Biomedical subjects

R F Wideman

Publications and source records attributed to R F Wideman.

At least 19 recordsLinked to original sources

PubMed2001

Minimal number of chicken daily growth velocities for artificial neural network detection of pulmonary hypertension syndrome (PHS).

Previously, evaluation of the first 2 wk of daily growth velocity with an artificial neural network (ANN) provided an effective noninvasive approach for predicting the susceptibility of broilers to pulmonary hypertension syndrome (PHS). This study was conducted to define the minimum number of days of growth data and the type of ANN required for the best prediction of PHS susceptibility. Four experiments were conducted in which broilers were weighed daily at 0800 h. In Experiment 1, Hubbard male broilers were reared to 50 d of age, with 13 developing PHS and 33 remaining normal (N), for a PHS:N ratio of 13:33. In Experiment 2, ANAK broilers were exposed to cool temperatures (16 to 17 C) from 17 to 42 d of age, resulting in a PHS:N ratio of 16:46 for males. In Experiments 3 and 4, Hubbard male and female chicks from a base population and a PHS-resistant line were exposed to cool temperatures from 17 to 42 d (Experiment 3) or 49 d of age (Experiment 4). The PHS:N ratios were 40:68 for males and 6:96 for females in Experiment 3 and 26:91 for males and 10:58 for females in Experiment 4. Four ANN, back propagation (BP3), Ward back propagation (WardBP), probabilistic (PNN), and general regression (GRNN), were evaluated for their ability to predict PHS in the shortest number of days based on daily growth velocities (BWd+1-BWd). A 100% prediction of PHS and N birds was considered the criterion of success. Starting with 14 d of data, each ANN was trained on daily growth velocity, and the number of predictive days was reduced with each run of the ANN. The best ANN was a GRNN, which correctly diagnosed PHS and N male broilers on 4 and 6 d of growth velocity data for Experiments 1 and 2, respectively. The results were poorer with the BP3, WardBP, and PNN. The diagnostic ability of the neural network was not consistent over all four experiments. In Experiment 2, a minimum of 6 d was required for 100% PHS detection for males. In Experiment 3, the best diagnostic value for males was 93% PHS detection and 100% N detection at 15 d. For females, the 100% PHS detection occurred at a minimum of 8 d. In Experiment 4, males had 100% PHS and N detection at a minimum of 11 d. Females had a 100% PHS and N detection at a minimum of 10 d. An attempt to build a single neural network that would detect PHS susceptibility in Hubbard (Experiment 1) and ANAK (Experiment 2) broilers was unsuccessful. The application (validation) of neural networks between experiments also was not successful (data not presented). However, these studies demonstrate that within a breed or line reared under similar selection pressures for ascites, a GRNN based on the first 14 d of growth velocity can detect, with at least 93% accuracy, broilers susceptible to PHS.

Age Factors↗

PubMed2001

Plasma levels of arginine, ornithine, and urea and growth performance of broilers fed supplemental L-arginine during cool temperature exposure.

Two experiments (Experiment 1 and 2) were conducted to evaluate growth performance, ascites mortality, and concentrations of plasma Arg, urea, and ornithine in male broilers raised in floor pens (2 x 4 factorial experiment, six pens for treatment) and exposed to cool temperatures averaging 16 C after 21 d of age. Broilers were fed low- or high-CP diets in both Experiments. In Experiment 1, Arg treatments consisted of control (no supplemental Arg); 0.15 or 0.3% supplemental Arg in the diet (low- and medium-Arg feed, respectively); and 0.3% supplemental Arg in the drinking water (Arg-water). Arginine levels were increased in Experiment 2 and consisted of the following: control (no supplemental Arg); 0.3 or 0.85% supplemental Arg in the diet (medium- and high-Arg feed, respectively); and 0.6% supplemental Arg in the drinking water (Arg-water). The water treatment followed a 3-d cyclic regimen, with supplemental Arg being provided for 24 h, followed by tap water for 48 h. When the broilers reached 37 d of age and all groups had consumed tap water for the previous 48 h, blood samples were collected from one bird per pen (Time 0, 0700 h); then supplemental Arg was provided in the Arg-water group, and additional blood samples were collected from the control and Arg-water groups at 3, 6, 12, and 36 h after Time 0. Plasma amino acids were analyzed using HPLC. Birds fed the high-CP diet were heavier at 49 d than birds fed the low-CP diet in Experiment 1, but not in Experiment 2. No differences were found in feed conversion or ascites mortality due to CP or Arg treatments in either experiment. In both experiments, plasma Arg was similar for all groups at Time 0, but increased in the Arg-water group at 3, 6, and 12 h after Arg was provided in the water. Within 12 h after returning to tap water, plasma Arg levels of the Arg-water group did not differ from the control group. Plasma urea and ornithine were parallel to plasma Arg concentrations, and the high-CP diets resulted in higher plasma levels of urea and ornithine compared with low-CP diets. These results indicate that kidney arginase was readily activated by Arg provided in the water, resulting in an immediate increase in plasma urea and ornithine. Plasma Arg was increased significantly, but no effects were observed in ascites mortality.

