BACKGROUND: Ascites is a metabolic disease that has negative effects on broiler chickens. OBJECTIVES: This study was performed to investigate the effect of cold induced ascites on performance, meat quality and quantity indices and some blood indices of broiler chickens with cold induced ascites. METHODS: Three hundred one-day-old female chicks (Ross 308) were used in a completely randomized design with two treatments of control (under normal temperature) and ascitic (under cold stress) with five replicates and 30 birds per each replicate. RESULTS: The results showed that cold-induced ascites caused the lower performance, carcass weight and thigh and breast meat (P<0.05). Furthermore, ascites caused the increased anus temperature and thigh lightness (L) and redness (a) at day 42 of age (P<0.05). Cold induced ascites decreased the enzymes of glutathione peroxidase and superoxide dismutase, uric acid, albumen and malondihaldehyde in blood at day 42 of age (P<0.05). The higher blood hematocrit and hemoglobin were observed in ascetic birds (P<0.05). CONLUSIONS: In conclusion, cold induced ascites increase the meat lightness through the increased peroxidation and decreased antioxidants of the body. Moreover, ascites cause the higher anus temperature by increasing the body basal metabolism.

A Jersey crossbred cow was admitted with the history of dystocia. A large sized anasarcous fetus along with ascites and hydrocephalus was delivered after puncture and draining of Àuid using William's long obstetrical hook and traction.

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56. Leptomeres were observed in cardiac myocytes of ducklings that had been fed furazolidone, but not in those fed only the control ration. Our clinical, gross pathologic, and ultrastructural findings indicate that regression of the cardiac lesions of furazolidone toxicosis may be essentially complete by 28 days after cessation of furazolidone intake. Our ultrastructural findings indicate that furazolidone consumption may result in cardiac dilatation by altering myofibrillar/cytoskeletal attachments of myocytes.

A 2-year-old, female, American cocker spaniel dog presented for a 1-year history of severe ascites, exercise intolerance, tachypnea. At that time, she was in an emergency state. First, the dog was stabilized with oxygen therapy. A diagnosis of cardiac problem was made from history, auscultation, radiograph, ECG, and echocardiography. Jugular pulsation was palpated and a harsh, systolic murmur of tricuspid regurgitation was prominent at the right cardiac apex. Tricuspid valve dysplasia (TVD) was confirmed with echocardiography, accompanying enormous myocardial hypertrophy.

A female Labrador dog presented with a history of distended abdomen was subjected for clinical, physical, hemato-biochemical, eletrocardiographic, and ultrasonographic evaluations. Respiratory distress, weakness, fluid thrill on palpation of abdomen, cough, cyanotic tongue, and syncope were the significant manifestations. Elevated levels of creatine kinase, lactate dehydrogenase, alanine amino transferase, and alkaline phosphatase with normal blood urea nitrogen and creatinine were the common serum chemistry findings. Low voltage QRS complexes were the electrocardiographic abnormalities. Classical ground glass appearance of abdomen, and enlarged heart with increased sternal contact were the radiographic findings of abdomen and thorax. Ultrasonography of abdomen revealed floating viscera in the anechoic effusion with engorged and distended hepatic vasculature. 2-dimensional echocardiography revealed dilated right ventricle both on B- and M-mode. Further, insufficiency in mitral and tricuspid valves were recorded on pulsed and color flow Doppler. Hence, right heart failure due to ascites was confirmed, and the condition was successfully managed with losartas, spiranolactone, co-enzyme Q10 and tricholine citrate, and sorbitol.