and ATP:CrP ratios increased with age in both leghorn and Broilers-Res, declined in fast growing broilers, and were the lowest in broilers that developed heart failure. The changes in heart high energy phosphate profile in broilers suggest that the energy demand of the heart during a rapid growth phase may exceed the bird's metabolic capacity to supply adequate levels of high energy phosphate substrate. The insufficiency of energy substrate likely contributes to the declining heart rate. In some individuals this may lead to impaired heart pump function, and in more severe cases may progress to heart pump failure.

This study reports novel insight into the aetiology of pulmonary hypertension and ascites in broiler chickens. The scope of measurements was focused on anatomical and functional parameters, and blood flow patterns in leghorns (resistant to ascites), fast-growing broilers (susceptible to ascites), broilers developing ascites, and ascitic broilers evaluated in vivo using echocardiography, and further examined in the context of postmortem findings. Both, in vivo observed features and postmortem findings, showed clear differences between broilers and leghorns, and between normal and ascitic broilers. Abnormalities in the heart chamber geometry and blood flow patterns were detected upon echocardiographic examination in all ascitic broilers. Right and left atrio-ventricular (AV) valve regurgitation were common findings in ascitic broilers and some apparently normal broilers, with left AV valve insufficiency being a predominant feature with respect to degree and frequency of occurrence. Blood flow disturbances were not detected in leghorns. Left ventricular fractional shortening (functional parameter) was considerably reduced (P < 0.01) in ascitic birds (mean: 21.7 +/- 2.0 SE) in comparison with normal broilers (mean: 39.1 +/- 3.6 SE), or leghorns (mean: 43.3 +/- 2.4 SE). The presented findings indicate that pathological and functional changes in the left ventricle and atrium play a significant role in the pathogenesis of ascites in broilers. Severe dilation of the left atrium and pulmonary veins seen on postmortem examination, as well as regurgitant blood flow in the left atrium, demonstrated by Doppler study in ascitic birds, provide evidence that chronically elevated pressure in the left atrium is involved in the aetiology of pulmonary hypertension and ascites in fast-growing broilers.

The present study examines ultrastructural and molecular changes in ventricular myocardium associated with ascites cases in fast-growing broilers raised at low altitude. Extensive ultrastructural lesions were seen in the left and right ventricular myocardium of broilers with fulminant heart failure and ascites. Significant changes included lesions in the myofibril contractile apparatus, altered mitochondria, marked reduction in the myofibril component, and changes in the extracellular matrix (ECM) architecture. No lesions were observed in hearts of slow growing broilers, but mild to moderate changes (predominantly in the left ventriculum) were apparent in the hearts from some clinically normal, fast-growing broilers. SDS-PAGE profiles of washed myofibrils showed several distinctly different bands in preparations from left ventricular myocardium of ascitic birds. Western blot analysis of these samples revealed several fragments of myosin heavy chain, M-protein, and titin. Based on gelatinolytic activity, matrix metalloproteinases (MMP) in the cytosolic fraction of ventricular myocardium homogenates were identified as MMP-2. The relative activity of this enzyme appears to be considerably higher in preparations from broilers, particularly in the preparations from the left ventriculum of fast-growing broilers, in comparison to leghorns or slow growing broilers. The nature and distribution of the changes in the heart indicate that chronic cardiomyopathic process in the left ventricular myocardium occurs during the development of ascites. It is postulated that progressive deterioration of the left heart pump function caused by initial lesions in the left ventricular myocardium is a significant factor in the development of pulmonary hypertension and the pathogenesis of ascites in broilers raised at low altitude.

