Hypertension In Broiler Chickens Research Articles

Garlic powder attenuates pulmonary hypertension in broiler chickens: an electrocardiographic-based study

One of the most severe health-threatening issues in broiler chickens is believed to be pulmonary hypertension, characterized by inadequate oxygen levels in blood, elevated workload of the cardiopulmonary network, right ventricle hypertrophy, and death. A total of 180 one-day-old male chickens were dividedinto four equal groups, with 3 replicates per group (45 birds per group, 15 birds per replicate). To induce pulmonary hypertension syndrome, triiodothyronine was added to their diet. A corn-soy based feed was formulated for all treatment groups, and birds were treated with different doses of dietary garlic powder (0.2%, 0.6%, and 1%) for 49 days.Right ventricle/total ventricles (RV/TV), RV/body weight, TV/body weight ratio,and electrocardiographic records were assessed. RV to TV ratio was significantly reduced in all treatment groups at 49 days of age (P <0.05). The S-wave amplitude was decreased significantly (0.2% and 1% garlic powder groups, lead II; and all treatment groups, lead aVF) at 49 days of age. R-wave amplitude showeda significant reduction at 49 days of age (0.6% and 1% garlic powder receivers, lead aVR; all treatment groups, lead II) (P<0.05). QT interval showed a significant increase at 14 days (0.2% garlic powder group, lead III) and at 49 days (0.6% garlic powder group, lead II) (P<0.05). RR interval at 49 days of age (0.6% and 1% treatment groups, lead II; and1% garlic powder receivers, leads III, aVR, and aVF) showed a significant increase compared with controls (P<0.05).According to our study, garlic powder canimprove the electrocardiographic patterns and reversethe detrimental effects offree radicals and oxidative stress in birds withpulmonary hypertension.

Hawthorn flavonoid extract can use as an effective herbal drug to prevent pulmonary hypertension in broiler chickens

Hawthorn flavonoid extract can use as an effective herbal drug to prevent pulmonary hypertension in broiler chickens

Metabonomics Profiling Reveals Biochemical Pathways Associated with Pulmonary Arterial Hypertension in Broiler Chickens.

Pulmonary arterial hypertension (PAH) is the major cause of death in fast growing meat-type chickens (broiler chickens). At present, the underlying mechanisms that give rise to PAH are not fully understood. To identify the metabonomics profiles characterizing the process, we conducted a comprehensive gas chromatography-mass spectrometry (GC-MS)-based metabolic profiling of lung tissues from PAH broilers and age-matched controls. PAH was induced by excess salt in drinking water. Medial hypertrophy of pulmonary arteries was present in PAH birds as compared with controls. The metabonomics profiles of lung tissues well distinguished PAH broilers from control subjects. Significant changes in the levels of 41 metabolites were detected in PAH vs normal birds. Aside from the metabolic alterations indicating a status of oxidative stress and inflammation, evidence of reduced cellular uptake of arginine due to increased lysine biosynthesis and of a shift of arginine metabolism to arginase pathway were observed. In addition, PAH birds showed increased biosynthesis of fatty acids, which may be associated with excessive proliferation of vascular cells during pulmonary vascular remodeling. Furthermore, we observed significant changes in pentose phosphate pathway and increased aminomalonic acid in PAH broilers. These results provide additional biochemical insights into the pathogenesis of the PAH. Our data may lead to the development of new strategies to control PAH in broilers.

Antioxidant supplementation of low-protein diets reduced susceptibility to pulmonary hypertension in broiler chickens raised at high altitude.

A reduced-protein diet (designated as RPD) was prepared and its effects on growth performance and the development of pulmonary hypertension syndrome (PHS) were evaluated in broiler chickens compared to a normal-protein diet (designated as NPD) or to the RPD supplemented with CoQ10 alone (30 mg/kg) or in combination with vitamin E (30 mg/kg CoQ10 + 100 mg/kg vitamin E). The RPD had 30 g/kg less crude protein compared to the NPD. A total of 208 1-day-old male broilers (Ross 308 strain) were used in a 42-day trial. Serum concentrations of uric acid (UA) and nitric oxide (NO) significantly (p < 0.05) declined when chickens fed on the RPD. However, supplementing RPD with the antioxidants significantly (p < 0.05) increased the serum NO concentration. Although serum malondialdehyde (MDA) concentration was significantly (p < 0.05) higher in the RPD than the NDP, supplementing RPD with CoQ10 and CoQ10 + VE decreased serum MDA concentration to similar levels found in the NPD. Significant overexpression in GPX1 gene observed in the heart and lungs of broilers fed on the RPD, which was effectively restored by supplementation of CoQ10 . The right to total ventricular weight ratio (RV:TV) was significantly (p < 0.05) increased in birds fed the RPD, which concurred with an increase in mortality from pulmonary hypertension syndrome (PHS). However, a significant decline in mortality from PHS was observed when birds on RPD received CoQ10 or CoQ10 + VE. In conclusion, antioxidant supplementation effectively improves pulmonary hypertensive response in broiler chicken fed of reduced-protein diets.

