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Biomedical subjects

R J Julian

Publications and source records attributed to R J Julian.

At least 19 recordsLinked to original sources
PubMed2005

Heritability of sudden death syndrome and its associated correlations to ascites and body weight in broilers.

(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 (h2) of SDS on the liability scale was 0.30 +/- 0.002 and 0.25 +/- 0.002 in the Cornish and White Rock breeds, respectively. (3) A positive genetic correlation (r(g)) with ascites (AS) was determined (approximately 0.3 +/- 0.006). However, it was not possible to estimate the rg of SDS with body weight because of the low prevalence of the defect trait studied (1.8% in the Cornish and 1-5% in the White Rock). (4) Heritability of SDS calculated using male records only was 0.45 +/- 0.009 and 0.35 +/- 0.009, and r(g) with body weight was 0.30 +/- 0.010 and 0.27 +/- 0.009, 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.

Animals↗
PubMed2001

The effect of dietary chloride and bicarbonate on blood pH, haematological variables, pulmonary hypertension and ascites in broiler chickens.

1. The effect of supplementing grower diets with bicarbonate or chloride on haematological variables, pulmonary hypertension syndrome and ascites in broilers exposed to cold temperature was investigated. 2. High concentrations of dietary chloride had no effect on the pH of the venous blood but a low chloride/high bicarbonate diet significantly increased blood pH. There was no consistent effect of dietary chloride or bicarbonate concentrations on growth performance, although in 1 experiment birds given a low chloride/high bicarbonate diet consumed less food and gained less weight than controls. 3. Birds fed on high-chloride diets tended to have a higher incidence of ascites and pulmonary hypertension than controls. Birds fed on low-chloride and high-bicarbonate diets had significantly lower pulmonary hypertension and lower heart weights, which may have indicated a decrease in pulmonary and systemic blood pressure. 4. We conclude that increasing dietary bicarbonate and reducing dietary chloride has potential as a low cost and effective method to reduce the pulmonary hypertension which leads to ascites in broiler chickens.

Animals↗
PubMed2001

Estimation of genetic parameters for ascites syndrome in broiler chickens.

Genetic parameters for the ascites syndrome (AS) were estimated for meat-type chickens. Data had been collected over 11 generations of selection for body weight and other traits within two distinct breeds (Cornish and White Rock). Linear methods (LM) were used to estimate genetic parameters and also to analyze a binary measure of survival. Survival analyses (SA) were also conducted to estimate the effects of various factors influencing the incidence of AS by evaluating the number of days that the birds survived. The animal model was used exclusively with linear methods. Heritabilities (h2) on the liability scale were 0.12 +/- 0.02 and 0.22 +/- 0.01 in the White Rock and Cornish breeds, respectively; however, the genetic correlation (r(g)) with body weight was not possible to estimate due to the low prevalence of the defect trait studied (1.5% in the Cornish and 1.1% in the White Rock). Because males are more prone to AS, the h2 using the male records only were 0.22 +/- 0.017 and 0.41 +/- 0.009, and the r(g) were 0.35 +/- 0.007 and 0.22 +/- 0.009 in the dam and sire populations, respectively. In conclusion, the heart defect investigated was heritable and had a positive genetic correlation with body weight.

Animals↗
PubMed2001

The effects of dietary flax oil and antioxidants on ascites and pulmonary hypertension in broilers using a low temperature model.