1. The first objective was to evaluate baseline heart rate (HR) responses in fast growing broilers fed ad libitum from 1 to 45d or subjected to a food restriction (85%, 70% and 55% of ad libitum from 7 to 21d) and a refeeding (22 to 45d) regimen in a normal thermal environment. The second was to evaluate HR and haematocrit responses in fast growing broilers reared at a low environmental temperature and fed ad libitum (A-L) from 1 to 42d, subjected to food restriction (70% ad libitum) between 7 to 21d and refed thereafter (R-R), or subjected to food restriction between 7 to 42d (R), and to follow the changes in normal birds and those prone to ascites. 2. The baseline HR in the normal thermal environment at 21 and 45d in birds fed ad libitum was lower (P < 0.001) than at 7d. The food-restricted groups had higher HRs at 21d than at 7d, with the differences significant (P < 0.01) for the 70% and 55% treatments. At 21d the HRs in restricted groups were significantly higher (P < 0.01) than in ad libitum-fed birds. After returning to ad libitum feeding the HRs in these birds tended to decline, with the differences significant (P < 0.05) for the 70% and 55% treatments. 3. In the birds exposed to cold, each feeding regimen produced distinct patterns of change in HR and haematocrit. Both feeding regimen and age had significant (P < 0.001) effects on the changes of both variables. Relative to 7d, on 14d and 21d the HRs decreased and haematocrits increased in all groups, but the rates of change were highest in the A-L and R-R birds. The first fulminant cases of ascites were observed during the third week in the A-L group and during the fourth week in the R-R group. None of the chickens from the R group developed ascites. Altogether, the incidence of ascites was 48% in the A-L group and 28% in the R-R group. 4. Among the birds exposed to cold, the ascitic birds had significantly (P < 0.001) lower HRs and higher haematocrits than normal birds from the same feeding regimen group. The time trends in the rates of change in HR and haematocrit were distinctly different (P < 0.001) for ascitic and normal birds. The change in feeding regimen from restricted to ad libitum in the R-R group resulted in a significant (P < 0.001) decrease in HR and increase in haematocrit. 5. In view of the evidence presented, it appears that hypoxaemia and tissue hypoxia in broiler chickens may be a result of circulatory insufficiency associated with progressive bradycardia rather than, as commonly believed, pulmonary insufficiency. In this situation the pulmonary hypertension may be a secondary symptom.

Background: The goal of this study was to evaluate marker-assisted selection (MAS) in broiler chickens using previously mapped gene regions associated with ascites syndrome incidence. The second-generation MAS products were assessed for impact on ascites phenotype and whether there were associated changes in important production traits. Previously, we used whole genome resequencing (WGR) to fine-map 28 chromosomal regions as associated with ascites phenotype in our experimental ascites broiler line (Relaxed, REL) based on a hypobaric chamber challenge. Genotypes for single nucleotide polymorphisms (SNPs) in mapped regions on chromosomes 2 and 22, were used for MAS in our REL line. After two generations, birds homozygous for the genotypes associated with resistance for both chromosomal regions were established. The MAS F2 generation was then compared to the REL line for ascites susceptibility and 25 production traits. Results: Selection based on SNPs in the carboxypeptidase Q (CPQ, Gga2) and leucine rich repeat transmembrane neuronal 4 (LRRTM4, Gga22) gene regions resulted in a sex- and simulated altitude- dependent reduction of ascites incidence in two F2 cohorts of the MAS line. Comparisons of the F2 MAS and REL lines for production traits when reared at ambient pressure found no significant negative impacts for feed intake (FI), feed conversion ratio (FCR), or deboned part yields for either sex for two F2 cohorts. There were, however, improvements in the MAS for full-trial body weight gain (BWG), FCR, absolute and relative tender weights, and relative drumstick weight. Conclusions: These results validate the mapping of the 28 chromosomal regions and demonstrate that fine mapping by WGR is an effective strategy for addressing a complex trait; it also stands as the first successful SNP-based selection program against a complex disease trait, such as ascites. The MAS line is comparable and, in some instances, superior, in growth performance to the REL control while being more resistant to ascites. This study indicates that MAS based on WGR can provide significant breeding potential in agricultural systems. [ABSTRACT FROM AUTHOR]

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Ascites syndrome (AS) is a harmful disease in fast-growing broilers characterized by heart failure and serious fluid accumulation in the abdominal cavity. One of the known functions of zinc transporter ZIP12 is an important regulator in pulmonary hypertension (PH) in rat. Whether chicken ZIP12 is involved in the process of AS need to be explored. Here, chicken ZIP12 was sequenced and expression pattern and histological distribution were detected in broilers of AS induced by intravenous cellulose microparticle injection. Phylogenetic analysis showed that ZIP12 was significantly different between chicken and mammalian. The relative mRNA expression level of ZIP12 in the liver and lung in AS and pre-ascites (PAS) groups were significantly higher (P < 0.01) than that in control. The immunohistological staining using rabbit anti-chicken ZIP12 IgG and integrated optical density analysis showed the positive cells of ZIP12 distributed in detected tissues and the expression level of ZIP12 protein increased in AS and PAS groups compared to control. The results will provide the basic data of ZIP12 in the pathological process of AS in broiler chickens and offer an important reference for prevention and control of the disease. [ABSTRACT FROM AUTHOR]