Nutritional approaches to ameliorate pulmonary hypertension in broiler chickens.

This article reviews recent nutritional approaches for counteracting the development of pulmonary hypertension syndrome (PHS; ascites) in broiler chickens especially when they are reared at high altitudes. High altitudes impose the sustained stress of hypobaric hypoxia, which reduces the availability of atmospheric oxygen to red blood cells passing through the lungs, thereby causing systemic arterial hypoxaemia (undersaturation of haemoglobin with oxygen), pulmonary arterial hypertension and PHS/ascites in susceptible broilers. Proper nutritional strategies are needed to reduce metabolic activity and prevent the development of ascites especially when modern broilers are reared in regions where the existing altitudes limit the availability of atmospheric oxygen. This article also addresses controversies with regard to broiler nutrition in relation to PHS. For example, the catabolism of protein from feed ingredients incurs increased oxygen consumption, suggesting that feeding reduced-protein diets to broiler chickens may result in reduced PHS incidences. However, experimental and field data indicate that feeding reduced-protein diets to broilers subjected to hypobaric hypoxia increases the development of PHS. Controversies on the nutrition of unsaturated fat in relation to PHS are also discussed. In conclusion, hypoxia, acidosis, vasoconstriction and enhanced metabolic rate are triggers of PHS. Feeding reduced-protein diets might promote the susceptibility of broilers to PHS by decreased dietary intake of arginine, decreased uric acid production and increased lipogenesis. Feeding high-protein diets, dietary arginine supplementation, partial substitution of sodium bicarbonate for sodium chloride, feeding low-fat diets and effective feed restriction programmes can be considered as nutritional approaches to prevent PHS.

L-carnitine supplementation decreases lipid peroxidation and improves cardiopulmonary function in broiler chickens reared at high altitude.

An experiment was carried out to examine the effects of L-carnitine supplementation on growth performance and cardiopulmonary function of broiler chickens reared at high altitude (2100 m above sea level). A total of 96 day-old male chicks (Cobb 500) were randomly assigned into two dietary treatments containing 0 (control group) and 200 mg/kg L-carnitine. The experimental diets were fed for a period of 42 days consisting of the starting (days 1 to 21) and growing periods (days 21 to 42). Nutrient requirements of chickens met the NRC (1994) recommendations. The results showed that dietary L-carnitine had no significant influence on body weight gain, feed intake and feed conversion ratio. L-carnitine reduced plasma concentration of malondialdehyde, packed cell volume (PCV) and abdominal fat deposition compared to the control (P < 0.05). A significant (P < 0.05) decrease was observed in the right to total ventricular weight ratio (RV:TV) in birds receiving L-carnitine when compared to the control. Supplementation of L-carnitine increased plasma nitric oxide and immune responsiveness, which manifested in an increased toe-web thickness index measured at 24 h following the injection of phytohaemagglutinin P. In conclusion, supplementation of L-carnitine had beneficial effects on preventing lipid peroxidation and pulmonary hypertension in broiler chickens raised at high altitude.

Kelussia odoratissima Mozzaf – A promising medicinal herb to prevent pulmonary hypertension in broiler chickens reared at high altitude