Animals↗

PubMed2001

Pulmonary wedge pressures confirm pulmonary hypertension in broilers is initiated by an excessive pulmonary arterial (precapillary) resistance.

High retrograde pressure through the pulmonary venous system caused by failure of the left ventricle or left atrio-ventricular valve may result in the elevated pulmonary arterial pressure and right ventricular hypertrophy associated with pulmonary hypertension syndrome (PHS; ascites) in broiler chickens. In the present study, unanaesthetized male broilers from an ascites-resistant line, the base population from which the resistant line was derived, and a separate unselected line were used to determine whether changes in wedge pressure (thought to be similar to left atrial pressure) are predictive of differences in the pulmonary arterial pressure of clinically healthy and pre-ascitic broilers. Venous, right atrial, right ventricular, pulmonary arterial, and wedge pressures were obtained by inserting a catheter into a wing vein and progressively advancing the catheter into a pulmonary branch artery until the catheter tip became wedged in and occluded the flow through a terminal artery. Mean right ventricular and pulmonary arterial pressures were lower in the resistant line than in the base population, but wedge pressures did not differ between the resistant, base, and unselected lines. Right:total ventricular weight ratios (RV:TV) and the percentage saturation of hemoglobin with oxygen in arterial blood ranged in value from 0.18 to 0.44 and 65 to 96%, respectively. Wedge pressure, however, remained similar when pre-ascitic broilers with high RV:TV values and low oximetry values were compared with clinically healthy broilers. In all birds, whether healthy or showing pre-ascitic characteristics, the wedge pressure was slightly higher than the right atrial pressure but substantially lower than pulmonary arterial pressure. These observations provide definitive proof that pulmonary hypertension is initiated as a consequence of excessive pulmonary arterial or arteriole resistance. Pulmonary venous pressure is estimated by measuring the pulmonary arterial wedge pressure, and high wedge pressures would be evident if pulmonary hypertension was caused by the elevated downstream resistances associated with left-sided heart failure.

Animals↗

PubMed2001

Lung mitochondrial dysfunction in pulmonary hypertension syndrome. I. Site-specific defects in the electron transport chain.

The main objectives of this study were to determine a) site-specific defects in the electron transport chain of lung mitochondria of broilers with pulmonary hypertension syndrome (PHS), b) if these defects are attenuated by high dietary vitamin E, and c) if these defects have a genetic basis. In Experiment 1, lung mitochondria were isolated from broilers with and without PHS fed diets containing 15 IU and 100 IU dl-alpha-tocopherol acetate/kg (VE); the four treatments were control, VE, PHS, and VE-PHS, respectively. Hydrogen peroxide (H2O2) generation in isolated lung mitochondria was monitored by dichlorofluorosein (DCF) fluorescence in response to chemicals that inhibit electron flow at specific sites on the electron transport chain using a 96-well microplate with Cytoflour (excitation/emission 480/530 nm). Basal H2O2 production was higher in PHS than in control mitochondria. Differences in H2O2 production between control and PHS were magnified by inhibition of Complexes I and III (Coenzyme Q) of the respiratory chain in mitochondria. Functional defects in PHS mitochondria were attenuated by high dietary VE. In Experiment 2, basal H2O2 production and that following inhibition of Complexes I and III were lower in lung mitochondria isolated from broilers selected for genetic resistance to PHS than in nonselected birds in the base population. The results of this study indicate that site-specific defects in Complexes I and III may underlie lung mitochondrial dysfunction in broilers with PHS, that these defects are attenuated by high dietary vitamin E, and that these defects may be related to genetic predisposition to PHS.