1. Three experiments were conducted using a low temperature model to induce pulmonary hypertension (PH) and ascites in broiler chickens. Diets containing 25 g or 50 g flax oil/kg food and control diets with an equivalent amount of animal/vegetable (A/V) blend oil, with and without supplemental antioxidants (vitamin C and vitamin E) were used. The amount of PH was assessed by the ratio of right ventricle weight to total ventricle weight (RV/TV ratio). Birds were considered to suffer from pulmonary hypertension syndrome (PHS) if the RV/TV ratio was greater than 0.299. 2. In experiment 1, the test diets contained 50 g oil/kg food and were given during the grower period only. Birds fed on the flax oil diet tended to have a lower incidence of PHS, ascites and lower RV/TV ratios than birds fed on the control diet. However, when the flax oil diet was supplemented with antioxidants, the incidence of ascites, PHS, haematocrit and whole blood and plasma viscosity increased compared with birds fed on the flax oil diet without antioxidants. These effects were not seen in experiment 2, when the test diets containing 30 g oil/kg food (25 g flax oil plus 5 g A/V blend oil/kg food compared to 30 g A/V blend oil/kg food) were given during the grower period. However, in experiment 3, when the test diets containing 30 g oil/kg food were given from day 1 to week 8, birds fed on the control diet supplemented with antioxidants had a higher incidence of PHS than those fed on the control diet alone. 3. In all 3 experiments, there was no significant effect of dietary fat source or supplemental antioxidants on total food intake or food conversion. 4. We conclude that diets containing 50 g flax oil/kg food tend to reduce the incidence of PHS and ascites in broilers using a low temperature model but the results were not statistically significant. In some cases, supplementing diets with a combination of vitamin E and vitamin C increased the incidence of ascites and PHS.

Animal Nutritional Physiological Phenomena↗
PubMed1999

Effect of dietary flax oil and hypobaric hypoxia on pulmonary hypertension and haematological variables in broiler chickens.

1. Three experiments were conducted with broiler chickens using hypobaric chambers and control pens, feeding diets containing 25 or 50 g flax oil/kg food or control diets with equivalent amounts of animal/vegetable (A/V) blend oil for 4 weeks. The effect of these diets on haematological variables and the extent of right ventricular hypertrophy (RVH) leading to ascites was determined. 2. Overall growth rate was not consistently affected by dietary treatment, although feeding the 25 g flax oil/kg diet reduced weight gain in week 4 of one experiment. Feeding the 50 g flax oil/kg diet but not the 25 g flax oil/kg diet reduced RVH in birds exposed to hypobaric conditions compared to feeding control diets. 3. Feeding the 50 g flax oil/kg diet under hypobaric conditions reduced the haematocrit and haemoglobin content, increased the erythrocyte deformability and the proportion of unsaturated fatty acids in the erythrocyte membranes, and reduced the whole blood viscosity compared to feeding control diets. These effects were not seen when the 25 g flax oil/kg diet was fed. The ratio of n-3 to n-6 fatty acids in erythrocyte membranes was increased in the 50 g flax oil/kg treatment group compared to controls. 4. Including 50 g flax oil/kg broiler diet reduces RVH in broiler chickens. This may be attributable in part to an increase in erythrocyte deformability from an increased proportion of unsaturated fatty acids in the erythrocyte membranes.

Animal Nutritional Physiological Phenomena↗
PubMed1998

Rapid growth problems: ascites and skeletal deformities in broilers.

Over the last 40 yr, genetic selection for rapid growth and improved feed efficiency has been very effective in meat-type poultry. Combined with changes in the feed that have increased both the nutritional and physical density to encourage a high nutrient intake, growth rate has more than doubled. The effect of genetic selection for high muscle to bone ratio and high calorie intake of a ration that supplies all nutritional requirements causes significant mortality from cardiovascular disease. In the chicken, sudden death syndrome (flip-over) and pulmonary hypertension syndrome resulting in ascites are the most important. Ruptured aorta, spontaneous turkey cardiomyopathy (round heart), and cardiomyopathy causing sudden death produce high mortality in turkeys. Rapid growth induced by high nutrient intake alone can cause severe lameness, bone defects, and deformity, as these problems are seen in animals that have not been selected for rapid growth: dogs, horses, pigs, ratites and wild birds kept in zoologic gardens. In meat-type poultry, growth-related disease can be reduced or eliminated by reducing feed intake without affecting final body weight. Rapid growth alone may not be the pathogenic mechanism that results in cardiovascular or musculoskeletal defects. Metabolic imbalance induced by high nutrient intake may cause some of the conditions. These metabolic problems might be corrected without reducing growth rate.