Ethnopharmacological relevanceKelussia odoratissima Mozzaf, formerly Apium odoratissima, is a plant locally called “Karafs”, found in central Zagros region of Iran. Leaves and stems of the plant are traditionally used in the treatment of hypertension and inflammation. Lowering blood pressure effects of Kelussia odoratissima Mozzaf (wild celery) was evaluated in preventing pulmonary hypertension syndrome (PHS) in broiler chickens reared at high altitude (2100m). Materials and methodsA total number of 208 day-old male broilers (Ross 308) were randomly assigned to four treatments including different levels of Kelussia odoratissima Mozzaf (0%, 0.25%, 0.5%, and 0.75%) in a 42-day trial. ResultsBody weight gain and feed:gain responses significantly (P<0.05) improved when Kelussia odoratissima Mozzaf was included in broiler diets at 0.75% in the growing stage and throughout the trial. Over-expression of inducible nitric oxide (NO) synthase in the heart was observed in chickens fed Kelussia odoratissima Mozzaf. Birds received Kelussia odoratissima Mozzaf at 0.5% and 0.75% had significantly (P<0.05) higher circulatory concentrations of NO though significantly (P<0.05) lower serum malondialdehyde concentration, hematocrit and heterophil to lymphocyte ratio when compared to the birds fed the control diet. Feeding Kelussia odoratissima Mozzaf at 0.5% and 0.75% prevented from right ventricular hypertrophy and led to a significant decline in mortality from PHS. ConclusionIt can be concluded that Kelussia odoratissima Mozzaf is a promising medicinal herb to prevent PHS in broiler chickens by improving blood pressure and antioxidant responses.

Influence of cold&amp;ndash;dry (harmattan) season on colonic temperature and the development of pulmonary hypertension in broiler chickens, and the modulating effect of ascorbic acid

Influence of cold&ndash;dry (harmattan) season on colonic temperature and the development of pulmonary hypertension in broiler chickens, and the modulating effect of ascorbic acid Ndazo S Minka,1 Joseph O Ayo2 1Department of Animal Health and Husbandry, College of Agriculture and Animal Science, Division of Agricultural Colleges, Ahmadu Bello University, Mando-Kaduna, Nigeria; 2Department of Physiology, Faculty of Veterinary Medicine, Ahmadu Bello University, Zaria, Nigeria Abstract: The influence of cold&ndash;dry (harmattan) season on colonic temperature (CT) and the development of pulmonary hypertension (PH), as well as the effect of ascorbic acid (AA), were investigated in Anak male broilers during the harmattan season (November&ndash;January) of 2010&ndash;2013. A total of 150 broiler chickens per season served as subjects. At the age of 4 weeks, the broilers were randomly divided into two groups consisting of three replicates of 25 birds each: group I, the control, was not administered AA; group II was AA-treated, administered with 200 mg/kg body weight of AA, every day at 7 am and 7 pm for a period of 3 weeks. The mortality rate and CT of the birds were recorded during the daytime and nighttime. Ten birds from each group were sacrificed at weeks 4, 5, 6, and 7 for the assessment of PH and ascites syndromes. The mean ambient temperature value of 24.3&deg;C&plusmn;0.1&deg;C recorded in the daytime was higher (P&lt;0.05) than the value of 17.2&deg;C&plusmn;0.1&deg;C recorded during the nighttime. The average level of dust was 8.2 mg/m3. The control birds were hypothermic during the nighttime and had high mortality rates compared with the AA-treated birds. Broilers with obvious signs of ascites demonstrated a uniquely continuous increase in CT. At weeks 6 and 7 of age, 80% of the control broilers that were sacrificed exhibited an increase (P&lt;0.05) in the weight of right ventricle to the weight of total ventricles, packed cell volume, and erythrocyte count with low hemoglobin content, which indicated PH syndrome. The remaining 20% of the control birds and those that died had ascites syndrome in addition to the PH syndrome. These syndromes were not observed in the AA-treated birds. In conclusion, the harmattan season induced PH in broilers with no obvious clinical signs; the harmattan may compromise the welfare, health, productivity, and meat quality of the birds, effects which were ameliorated by AA. Keywords: ascorbic acid, broilers, cold&ndash;dry (harmattan), colonic temperature, hypothermia, pulmonary hypertension/ascites

Caspase-1, -2, and -3 gene expression is enhanced in the heart and lung of chickens with pulmonary hypertension (ascites)

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/TV 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.

Diminished gene expression of cardiac heat shock proteins in pulmonary hypertensive chickens