Animals↗

PubMed2001

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 (> or = 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.

Animals↗

PubMed2001

Lung mitochondrial dysfunction in pulmonary hypertension syndrome. II. Oxidative stress and inability to improve function with repeated additions of adenosine diphosphate.

The major objective of this study was to examine lung mitochondrial dysfunction and antioxidants in pulmonary hypertension syndrome (PHS) in broilers. Lung mitochondria were obtained from broilers fed diets containing 15 IU (control) and 100 IU dl-alpha-tocopherol acetate, i.e., vitamin E (VE)/kg with and without PHS; the four treatment groups were control, VE, PHS, and VE-PHS, respectively (Experiment 1), or from healthy broilers genetically selected or not selected for resistance to PHS (Experiment 2). Mitochondrial function was assessed with sequential additions of adenosine diphosphate (ADP) to mimic a repeated demand for energy. Compared to controls, PHS mitochondria in Experiment 1 exhibited mitochondrial dysfunction [lower respiratory control (RCR) and ADP:O ratios and an inability to improve function with repeated energy demand] and oxidative stress [lower alpha-tocopherol and reduced glutathione (GSH) and higher oxidized glutathione levels (GSSG)]. High dietary alpha-tocopherol had no effect on lung mitochondrial function in healthy broilers (VE vs. controls) but attenuated dysfunction in VE-PHS mitochondria. In Experiment 2, there were no differences in selected and nonselected mitochondrial function following a single addition of ADP, but nonselected mitochondria exhibited lower RCR and ADP:O values with repeated energy demand. Higher GSSG levels were also observed in nonselected lung. The results indicate that lung mitochondrial dysfunction present in broilers with PHS was associated with oxidative stress and may be attenuated by high dietary vitamin E. Furthermore, genetic resistance to PHS was associated with more efficient oxidative phosphorylation in lung mitochondria and an inherently lower degree of oxidative stress.

Adenosine Diphosphate↗

PubMed2001

Furosemide does not facilitate pulmonary vasodilation in broilers during chronic or acute unilateral pulmonary arterial occlusion.

Furosemide (FURO) is a diuretic and a putative pulmonary vasodilator that, when added to broiler diets, previously has been shown to reduce the cumulative pulmonary hypertension syndrome (PHS) mortality induced by cold temperatures. The objective of the present study was to evaluate the influence of dietary FURO on the pulmonary vasculature in broilers undergoing chronic or acute unilateral pulmonary arterial occlusion. Broilers were fed a standard ration throughout the entire experiment (Control group) or the same ration supplemented with 0.015% (wt/wt) FURO from Day 14 to 42 (FURO group). In the present study chicks were chosen at random at 16 to 18 d of age to undergo sham surgery or a chronic unilateral pulmonary artery clamp (PAC) procedure. Diet and surgical treatments resulted in Control-Sham, FURO-Sham, Control-PAC, and FURO-PAC groups. The Control-PAC and FURO-PAC groups did not differ in body weight or right:total ventricular weight ratios (RV:TV). The postsurgical mortality, ascites mortality, and mortality due to other causes did not differ between the Control-PAC and FURO-PAC groups. Plasma Na+ (P < or = 0.05) was lower in the FURO-Sham group than in the Control-Sham group. Broilers from the same hatch were fed Control or FURO diets and surgically prepared for acute unilateral pulmonary arterial occlusion by using a snare. Tightening of the snare triggered characteristic increases in pulmonary blood flow, pulmonary arterial pressure, and pulmonary vascular resistance. Across all of these variables, the Control and FURO groups did not differ during any sample interval. Dietary FURO did not affect body weight, hematocrit, or RV:TV. Dietary FURO at 0.015% (wt/wt) does not appear to influence the pulmonary vasculature in broilers, but it may prolong the survival of broilers during the pathophysiological progression of PHS.

Animals↗

PubMed2000

Measurements of pulmonary arterial pressure in anesthetized male broilers at two to seven weeks of age.