Animal Welfare↗
PubMed1996

Effect of dietary flax oil and hypobaric hypoxia on right ventricular hypertrophy and ascites in broiler chickens.

1. The effect of dietary flax oil on growth rate, blood haemoglobin content, mortality and incidence of pulmonary hypertension and ascites in broilers at ambient pressure and at reduced atmospheric pressure was examined. 2. Birds were housed either in hypobaric chambers simulating 1000, 1500 or 2200 m altitude or in pens at ambient atmospheric pressure and fed on diets containing 100 g/kg added fat as either an animal/vegetable (A/V) blend or flax oil. 3. Birds raised under hypobaric conditions had a decreased growth rate and increased mortality, blood haemoglobin content, and incidence of pulmonary hypertension and ascites compared to the groups at normal atmospheric pressure. 4. Broilers fed on the diet containing flax oil showed no difference in growth rate or blood haemoglobin content compared to birds fed on the A/V fat diet raised at the same altitude. 5. Inclusion of flax oil in the diet decreased mortality and the incidence of ascites at 2200 m and pulmonary hypertension at 1500 m. 6. Flax oil may be an effective method of reducing ascites and pulmonary hypertension in broilers without affecting performance.

Altitude↗
PubMed1994

Individual and combined effects of T-2 toxin and DAS in laying hens.

1. The individual and combined effects of T-2 toxin and 4,15-diacetoxyscirpenol (DAS) on laying hens were investigated in an experiment consisting of a 2 x 2 completely randomised factorial design with dietary concentrations of 0 and 2 mg/kg T-2 toxin and 0 and 2 mg/kg DAS. 2. Individually, T-2 toxin and DAS induced oral lesions in half of the hens and decreased significantly egg production and food intake. 3. The effects of T-2 toxin and DAS were additive for reduced food consumption and incidence of oral lesions. However, a synergism for reduced egg production was observed during the last experimental period. 4. No effects on body weight were observed during this study. Mild changes in selected plasma enzymes activities and no change in liver malondialdehyde content were detected. 5. The combination of T-2 toxin and DAS was more toxic than the single mycotoxins, for some parameters, and therefore, may pose a greater economic threat to the poultry industry than either of the toxins individually.

Animals↗
PubMed1994

Effect of selected dietary antioxidants on fatty liver-haemorrhagic syndrome in laying hens.

1. Single comb White Leghorn hens of an inbred line highly susceptible to fatty liver haemorrhagic syndrome (FLHS) were fed supplemented dietary ascorbic acid (200 mg/kg), alpha-tocopherol (75 mg/kg), or L-cysteine (3 g/kg, and 6 g/kg) for 28 d in order to evaluate the potential therapeutic effect of these compounds against the disease. 2. Supplementation of ascorbic acid, alpha-tocopherol, or a low level of L-cysteine (3 g/kg) did not significantly affect any of the hepatic variables evaluated. Hepatic glutathione was not increased by the supplementation of dietary L-cysteine. 3. L-cysteine supplemented at a level of 6 g/kg decreased hepatic dry matter and fat contents without affecting the hepatic malondialdehyde or the liver haemorrhagic score. 4. Because one of the predisposing factors of FLHS is a high hepatic fat content it was concluded that dietary supplementation of L-cysteine (6 g/kg) may be useful in the prevention of the disease.

Animals↗
PubMed1993

Clinical pathologic profiles of dogs and turkeys with congestive heart failure, either noninduced or induced by rapid ventricular pacing, and turkeys with furazolidone toxicosis.