1. The relative expression of heat shock protein (HSP) genes (HSP60, HSP70 and HSP90) was performed using quantitative real-time PCR on tissue from the heart ventricles to investigate the effect of 3,5,3′-l-triiodothyronine (T3)-induced pulmonary hypertension in broiler chickens.2. The ratio of the right ventricle to total ventricle (index of pulmonary hypertension) was increased in the treated groups at 12 and 42 d of age compared to controls but was significant only at 42 d.3. The HSP genes were expressed in the right and left ventricles of control but T3-treated broilers at 12 and 42 d of age. The relative amounts of HSP60 and HSP90 gene expression in the right ventricle of treated groups were significantly increased at 12 d and decreased at 42 d of age compared to controls.4. Variations of HSP60 and HSP90 mRNAs in the left ventricle were not significant. The relative amount of HSP70 mRNA expression in the right and left ventricles of treated groups was significantly decreased at 42 d of age compared to controls. HSP70 mRNA expression did not differ between the right and left ventricles at 12 d of age.5. It is concluded that gene expression of HSPs (i.e. HSP60 and HSP90) was upregulated in the heart of chickens developing pulmonary hypertension syndrome, probably to delay the pathological process of disease. The right ventricle from hearts of pulmonary hypertensive chickens showed considerable reductions of HSP60, HSP70 and HSP90, which is evidence of a loss of compensatory responsiveness in dilated heart.

Re-evaluation of Arginine Requirements for Broilers Exposed to Hypobaric Condition during the 3-to 6-week Period

In order to estimate arginine (Arg) requirements of male broilers (Ross 308) during the 21-to 42-day period and exposed to hypobaric condition, six diets (200 g/kg CP and 13.4 MJ ME/kg) with graded levels of Arg (8.8 to 14.3 g/kg) were allocated to four pens of twelve birds each. Body weight gain, feed:gain, breast meat yield, plasma nitric oxide (NO) concentration, and right to total ventricular weight ratio (RV/TV) were determined as response criteria. Responses to Arg supply were nonlinear and attained plateau values (ymax) within the studied range of Arg supply. The estimated Arg requirements for maximal body weight gain and optimal feed:gain during the 21 days under study were 12.4, and 12.2 g/kg of diet, respectively. The estimated Arg requirement for maximizing breast meat yield was 12.6 g/kg of diet. Based on the response in plasma NO and RV/TV, the estimated requirements were 13.0, and 13.2 g/kg of diet, respectively. Data obtained for the individual factors clearly indicate that the NRC recommendations for Arg are not sufficient for maximizing body weight gain, optimizing feed:gain and preventing the onset of pulmonary hypertension in broiler chickens exposed to hypobaric condition. Data may be used for future modeling of broilers’ Arg requirements.

Methylglyoxal and pulmonary hypertension in broiler chickens

Methylglyoxal (MG) is a dicarbonyl molecule that forms during glycolysis and normally is detoxified via the glyoxalase system. Methylglyoxal is highly reactive with various amino acid residues in proteins, leading to oxidative stress and irreversible protein damage. Increased levels of MG have been associated with endothelial damage and vascular remodeling contributing to the development of systemic arterial hypertension in mammals. This study was conducted to determine whether administering exogenous MG can trigger pulmonary hypertension (increased pulmonary arterial pressure) in broilers. Hematological assays and preliminary mass spectrometric analyses also were conducted using blood samples from broilers that had been injected intramuscularly with either saline or MG to determine whether MG triggers either a toxic response or oxidative posttranslational modification of hemoglobin within 24 h postinjection. Clinically healthy male broilers received 100-µL intravenous injections of saline and then MG, followed by a 500-µL intramuscular injection. Neither intravenous nor intramuscular injections of saline altered the pulmonary arterial pressure, whereas both intravenous and intramuscular MG injections triggered pulmonary hypertension attributable to increased pulmonary vascular resistance. The precise mode of action by which MG triggers pulmonary vasoconstriction remains to be determined. Pulse oximetry, hematology, and matrix-assisted laser desorption ionization-time-of-flight spectra data did not provide evidence of an overt toxic response to MG, nor was modification of hemoglobin detected, although increased heterophil:lymphocyte ratios did demonstrate that MG caused a stress response. To the best of our knowledge the present results constitute the first demonstration in any vertebrate species that exogenously administered MG rapidly initiates pulmonary hypertension attributable to pulmonary vasoconstriction.