Pulmonary hypertension (an elevated pulmonary arterial pressure) is the defining symptom of the pathophysiological progression leading to pulmonary hypertension syndrome (ascites) in broilers. Previously, closed-thorax techniques had not been reported for measuring the pulmonary arterial pressure in young (<5 wk of age) broilers. The objective of this research was to evaluate continuous pulmonary arterial pressure in anesthetized male broilers at weekly intervals (2 to 7 wk of age) by inserting a cannula directly into the pulmonary artery. Body weights, heart rates, and the right:total ventricular weight ratio were also recorded. Clinically healthy individuals were selected from two separate hatches without prior assessment of electrocardiograms or the percentage of saturation of hemoglobin with oxygen. The pulmonary arterial pressure increased (P < or = 0.05) from 20 to 25 mm Hg between Weeks 2 and 3, remained at approximately 25 mm Hg during Weeks 4 and 5, and then returned to 19 mm Hg during Weeks 6 to 7. Body weight increased with age, the heart rate and body weight-normalized right and total ventricular weights remained constant through Week 5, and the right:total ventricular weight ratio remained constant through Week 7. This technique is useful for determining age-related changes in pulmonary arterial pressure that may contribute to a mismatch between pulmonary vascular capacity and cardiac output in apparently healthy broilers during the pathogenesis of pulmonary hypertension syndrome.

Aging↗

PubMed2000

Evaluation of broiler growth velocity and acceleration in relation to pulmonary hypertension syndrome.

An evaluation was made of the relationship between individual daily growth patterns and susceptibility of broiler chickens to pulmonary hypertension syndrome (PHS). In the first experiment, 46 male broilers were weighed for each of 50 d, during which time 13 developed PHS. Three temporal phases (0 to 15, 16 to 35, and 36 to 50 d) of broiler growth velocity and acceleration were examined. Correlation dimensions and Lyapunov exponents suggested evidence of chaos in growth velocity and acceleration, but the absence of detectable differences between broilers in the normal and PHS categories led us to reject the hypotheses that growth is more chaotic in normal broilers than in broilers susceptible to PHS. Growth velocity and acceleration values for mean and SD were statistically evaluated as response variables for each growth phase. Mean values for velocity during the third phase were different between broilers in the normal and PHS categories (velocity: 68.8 vs 48.9 g/d, P = 0.03, respectively) and (acceleration: 0.3 vs -1.4 g/d2, P = 0.07, respectively). The third phase SD (reflecting oscillation for velocity and acceleration) was greater for normal than for PHS birds (velocity: 26.1 vs 21.3 g/d, P = 0.13, respectively; acceleration: 39.7 vs 28.2 g/d2, P = 0.03, respectively). The hypothesis was accepted that normal birds have greater oscillations in growth velocity and acceleration than birds susceptible to PHS. A general regression neural network (GRNN) with genetic adaptive calibration was trained to predict PHS based on individual growth phases and their combinations. Data representing the first, first two, and all three phases of growth were determined to have potential for computerized diagnostic weighing. With the GRNN, birds in all three data sets were successfully classified (100%) with or without PHS. A third hypothesis, therefore, was accepted that artificial neural networks could be used to distinguish the difference between normal broilers and those susceptible to PHS. In the second experiment, only one bird was diagnosed with PHS. Velocity and acceleration neural networks from Phase 1 and Phases 1 and 2 in the first experiment were applied to the growth velocity and acceleration data of Experiment 2. The Phase 1 neural networks were the most promising in that they correctly identified 71.6 and 72.4% of the birds as normal for velocity and acceleration data, respectively. In general, data in the second experiment exceeded the neural network range of training for both velocity and acceleration, which reflected increased oscillation during the second phase of growth.

Animals↗

PubMed2000

Cardio-pulmonary function in broilers reared at warm or cool temperatures: effect of acute inhalation of 100% oxygen.