Characteristic alterations in the serum and urine biochemical profiles of Doberman Pinschers with congestive heart failure (CHF) resulting from idiopathic dilated cardiomyopathy were determined. We compared these alterations with those observed in 2 other models of CHF: rate overload induced by rapid ventricular pacing in dogs, and biventricular hypertrophy and dilatation induced in turkey poults by furazolidone toxicosis. Serum and urine biochemical changes in both models of CHF in dogs were mild to moderate in degree, and were moderately consistent. They could be attributed to secondary neurohumoral, hepatic, and renal effects of heart failure. The most marked and consistent changes observed were mildly decreased anion gap that developed, in part, because of decreased serum sodium concentration, moderately increased catecholamine concentrations, moderate lactaciduria, hyposthenuria, and mildly increased urea concentrations and liver enzyme activities. In birds with furazolidone cardiomyopathy, we observed mild increases in serum urate concentration, liver and muscle enzyme activities, but moderately increased sodium concentration with decreased chloride concentration. In the pacing and furazolidone models, in which CHF was rapidly induced, moderate to marked hypoproteinemia was attributable to decreases in albumin and globulin concentrations. Using the avian model we found that the hypoproteinemia could be largely attributed to blood volume expansion, and to a lesser extent, inanition. Development of hypoalbuminemia during rapid ventricular pacing and furazolidone treatment may contribute to the effects of rate overload or drug toxicity in the pathogenesis of CHF, because hypoalbuminemia may contribute to altered hemodynamics and neuroendocrine system activation. Our data indicate that clinical biochemical analysis of serum and urine may be useful for assessing progression of CHF.

Animals↗
PubMed1993

Blood volume increase in salt-induced pulmonary hypertension, heart failure and ascites in broiler and White Leghorn chickens.

In this study we tested the hypothesis that excess dietary salt produces an expansion of extracellular fluid volume which may be associated with pulmonary hypertension-induced right ventricular failure in chickens with rapid growth rates. One-week-old broiler and White Leghorn chickens were given 0.5% salt in their drinking water for three weeks. Saline water had a minimal effect on White Leghorns. The hypothesis appears to be correct since salt-treatment in broilers resulted in up to 30% expansion in blood volume and there was 50% mortality from pulmonary hypertension-induced right ventricular failure and ascites. There was marked (up to 88% in some broilers) right ventricular hypertrophy, an indicator of pulmonary hypertension. There was less left ventricular hypertrophy as shown by an increase in the ratio of the right to total ventricle weight. There was up to 32% decrease in growth rate. There was renal hypertrophy in the salt-treated birds as shown by a higher kidney to body weight ratio.

Animals↗
PubMed1992

Rapid, simple and sensitive microassay for skeletal and cardiac muscle myoglobin and hemoglobin: use in various animals indicates functional role of myohemoproteins.

A novel, simple, rapid, sensitive and reproducible microassay is described for determination of myoglobin and hemoglobin content of myocardial and skeletal muscle biopsy specimens from various mammals, birds and fish. As little as 50 mg of tissue is needed and myoglobin concentrations lower than 1 mg% can be detected. Myoglobin and hemoglobin are separated at alkaline pH by ammonium sulfate extraction followed by ultrafiltration. Heme content is determined by absorption of the Soret band when the hemoprotein extract is visibly colored or more sensitively by its peroxidase activity when the extract has low color. The heme reacts with tertiary-butyl hydroperoxide and orthotolidine to generate a blue color. Hemoglobin content is correlated with myoglobin content and is related to aerobic capacity and blood flow to the tissue. Myoglobin content varied over 5 orders of magnitude up to 7 per cent of the weight of tissue, whereas hemoglobin content varied over 2 orders of magnitude up to 6 per cent of tissue weight. Myoglobin content is increased in species with high basal metabolic rate, high physical activity, prolonged diving capacity, fatigue resistance, and red muscle, whereas it is decreased in white muscle, iron-deficient animals, animals with sedentary lifestyles, and in animals and tissues with small fiber diameters such as avian or fish hearts.

Animals↗
PubMed1992

Myocardial myoglobin deficiency in various animal models of congestive heart failure.