Acetic acid modulates induction of pulmonary hypertension in broiler chickens: based on electrocardiographic parameters

To clarify the effect of acetic acid on the electrocardiographic parameters of pulmonary hypertensive broilers, chicks were reared at high altitude and treated with acetic acid (0.4 and 0.9 g/L) for 45 days. The right ventricle-to-total ventricle ratio was noted as an index of pulmonary hypertension that was significantly (P < 0.05) decreased in the treated groups. S amplitudes were significantly decreased only at 36 days (leads II and III) and 45 days (lead aVF) in many treated groups. There were significant (P < 0.05) reductions of T amplitudes at 28 days (leads aVR and aVL) and 36 days (lead aVL), and significant elevations of QRS (leads II, III, and aVF) and QT intervals (leads II, aVR, aVL, and aVF) at different ages of many treated groups. R amplitudes were significant (P < 0.05) at 28 days (leads aVL and aVF, at both doses of acetic acid), 36 days (leads aVR and aVL, at 0.4 g/L of acetic acid), and 45 days (lead aVR, at both doses of acetic acid). The RR interval also significantly increased at 28 days (leads aVR and aVL) and 45 days (lead aVL). It was concluded that acetic acid modulates induction of ventricular hypertrophy, dilation, and arrhythmia. These effects are detectable in many electrocardiographic parameters.

Intravenous micro-particle injections and pulmonary hypertension in broiler chickens: acute post-injection mortality and ascites susceptibility

Intravenously injected micro-particles become trapped within the pulmonary vasculature where they increase the resistance to blood flow and trigger pulmonary hypertension. We tested the hypothesis that i.v. micro-particle injections can be used to trigger acute (24 to 48 h) post-injection mortality in broilers having the most limited pulmonary vascular capacity, or ascites in broilers whose marginal cardiopulmonary capacity renders them susceptible to pulmonary hypertension syndrome (PHS). Progressive inflammation-associated responses were initiated within the lung parenchyma by 10 to 80 microm diameter dextran polymer (Sephadex) and 30 microm diameter cellulose micro-particles, leading to the scavenging of Sephadex micro-particles from the pulmonary vasculature by <5 d post-injection, whereas the cellulose micro-particles persisted for >7 d post-injection. The persistency and size of the cellulose apparently facilitated chronic occlusion of blood flow through precapillary arterioles, thereby triggering appreciable post-injection mortality and PHS at relatively low injection volumes (0.3 to 0.6 mL at 0.02 g/mL). In contrast, the small size of the polystyrene microspheres (15 microm), and the lack of persistency of the Sephadex micro-particles, apparently precluded the reliable occurrence of post-injection mortality or PHS until higher volumes (>0.8 mL at 0.02 g/mL) were injected. Values for the total susceptibility index (TSI: 24 to 48 h post-injection mortality + PHS mortality) following cellulose injections were higher for broilers reared at cool temperatures than at thermoneutral temperatures. The incidences of PHS induced by exposing broilers from different genetic lines to constant cool temperatures qualitatively paralleled the respective post-injection mortalities elicited by injecting the cellulose micro-particle suspension into the same lines. These observations indicate the micro-particle injection methodology potentially can replace unilateral pulmonary artery occlusion as the technique of choice for genetically selecting broilers that have a sufficiently robust pulmonary vascular capacity to resist the onset of pulmonary hypertension and PHS. The functional importance of the relative antigenicity of different micro-particle types, and the extent to which key immune-mediated responses, either beneficial or detrimental, might be co-selected by the micro-particle injection technology, remain to be clarified.

Intravenous micro-particle injection and pulmonary hypertension in broiler chickens: cardio-pulmonary hemodynamic responses

Experiments were conducted to determine whether intravenous injections of micro-particles, having a size suitable to be trapped by the pulmonary precapillary arterioles, could be used to increase the pulmonary vascular resistance and thereby trigger an acute increase in the pulmonary arterial pressure (pulmonary hypertension). Anesthetized male broilers injected intravenously with inorganic (silica gel, polystyrene) or organic (cellulose, Sephadex) micro-particles developed an immediate pulmonary hypertension in proportion to the cumulative quantities of micro-particles injected. Micro-particle occlusion of a portion of the pulmonary arterioles forced the cardiac output to flow at a higher rate through the remaining vascular channels, thereby exposing a diffusion limitation characterized by undersaturation of the systemic arterial blood with oxygen (hypoxemia). The concurrent onset of systemic hypotension (reduced systemic arterial blood pressure) was not due to a reduction in cardiac output but rather was attributed to hypoxemic vasodilation of the systemic vasculature (reduced total peripheral resistance). Preliminary histological evaluations revealed micro-particles lodged in inter- and intraparabronchial arterioles, surrounded by aggregates of thrombocytes and mononuclear leukocytes within 30 min post-injection. These observations infer that intravenously injected micro-particles are carried to the lungs by the returning venous blood, where trapping of the micro-particles by the pulmonary vasculature triggers acute responses (increased pulmonary vascular resistance, pulmonary hypertension, systemic hypoxemia, systemic hypotension) that mirror those previously observed following acute occlusion of one pulmonary artery. Additional studies will be required to determine the extent to which the focal immune response to trapped micro-particles promotes local vasoconstriction that amplifies the pulmonary hypertension attributable to direct physical obstruction of precapillary arterioles.