Ascites syndrome (AS) is a metabolic disorder in fast-growing broilers that is characterized by non-tumult fluid collection in the abdomen. The objective of this study was to evaluate the effects of variable feeding and rearing temperature on AS occurrence in broilers. A total of 360 one-day-old male Ross-308 chicks were assigned to three equal groups (n = 120) fed pellet, crumble or mash diets and within each group, half of birds (n = 60, starting from the 22nd day of age) were reared under two different temperatures: at 23°C (comfort) or at 14°C (cold), respectively. There were six treatments and four replicates including 15 broilers per replicate per treatment. Birds' growth performances and blood parameters as well the incidence of ascites were assessed. The haematocrit percentage, T3 and T4 hormones activity in pellet-fed group under cold temperature conditions were significantly higher (P < .05) than the other groups. Based on the results, the occurrence of AS under mash-fed regime was less than pellet and crumble dietary groups (P > .05). Further, feeding of mash diet reduced broilers' feed consumption per unit of time, especially by level of achieving energy that is reducing the growth and AS. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of hypoxic stresses on vascular endothelial growth factor (VEGF) in cultured lung fibroblasts of meat-type chickens. Isolated and subcultured primary lung fibroblasts were exposed to hypoxia. The presence of VEGF and the effects of hypoxia on cultured lung fibroblasts and in the culture media were evaluated. Immunocytochemistry using streptavidin-biotin-peroxidase method and ELISA using commercially available primary monoclonal antibodies were used for evaluation in both 6-h and 12-h hypoxic fibroblasts. The level of VEGF was slightly higher in the 6-h hypoxic group (1.22 ng/mL) than in the 6-h control group (1.27 ng/ml) in cell culture media by LISA. In the 6-ah hypnotic group, a correlation between the decrease in imminency score and increase in medium with VEGF was observed. The presence of VEGF was shown in cultured chicken lung fibroblasts from meat-type chickens. In conclusion, a significant decrease in immunocytochemical staining score was observed along with a slight increase in the amount of VEGF in culture media under hypoxic conditions. The results suggest that VEGF might have a role in edema formation via permeability increase in the lungs of ascitic meat-type chickens. [ABSTRACT FROM AUTHOR]

Increasing susceptibility of broiler chickens to ascites syndrome has coincided with a continuing genetic and nutritional improvement in their feed efficiency and growth rate. Imbalance between oxygen supply and the oxygen required to sustain rapid growth rates and high food efficiencies is believed to be the primary cause of ascites. This imbalance is caused by exogenous and/or endogenous factors. Selection in fast growth broilers, have also resulted in the development of birds with changed anatomical, physiological, metabolic and hematological parameters including thyroid hormone activity, partial pressure of O2 and carbon dioxide in venous blood, cardiac β-adrenergic receptors and hematocrit levels that coincide with susceptibility to ascites in broiler chickens. Observations to date have indicated that the structural or endocrine changes are often linked with ascites susceptibility and may be influenced during the early stages of development, embryogenesis and incubation. In this review, particular attention is paid to the interactions between endogenous and exogenous factors as predisposing factors for development of ascites syndrome. Additionally, preventive management procedures like different lighting schedules, feed restriction protocols and supplementation of feed with antioxidants which reduce the incidence of ascites in broiler chickens are highlighted. [ABSTRACT FROM AUTHOR]

To investigate the involvement of apoptosis in the pathogenesis of T3-induced pulmonary hypertension in broiler chickens, caspase-1, -2, and -3 gene expressions were evaluated by semiquantitative RT-PCR in the lungs and left and right heart ventricles. One-day-old fast-growing chickens were randomly divided into 2 equal groups with 3 replicates per group. Chicks were reared for 7 weeks under standard conditions. T3 as a thyroid hormone was added to the ration after week 1 of rearing. Pulmonary hypertension was induced at 49 days based on RV/T V ratio index. The caspase genes were constitutively expressed in the lung and right and left ventricles of intact and pulmonary hypertensive broiler chickens. The relative amount of caspase-1, -2, and -3 mRNA in the lung and right and left ventricles of the heart was higher in pulmonary hypertensive broilers than in control broilers (P < 0.05). It is speculated that increased mRNA levels of caspase in the lungs and hearts of pulmonary hypertensive broilers could be evidence of upregulated apoptosis, which is involved in the pathophysiology of broiler chickens with pulmonary hypertension. [ABSTRACT FROM AUTHOR]