Fast growth and cool temperatures are the primary triggers for pulmonary hypertension syndrome (PHS, ascites) during commercial broiler growout. We evaluated cardio-pulmonary function in male broilers that initially were reared together at normal brooding temperatures and then were randomly assigned to chambers maintained at 28 C (warm group) or 16 C (cool group). Cardio-pulmonary evaluations were conducted between 35 and 42 d of age. The groups initially did not differ in body weight, right:total ventricular weight ratio, respiratory rate, heart rate, total peripheral resistance, or pulmonary vascular resistance, nor did their arterial blood gas values differ for the partial pressure of carbon dioxide, bicarbonate concentration, or hydrogen ion concentration. When compared with the warm group, the cool group had heavier total ventricular weights and higher values for pulmonary arterial pressure, cardiac output, stroke volume, mean systemic arterial pressure, and hematocrit and a marginally lower (P = 0.06) partial pressure of oxygen. Inhaling 100% O2 for 20 min caused equivalent increases in the arterial partial pressure of oxygen (> or =388 mm Hg) and the percentage saturation of hemoglobin with oxygen (99.9%) in both groups. The respiratory rate was reduced and total peripheral resistance in both groups was increased; the pulmonary arterial pressure, cardiac output, and heart rate in the cool group were also reduced. Cool temperatures contributed to the increase in pulmonary arterial pressure primarily by increasing the metabolic demand for oxygen, as reflected by incipient hypoxemia (reduced blood oxygen and elevated hematocrit), generalized ventricular hypertrophy, and an elevated cardiac output. It was the elevated cardiac output rather than hypoxemic pulmonary vasoconstriction that increased the pulmonary arterial pressure in the cool group when compared with the warm group.

Animals↗

PubMed2000

Ascites resistance of progeny from broiler breeders selected for two generations using chronic unilateral pulmonary artery occlusion.

Broilers that survived unilateral pulmonary artery occlusion and lived to maturity comprised the first generation (GEN1) of an ascites-resistant line. Progeny from the GEN1 line previously were shown to tolerate fast growth and cool temperatures with a 50% lower incidence of ascites than chicks from the breeder pullet line serving as the base population for the resistant line. In the present study, progeny from the GEN1 line were subjected to unilateral pulmonary artery occlusion, and survivors were reared to breeding age to serve as the parent stock for the second generation (GEN2) ascites-resistant line. In two experiments (EXP1 and 2), chicks were reared separately by sex but were mixed by line within environmental chambers, where they were grown as rapidly as possible and exposed to cool (14 C) temperatures from 17 to 49 d of age. In EXP1, the ascites incidences in the base population, GEN1, and GEN2 lines, respectively, were 31% (48/157), 15% (8/52), and 4% (3/69) for males and 10% (13/128), 11% (5/46), and 3% (1/36) for females. In EXP2, the ascites incidences in the base and GEN2 lines, respectively, were 44% (71/163) and 6% (7/110) for males and 12% (19/155) and 0% (0/92) for females. The final BW for nonascitic broilers did not differ across lines in EXP1. In EXP2, the final BW was lighter for nonascitic GEN2 males (2,915+/-43 g) and females (2,382+/-17 g) than for nonascitic base population males (3,088+/-42 g) and females (2,493+/-22), respectively. Right:total ventricular weight ratios were higher for ascitic than nonascitic broilers, confirming the primary role for pulmonary hypertension in the pathogenesis of ascites. These experiments demonstrate ongoing improvement in the ascites resistance of progeny from broiler breeders that, for two consecutive generations, have survived the rigorous selection pressure imposed by unilateral pulmonary artery occlusion.

Animal Husbandry↗

PubMed2000

Cardio-pulmonary function in preascitic (hypoxemic) or normal broilers inhaling ambient air or 100% oxygen.

We evaluated the influence of the percentage saturation of hemoglobin with oxygen (HbO2) on the pulmonary arterial pressure in normal and preascitic (hypoxemic) broilers breathing ambient air or 100% O2. In Experiment 1, unanesthetized preascitic broilers (right:total ventricular weight ratios [RV:TV] = 0.32+/-0.02) breathing ambient air had initial values of 67% for HbO2 and 32 mm Hg for pulmonary arterial pressure. The HbO2 increased to > or =96.6% during inhalation of 100% O2; however, pulmonary arterial pressure was not reduced. In Experiment 2, anesthetized normal (RV:TV = 0.23; HbO2 = 88%) and preascitic broilers (RV:TV = 0.28; HbO2 = 76%) were compared. The groups did not differ in body weight or respiratory rate, but preascitic broilers had lower values for mean arterial pressure, total peripheral resistance, and partial pressure of O2 in arterial blood and had higher values for pulmonary arterial pressure. Inhaling 100% O2 increased HbO2 to 99.9% in both groups; however, pulmonary arterial pressure remained higher in preascitic than in normal broilers, and the pulmonary vascular resistance was not reduced during 100% O2 inhalation. Cardiac output was higher in preascitic than in normal broilers before and after, but not during, 100% O2 inhalation. Mean arterial pressure and total peripheral resistance increased in the preascitic but not in the normal group during 100% O2 inhalation. Low coefficients of determination (R2) were obtained for linear regression comparisons of HbO2 vs. pulmonary arterial pressure in both experiments. Overall, acute reversal of the systemic hypoxemia in preascitic broilers had little direct impact on pulmonary hypertension, providing no evidence of hypoxemic or hypoxic pulmonary vasoconstriction. Instead, acute reversal of the systemic hypoxemia primarily increased the total peripheral resistance and normalized the mean arterial pressure and cardiac output. A sustained reduction in cardiac output theoretically should attenuate pulmonary hypertension, but this was not observed because of the overriding influence of sustained pulmonary vascular resistance.