Intravenous Endotoxin Triggers Pulmonary Vasoconstriction and Pulmonary Hypertension in Broiler Chickens

Bacterial endotoxins stimulate endothelin-mediated, thromboxane-dependent increases in pulmonary vascular resistance in mammals, and thromboxane has been shown to cause an immediate but transient pulmonary vasoconstriction in broiler chickens. In the present study, i.v. injections of 1 mg endotoxin into anesthetized male broilers caused a pulmonary vasoconstrictive response that was delayed in onset by 15 min and that elevated the pulmonary arterial pressure by 10 mm Hg within 25 min postinjection. Thereafter, pulmonary hemodynamic variables gradually (≥15 min) returned toward pre-injection levels, and supplemental injections of 4 mg endotoxin during this recovery period failed to reinitiate pulmonary hypertension. In contrast, injecting the thromboxane A2 mimetic U44069 during the endotoxin recovery period triggered pulmonary vasoconstriction and pulmonary hypertension similar in magnitude to the responses triggered by U44069 before endotoxin had been administered. The time course and magnitude of the pulmonary hemodynamic responses to endotoxin were highly variable among individual broilers, whereas the individual responses to U44069 were more consistent. Unanesthetized broilers resembled anesthetized broilers in the time course, magnitude, and variability of their pulmonary hemodynamic responses to endotoxin. Overall, these observations are consistent with the hypothesis that endotoxin initiates a biochemical cascade, culminating in the delayed onset of pulmonary vasoconstriction and pulmonary hypertension within 20 min postinjection. Subsequently, the pulmonary vasculature remains responsive to large bolus injections of exogenous thromboxane mimetic; however depletion of endogenous vasoconstrictive components of the endotoxin-mediated cascade, a compensatory increase in endogenous vasodilators, or the induction of a transient cellular tolerance to endotoxin prevented fourfold higher doses of endotoxin from reversing the return toward a normal pulmonary vascular tone. Individual differences among broilers in their susceptibility to pulmonary hypertension syndrome (ascites) may be related to innate or acquired variability in their pulmonary vascular responsiveness to vasoactive mediators.

Effect of graded levels of dietary nickel and manganese on blood haemoglobin content and pulmonary hypertension in broiler chickens

Dietary supplementation with high levels of cobalt increases blood haemoglobin content and causes pulmonary hypertension (PH) in broiler chickens. Since cobalt, nickel and manganese can stimulate erythropoietin synthesis in vitro, a trial was conducted to investigate the effect of graded levels of dietary nickel and manganese on blood haemoglobin content and PH in broiler chickens. Results showed that dietary supplementation with high levels of Ni (494 parts/10(6)), and to a lesser extent Mn (372 parts/10(6)), significantly increases blood haemoglobin content and PH, as measured by the right ventricle weight to total ventricle weight ratio (RV/TV). Dietary Ni at 494 parts/10(6) significantly increases the incidence of ascites and right ventricular hypertrophy. Results show that dietary supplementation with high levels of Ni can be used as an experimental model to induce PH and ascites in broilers.

Effect of graded levels of dietary nitrite on pulmonary hypertension in broiler chickens and dilatory cardiomyopathy in turkey poults

In two separate trials, day-old broiler chicks and turkey poults were fed graded levels of dietary sodium nitrite in order to investigate the possible role of nitrite-induced methaemoglobinaemia on the incidence of chicken pulmonary hypertension and spontaneous turkey cardiomyopathy (STC). A transient low level of methaemoglobinaemia was observed after 7 days of exposure to dietary nitrite, but the levels returned to normal afterwards in spite of the presence of nitrite in the diet throughout the experiment. No effect on pulmonary hypertension, as measured by the right ventricle weight to total ventricle weight ratio, was observed in chickens exposed to dietary nitrite. The group of turkey poults receiving 1200 mg/kg nitrite in the diet had a higher incidence of STC than controls (20 v. 5%), although the difference was not statistically significant. The levels of nitrite-induced methaemoglobinaemia were probably too low to be considered as the aetiology of increased STC incidence.

Effect of chronic hypoxia on the pulmonary arterial blood pressure of the chicken

Effect of chronic hypoxia on the pulmonary arterial blood pressure of the chicken