1. B- and M-mode echocardiography was used to compare cardiac function in broilers with spontaneous ascites syndrome with that of normal chickens. 2. Thirty ascitic chickens and 15 normal chickens aged three, 4, 5 and 6 weeks from the same flock (180 birds in total) were examined. They were restrained gently in a natural standing position, and echocardiographs were obtained with a 7·0-MHz linear transducer placed on the left pectoral apterium. Indices of cardiac structure and functioning were calculated from the echocardiographs, and some were normalised to body weight. Heart rate was also measured. 3. All cardiac structural indices in both ascitic and normal chickens increased with age. Compared with normal chickens, right ventricular diameter at both the end of systole and of diastole was greater in ascitic chickens at all ages. Left ventricular diameter at the end of systole in ascitic chickens was greater at 4, 5 and 6 weeks of age. Ventricular septal thickness at the end of both systole and diastole was greater in ascitic chickens at 5 and 6 weeks. Left ventricular free wall thickness at the end of diastole was less in ascitic chickens at 3 weeks. However, all the structural indices decreased with age after normalisation with body weight. 4. The heart rate of ascitic chickens was lower at 4, 5 and 6 weeks. Normalised left ventricular fractional shortening was lower in ascitic chickens at 4, 5 and 6 weeks, as was normalised right ventricular fractional shortening. Incrassation of the ventricular septum (ΔT), which changed little in normal chickens, was less at 4, 5 and 6 weeks in ascitic chickens. Left ventricular fractional shortening, right ventricular fractional shortening and ΔT were all negatively correlated with ascites heart index at all ages. 5. Taken together the results suggest heart failure of both ventricles, but that right ventricular dysfunction is more extensive than left ventricular dysfunction. We suggest that secondary pulmonary hypertension would result in these ascitic chickens due to volume overload. [ABSTRACT FROM AUTHOR]

Copyright of Avian Pathology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

1. Genetic parameters for the sudden death syndrome (SDS) were estimated in meat-type chickens. Data were collected over 11 generations of selection for body weight within two distinct breeds (Cornish and White Rock).2. The animal model was used exclusively with linear methods (LM) to estimate genetic parameters. Heritability (h 2 ) of SDS on the liability scale was 0&CenterDot;30?&PlusMinus;?0&CenterDot;002 and 0&CenterDot;25?&PlusMinus;?0&CenterDot;002 in the Cornish and White Rock breeds, respectively.3. A positive genetic correlation (rg) with ascites (AS) was determined (~0&CenterDot;3?&PlusMinus;?0&CenterDot;006). However, it was not possible to estimate the rg of SDS with body weight because of the low prevalence of the defect trait studied (1&CenterDot;8% in the Cornish and 1&CenterDot;5% in the White Rock).4. Heritability of SDS calculated using male records only was 0&CenterDot;45?&PlusMinus;?0&CenterDot;009 and 0&CenterDot;35?&PlusMinus;?0&CenterDot;009, and rg with body weight was 0&CenterDot;30?&PlusMinus;?0&CenterDot;010 and 0&CenterDot;27?&PlusMinus;?0&CenterDot;009, in the Cornish and White Rock breeds, respectively.5. In conclusion, the heart defect investigated was heritable with a positive genetic correlation with AS and body weight. [ABSTRACT FROM AUTHOR]

1. Pulmonary hypertension syndrome followed by ascites is a metabolic disorder in broilers that occurs more often in fast-growing birds and at cool temperatures.2. Knowledge of the genetic relationships among ascites-related traits and performance traits like carcase traits or feed efficiency traits is required to design breeding programmes that aim to improve the degree of resistance to ascites syndrome as well as production traits. The objective of this study was to estimate these genetic correlations.3. Three different experiments were set up to measure ascites-related traits (4202 birds), feed efficiency traits (2166 birds) and carcase traits (2036 birds). The birds in different experiments originated from the same group of parents, which enabled the estimation of genetic correlations among different traits.4. The genetic correlation of body weight (BW) measured under normal conditions and in the carcase experiment with the ascites indicator trait of right ventricle to total ventricle ratio (RV:TV) measured under cold conditions was 0&CenterDot;30. The estimated genetic correlation indicated that single-trait selecting for BW leads to an increase in occurrence of the ascites syndrome but that there are realistic opportunities of multi-trait selection of birds for improved BW and resistance to ascites.5. Weak but positive genetic relationships were found between feed efficiency and ascites-related traits suggesting that more efficient birds tend to be slightly more susceptible to ascites.6. The relatively low genetic correlation between BW measured in the carcase or in the feed efficiency experiments and BW measured in the ascites experiment (0&CenterDot;49) showed considerable genotype by environment interaction. These results indicate that birds with high genetic potential for growth rate under normal temperature conditions have lower growth rate under cold-stress conditions due to ascites. [ABSTRACT FROM AUTHOR]