Animals↗

PubMed1999

Electrocardiographic and genetic evaluation of giant jungle fowl, broilers, and their reciprocal crosses following unilateral bronchus occlusion.

Electrocardiography is useful as a noninvasive technique for detecting right ventricular hypertrophy in birds developing pulmonary hypertension (PH) and pulmonary hypertension syndrome (PHS, ascites). The objective of this study was to identify every aspect of the Lead II ECG wave form (amplitude or duration) that can be correlated with right ventricular hypertrophy [increased right:total ventricular weight ratios (RV:TV)] indicative of PH across a broad genetic background. Sham operations were conducted, or PH was induced by occluding one extrapulmonary primary bronchus in 14-d-old chicks produced from matings of broilers (B x B), Giant Jungle Fowl (J x J), and their reciprocal crosses (B x J and J x B). Standard three-lead electrocardiograms (ECG) were recorded on Days 28 and 42, and final necropsies were conducted to evaluate the incidence of ascites, confirm sex, and obtain ventricular weights for calculating RV:TV. Ascites did not develop in the J x J, and one each of the B x J and J x B chicks developed ascites; consequently, only data from birds that did not develop ascites were compared. Heart rate was recorded, and the following amplitudes and durations were measured or calculated for three consecutive wave cycles of the Lead II ECG: base of R to the peak of R (RbR), peak of R to base of S (RS), base of S to peak of R' (SR'), S, peak of R' to base of R' (R'R'b), and base of S to peak of T (ST). Differences between the ECG of sham and bronchus clamp groups were more prominent in B x B and B x J than in J x B, and bronchus occlusion did not affect the ECG, growth, or RV:TV ratios of J x J. In contrast, sex influences were more prominent in J x J and J x B than in B x J and B x B. These observations suggest a paternal pattern of inheritance for Lead II ECG wave forms, with crosses sired by broilers (B x B, B x J) exhibiting susceptibility to PH and few ECG differences related to sex, whereas crosses sired by Giant Jungle Fowl U x J, J x B) exhibited resistance to PH and numerous ECG differences related to sex.

Animals↗

PubMed1999

Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion.

We evaluated the hypothesis that venous congestion (increased venous volume), as reflected by venous hypertension (increased venous pressure), can arise when the right ventricle is unable to elevate the pulmonary arterial pressure sufficiently to propel the cardiac output through an anatomically inadequate or inappropriately constricted pulmonary vasculature. Changes in venous pressure were evaluated in clinically healthy broilers during modest increases in pulmonary vascular resistance induced by inhalation of 5% CO2 and during large increases in pulmonary vascular resistance accomplished by acutely tightening a snare around one pulmonary artery. Inhalation of 5% CO2 induced a pronounced respiratory acidosis, as reflected by increases the partial pressure of CO2 and the hydrogen ion concentration in arterial blood. Inhalation of 5% CO2 also increased pulmonary arterial pressure by approximately 3 mm Hg and increased venous pressure by approximately 1 mm Hg when compared with the pre-inhalation venous pressure. Tightening the pulmonary artery snare increased the pulmonary arterial pressure by approximately 10 mm Hg, and this degree of pulmonary hypertension was sustained until the snare was released. When compared with the pre- and post-snare intervals, tightening of the pulmonary artery snare induced a sustained increase in venous pressure of > or = 1 mm Hg. Veins have highly compliant walls that permit an approximate doubling in volume with only small (4 to 6 mm Hg) increases in central venous pressure. Presumably the apparently modest 1 mm Hg increase in venous pressure measured after CO2 inhalation or unilateral pulmonary artery occlusion reflects a large increase in venous volume and, thus, substantial venous congestion. These observations support the hypothesis that increases in pulmonary vascular resistance can initiate increases in venous pressure by challenging the capacity of the right ventricle to propel all of the returning venous blood through the lungs. Central venous congestion predisposes broilers to the onset of cirrhosis and ascites by impeding the outflow of hepatic venous blood and increasing the hydrostatic pressure within hepatic sinusoids.