Myoglobin is known to protect the mechanical function of the heart from hypoxia by acting as a sarcoplasmic oxygen reservoir and shuttle. We postulated a role for myoglobin in the pathogenesis of congestive heart failure. Several models of congestive heart failure were employed to test the hypothesis, including spontaneous inherited dilated cardiomyopathy in Doberman Pinschers, and heart failure produced by rapid ventricular pacing in dogs, volume overload in chickens and furazolidone toxicity in turkeys. Myocardial myoglobin was decreased by approximately 50% for all models (P less than 0.05). In Doberman Pinschers dogs which are predisposed to the development of dilated cardiomyopathy and have mild subclinical depression of cardiac performance, myocardial myoglobin (1.05 +/- 0.22 mg/g) is approximately 50% decreased compared to healthy mongrel dogs (2.15 +/- 0.52 mg/g), approximately twice as much as dobermans with heart failure (0.47 +/- 0.25 mg/g) but similar to the concentration found in dogs paced to heart failure (1.09 +/- 0.34 mg/g). Myocardium from poultry had remarkably decreased myoglobin compared to mammals (34 +/- 4 micrograms/g) with heart failure produced either by furazolidone or salt toxicity causing a further 50% reduction. In the canine models of heart failure, myocardial myoglobin concentration was demonstrated to be correlated with biochemical and physiological indicators of myocardial performance, namely, mitochondrial and sarcoplasmic reticular ATPase activities, and cardiac output, systemic vascular resistance, pulmonary capillary wedge pressure and mean arterial pressure, respectively. Our data implicates a role for myoglobin deficiency in the pathogenesis of congestive heart failure and in the predisposition of doberman pinschers to dilated cardiomyopathy.

Animals↗
PubMed1992

The effect of dietary sodium on right ventricular failure-induced ascites, gain and fat deposition in meat-type chickens.

Experiments were carried out using various levels of sodium (Na+) from NaCl or NaHCO3 to determine: 1) the level of Na+ required to induce ascites alone or in combination with cold temperature and 2) the effect of Na+ on weight gain and fat deposition in broiler chickens. In experiment 1, there were no cases of ascites using levels of Na+, from NaCl at 0.14% to 0.44% in the feed from day 3 or using added Na+, from NaCl at 0.0% to 0.12% in the water from day 3 with a level of 0.14% in the feed. There was no significant difference in 21 or 42 day body weight, feed conversion, or right ventricle:total ventricle (RV:TV) ratio between treatment groups. Day 3 to 4 body weight gains were significantly increased in all treatment groups with added Na+ (p less than 0.01). In experiment 2, with levels of added Na+, from NaCl, at 0.0% to 0.12% in the water with a level of 0.20% in the feed there were two cases of ascites, one at day 7 and one at day 40 at the 0.12% level. There were no significant differences in body weight at days 21 or 42 or in the RV:TV ratios between groups. Feed conversions were improved (p less than 0.01) with the lowest and highest levels of Na+ and a significant increase in day 3 to 4 body weight gain, with increasing Na+ in all treatment groups, was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1992

Changes in erythrocyte deformability in NaCl-induced right-sided cardiac failure in broiler chickens.

In this study, we tested the hypothesis that erythrocyte deformability is decreased in the development of cardiac failure induced by NaCl toxicosis. Deformability of erythrocytes and routine hematologic and biochemical variables were measured in 6 of 50 chickens that were given 5 g of NaCl/L in their drinking water from day 7 to day 42, and were compared with values in 6 of 50 healthy chickens given free access to tap water. Deformability was assessed by passing a 10% suspension of erythrocytes through a polycarbonate membrane with 5-microns pores. Chickens were euthanatized and heart and body weights were determined. Treatment with NaCl induced right-sided cardiac failure up to day 28. The ratios of heart weight to body weight were greater, for right ventricle by 20 to 64% and for left ventricle by 15 to 27%, attributable to NaCl treatment. Deformability of erythrocytes of NaCl-treated chickens was markedly decreased, in association with increased erythrocyte size and plasma Na+ concentration. However, only part of the decreased deformability could be explained by swelling of erythrocytes. Decreased deformability could not be explained by increased cell viscosity because mean corpuscular hemoglobin concentration, the primary determinant of erythrocyte viscosity, was decreased. Because decreased deformability of erythrocytes has been demonstrated previously to be associated with increased vascular resistance, decreased deformability may have contributed to the development of right-sided cardiac failure in these chickens.