Acidosis, Respiratory↗

PubMed1999

Plasma taurine levels in broilers with pulmonary hypertension syndrome induced by unilateral pulmonary artery occlusion.

Low plasma levels of taurine are associated with losses of cardiac sarcomeric proteins, leading to heart failure in mammals. Recently, it was proposed that cardiac taurine depletion serves to defend the heart against injury caused by regional ischemia in mammals. The role of taurine has not been well documented in broilers, particularly in relation to pulmonary hypertension syndrome (PHS; ascites). Three independent experiments evaluated plasma taurine in male broilers by utilizing the following treatments: unoperated controls (CONTROL; n = 10 in each experiment); sham operated (SHAM; n = 11, 12, and 10); or, unilaterally pulmonary artery clamped (PAC; n = 18, 29, and 24) that did (PAC-ascites) or did not (PAC-normal) develop ascites within 12 d postsurgery. Plasma samples were collected 9 and 11 d postsurgery in Experiments 1 and 2, respectively, and 2 d before and 4, 8, and 12 d after surgery in Experiment 3. Plasma taurine was analyzed by HPLC. Twelve days postsurgery, the birds were euthanatized, and ventricles were weighed for calculating the right:total ventricular weight ratio (RV:TV). The RV:TV of PAC birds (>0.35) consistently was higher (P < 0.01) than that of CONTROL and SHAM birds (<0.27 and 0.25, respectively). In Experiments 1 and 2, plasma taurine was higher (P < 0.05) in PAC-ascites (380 and 370 nmol/mL) than in SHAM broilers (183 and 186 nmol/mL), whereas CONTROL (262 and 278 nmol/mL) and PAC-normal (362 and 300 nmol/mL) broilers tended to have intermediate plasma taurine levels. In Experiment 3, PAC birds had higher (P < 0.05) plasma taurine at 8 and 12 d postsurgery when compared with presurgery levels, whereas plasma taurine was unchanged over time in CONTROL and SHAM birds. These results suggest cardiac taurine may be released into the plasma as a protective mechanism in response to the induction of pulmonary hypertension, hypoxemia, and right-side heart failure, similar to the mechanism reported for protecting cardiac muscle from ischemia in mammals.

Animals↗

PubMed1999

Renal responses of normal and preascitic broilers to systemic hypotension induced by unilateral pulmonary artery occlusion.

During the pathophysiological progression of pulmonary hypertension syndrome (PHS; ascites), broilers concurrently develop systemic hypotension (low mean systemic arterial pressure) that may initiate renal retention of water and solute, contributing to fluid accumulation in the abdominal cavity (ascites). In male Single Comb White Leghorns, glomerular filtration is autoregulated over a systemic arterial pressure range of 110 to 60 mm Hg, and corresponding reductions in urine flow are attributed to a phenomenon known as pressure natriuresis. Acute unilateral pulmonary artery occlusion was used in the present study to reduce systemic arterial pressure toward the lower autoregulatory limit for glomerular filtration, and to evaluate kidney function in normal and preascitic broilers. Preascitic broilers characteristically exhibited lower (P < or = 0.05) values for mean systemic arterial pressure (91 vs 100 mm Hg) and percentage saturation of hemoglobin with oxygen (73 vs 84%), higher hematocrits (35 vs 30%), heavier right ventricles (3.44 vs 2.32 g), and higher right:total ventricular weight ratios (0.32 vs 0.24) than normal broilers. Body weights (2,445 vs 2,429 g, respectively), left ventricle plus septum weights (7.16 vs 7.19 g), and heart rates (349 vs 341 beats/min) were similar. Preascitic broilers exhibited larger (P < or = 0.05) dependent reductions in glomerular filtration, urine flow, osmolal clearance, and solute excretion and had a higher free water clearance than normal broilers in response to pulmonary artery occlusion. The differences observed between normal and preascitic broilers demonstrate that systemic hypotension can trigger renal mechanisms contributing to fluid and solute retention during development of PHS.