Animals↗
PubMed1991

Myocardial calcium cycling defect in furazolidone cardiomyopathy.

We have previously demonstrated that in furazolidone-induced congestive heart failure in turkeys the specific Ca(2+)-ATPase activity of myocardial sarcoplasmic reticulum (SR) is 60% increased in compensation for a 50% depression in net Ca(2+)-sequestration activity. This study tested the hypothesis that SR Ca(2+)-uptake and Ca(2+)-ATPase activities were uncoupled in this cardiomyopathy because of increased Ca(2+)-release channel activity. A novel microassay was used to monitor Ca2+ transport by myocardial homogenates using the fluorescent Ca2+ dye indo 1 to indicate extravesicular ionized Ca2+. The method is applied to cyropreserved biopsy specimens of myocardium and requires only 50 mg tissue. Both SR Ca(2+)-pump and SR Ca(2+)-channel activity were estimated using the channel-inhibitor ruthenium red (RR) and the mitochondrial inhibitor sodium azide. The specificity of the RR inhibition was confirmed using ryanodine. Cardiomyopathy was induced in 2-week-old turkey poults by the addition of 0.07% furazolidone to their feed for 4 weeks. Compared with controls, myocardial maximal Ca(2+)-channel activity relative to maximal Ca(2+)-pump activity was 22% greater and duration of Ca(2+)-channel activity was 100% increased. However, the heart failure birds had 43 and 53% decreases in absolute maximal Ca(2+)-pumping and Ca(2+)-channel activities, respectively. The abnormal Ca(2+)-channel activity resulted in 200% greater time before initiation of net Ca2+ sequestration and 700% greater final myocardial Ca2+ concentrations. For all birds, the Ca(2+)-accumulating activity was highly correlated with Ca(2+)-release activity (all p less than 0.05). These data indicate that in this animal model of congestive heart failure there is defective SR Ca(2+)-channel function resulting in abnormal Ca2+ homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of mild cardiac hypertrophy, induced by volume overload in turkeys, on myocardial sarcoplasmic reticulum calcium-pump and calcium-channel activities and on the creatine kinase system.

Recent studies indicate that in animals with marked cardiac hypertrophy, there is depressed function of Ca2+ sequestration by myocardial sarcoplasmic reticulum (SR) because of down regulation of the Ca(2+)-ATPase gene. However, in several animal models we have observed enhancement of myocardial Ca2+ sequestration in response to chronic cardiac stimulation. We tested the hypothesis that in animals with mild cardiac hypertrophy, there is enhanced Ca(2+)-cycling activity by the SR Ca2+ pump and Ca(2+)-release channel. Because creatine kinase activity is consistently decreased in cardiomyopathy, we also determined whether enhanced Ca2+ cycling was accompanied by down regulation or inhibition of the creatine kinase system. Mild cardiac hypertrophy was induced by volume overload; 2% salt was added to the diet of 2-week-old turkey poults for 4 weeks. Compared with age-matched controls, volume overload resulted in 14.3% increase in heart weight and 21.5% increase in heart-to-body weight ratios. The hypertrophied heart had approximately 20% increased activities of the SR Ca2+ pump and the SR Ca2+ channel. Net Ca2+ transport was increased by 16.5%. Compared with controls and in contrast to several other myocardial enzymes, creatine kinase activity was diminished in the hypertrophied hearts by 23% and creatine content was decreased by 8%. Differences between groups were not detected for lactate dehydrogenase, aspartate transaminase, and alanine transaminase. We concluded that an early adaptation of the myocardium undergoing hypertrophy in compensatory response to functional overload is an enhancement of Ca2+ cycling activity by the Ca2+ pump and Ca2+ channel of the SR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