Animals↗

PubMed1999

Electrocardiographic evaluation of broilers following unilateral occlusion of an extrapulmonary primary bronchus.

This study was conducted to provide a comprehensive evaluation of both the amplitudes and durations of the Lead II electrocardiogram (ECG) in nonascitic and ascitic broilers. At 14 d of age, male and female broiler chicks were sham-operated (SHAM, n = 27), or pulmonary hypertension was initiated by occluding one extrapulmonary primary bronchus (BRONCHUS CLAMP, n = 57). Lead II ECG and BW were recorded on Days 28 (ECG1) and 42 (ECG2), necropsies were conducted on all birds dying after Day 28, and final necropsies were conducted on Day 49. Data collected at necropsy included the presence (ASCITIC) or absence (NONASCITIC) of ascites, sex, and ventricular weights for calculating the right:total ventricular weight ratio (RV:TV), which serves as a reliable index of pulmonary hypertension. In each bird, three consecutive ECG1 and ECG2 wave cycles were quantified for both amplitude and duration of the following wave segments: Rb-R, R-S, S-R', R'-R'b, and S-T. The S wave amplitude was calculated by subtracting R-S from Rb-R and heart rate (HR) was measured from the peak of one T wave to the peak of the next. In the majority of comparisons, ASCITIC and BRONCHUS CLAMP broilers had larger S, R'-R'b, and S-T amplitudes, longer R-S, R'-R'b, and S-T durations, and a slower HR than NONASCITIC and SHAM broilers, regardless of sex. The differences in ECG wave forms and durations between ASCITIC and NONASCITIC broilers were greater on Day 42 (ECG2) than on Day 28 (ECG1), but when both ECG were used to develop a regression equation to estimate RV:TV, the R2 was 0.79. The most important Lead II ECG parameters associated with the development of ascites were an increasingly negative S wave amplitude and greater amplitudes and durations for R'-R'b and S-T as well as a decrease in the HR.

Airway Obstruction↗

PubMed1999

Cardiac output in four-, five-, and six-week-old broilers, and hemodynamic responses to intravenous injections of epinephrine.

Female broilers were evaluated at 4, 5, and 6 wk of age (1.2, 1.8, and 2.3 kg BW, respectively) to assess changes in cardiac output and related hemodynamics associated with BW gain, and to evaluate cardiopulmonary hemodynamic adjustments occurring secondary to i.v. injections of epinephrine (0.1 mg/ kg BW). Cardiac output increased with BW (253, 348, and 434 mL/min at 4, 5, and 6 wk, respectively) due to increases in stroke volume (0.70, 1.03, and 1.33 mL/beat) that more than compensated for reductions in heart rate (362, 337, and 328 bpm). Normalization for BW eliminated the differences in cardiac output and stroke volume. Increases in cardiac output were not associated with age- or BW-related increases in mean systemic arterial pressure (101.5, 108.6, and 108.0 mm Hg) due to corresponding reductions in total peripheral resistance (0.41, 0.32, and 0.26 relative resistance units). Epinephrine initially triggered immediate (within 90 s) threefold increases in total peripheral resistance and pulmonary vascular resistance, which, in turn, increased the systemic arterial pressure and pulmonary arterial pressure in spite of concurrent reductions in cardiac output that were associated with diminished venous return and dependent reductions in stroke volume and heart rate. Within 150 s after epinephrine injection, the systemic and pulmonary vascular resistances returned to preinjection control levels. By 300 s postinjection, stroke volume and heart rate increased, causing cardiac output to rise above preinjection control levels, which, in turn, elicited variable pulmonary arterial pressure responses apparently reflecting individual variability in the capacity for flow-dependent pulmonary vasodilation. These studies demonstrate that chronic (age- and BW-related) and acute (epinephrine-induced) changes in cardiac output in broilers reflect complex interactions among hemodynamic variables that include stroke volume, heart rate, and systemic and pulmonary vascular resistances.

Age Factors↗