Biomedical subjects

R F Wideman

Publications and source records attributed to R F Wideman.

At least 55 records · Page 3Linked to original sources

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↗

PubMed1999

Broiler breeder survivors of chronic unilateral pulmonary artery occlusion produce progeny resistant to pulmonary hypertension syndrome (ascites) induced by cool temperatures.

Chronic occlusion of one pulmonary artery triggers a high incidence of pulmonary hypertension syndrome (PHS, ascites) in broilers. In the present study, the left pulmonary artery was chronically occluded in 295 male and 255 female chicks pedigreed from 18 sire families, leading to PHS in 74% of the males and 45% of the females. Survivors were reared to breeding age and served as parents for the resulting PHS-resistant chicks (Resistant), whereas control chicks were produced from the base population for this line (Base). In two experiments, male and female Resistant and Base chicks were reared separately by sex but mixed by group within environmental chambers, where they were exposed to cool (14 C) temperatures. In both experiments, the incidence of PHS was at least 50% lower in the Resistant males and females than in the Base males and females, respectively. When compared within a sex, the Base and Resistant broilers surviving to the end of both experiments did not differ in final body weight or body weight gain, nor did their right:total ventricular weight (RV:TV) ratios differ. These results demonstrate that broiler breeders capable of thriving after having their entire cardiac output forced to flow through one lung, subsequently produced male and female progeny with substantially improved resistance to the onset of PHS induced by fast growth and exposure to cool environmental temperatures. Fast growth and cool temperatures are primary triggers for PHS under most conditions of commercial broiler growout. In both experiments, final necropsies revealed higher RV:TV ratios in ascitic than in nonascitic broilers, whereas normalizing the left ventricle plus septum weight for differences in body weight generated similar values for ascitic and nonascitic males or females, respectively. These results support a primary role for pulmonary hypertension but not cardiomyopathy in the pathogenesis of ascites triggered by cool temperatures in both the Base and Resistant populations.

Animal Husbandry↗

PubMed1999

Thromboxane mimics the pulmonary but not systemic vascular responses to bolus HCl injections in broiler chickens.

Bolus i.v. injections of 1.2 N HCl elicit a rapid but transient pulmonary vasoconstriction in broiler chickens. In mammals, the pulmonary vasoconstrictive response to bolus acid injection depends on increased synthesis of thromboxane A2; however, the vascular responsiveness of domestic fowl to thromboxane previously had not been evaluated. In the present study, we tested the hypothesis that, if HCl triggers pulmonary vasoconstriction by stimulating thromboxane A2 synthesis in broilers, then bolus i.v. injections of the potent thromboxane A2 mimetic U44069 (9,11-dideoxy-9alpha,11alpha-epoxy-methanoprostaglandin++ + F2alpha; 1 micromol/mL; 0.5 mL injected volume) should trigger hemodynamic responses similar to those elicited by HCl (1.2 N; 1.5 mL injected volume). Both HCl and the thromboxane mimetic elicited twofold or greater increases in pulmonary vascular resistance, which in turn increased pulmonary arterial pressure by 50% despite concurrent reductions in cardiac output. The reductions in cardiac output were associated with reductions in stroke volume but not heart rate. The thromboxane mimetic also increased the total peripheral resistance, which minimized the reduction in mean systemic arterial pressure associated with the decrease in cardiac output. In contrast, HCl injections did not increase total peripheral resistance; consequently, the reduction in cardiac output caused the mean systemic arterial pressure to decrease by 30 mm Hg. Mannitol (2.5%; 1.5 mL) was injected i.v. as a volume control, and had no influence on any of the variables. This study provides the first direct evidence that thromboxane is a potent pulmonary vasoconstrictor in broilers, and provides support for the hypothesis that thromboxane mediates the pulmonary vasoconstrictive response to bolus i.v. injections of HCl. The differential response of the systemic vasculature to the thromboxane mimetic and HCl may indicate that cardiopulmonary responses to HCl injections are not mediated solely via thromboxane production. Alternatively, a direct dilatory effect of elevated hydrogen ion concentrations on the systemic vasculature may have counteracted any tendency for simultaneously evolved endogenous thromboxane to elicit systemic vasoconstriction.

Animals↗

PubMed1998

Evaluation of minimally invasive indices for predicting ascites susceptibility in three successive hatches of broilers exposed to cool temperatures.

Broilers from three consecutive hatches were exposed to cool temperatures to amplify the incidence of pulmonary hypertension syndrome (PHS, ascites). The largest apparently healthy individuals on Day 42 were evaluated using minimally invasive diagnostic indices [percentage saturation of hemoglobin with oxygen, hematocrit (HCT), heart rate, electrocardiogram (ECG) Lead II, body weight), then they were subjected to the ongoing pressures of fast growth and cool temperatures to determine which of these indices are predictive of the subsequent onset of PHS. Approximately 20% of the males and females evaluated on Day 42 subsequently developed PHS by Day 51. When data for all hatches were pooled and broilers that subsequently developed ascites were compared with those that did not (nonascitic), body weights, heart rates, and percentage saturation of hemoglobin with oxygen were lower on Day 42 for ascitic than for nonascitic males, and HCT was higher in ascitic males and females than in nonascitic males and females, respectively. Comparisons of the ECG Lead II wave amplitudes for all hatches pooled indicated that RS-wave amplitude was larger in ascitic than in nonascitic males, and that S-wave amplitude was more negative in ascitic males and females than in nonascitic males and females. Necropsies conducted on Day 51 revealed higher right:total ventricular weight ratios in ascitic than in nonascitic broilers, whereas normalizing the left ventricle plus septum weight for differences in body weight generated similar values for ascitic and nonascitic males and females, respectively. These results support a primary role for pulmonary hypertension but not cardiomyopathy in the pathogenesis of ascites triggered by cool temperatures. Values obtained for minimally invasive diagnostic indices on Day 42 also establish predictive thresholds that can be used to evaluate the PHS susceptibility of large and apparently healthy male and female broilers.

Animals↗

PubMed1998

Influence of feed deprivation on ventilation and gas exchange in broilers: relationship to pulmonary hypertension syndrome.

Fast-growing broiler chickens not uncommonly exhibit elevated pulmonary vascular resistance that leads to pulmonary hypertension and right ventricular failure. We tested the hypothesis that a distended gastrointestinal tract in these full-fed birds results in an abnormally low tidal volume and minute ventilation that could lead to pulmonary hypoxia, pulmonary arterial vasoconstriction, right ventricular failure, and ascites. Tidal volume, respiratory frequency, heart rate, percentage saturation of hemoglobin with oxygen (HbO2), O2 consumption, and carbon dioxide elimination were measured on fast-growing broiler chickens when full-fed and after 3, 6, and 9 h of feed deprivation. Tidal volume of full-fed birds was not abnormally low despite HbO2 values varying from above 80% to nearly 60%. Importantly, HbO2 was found to be markedly increased in the hypoxemic birds at and beyond a 3-h period without feed, despite a reduction in minute ventilation. This response was not caused by a decrease in O2 consumption. Thus, limitation of gas intake at the mouth was not the cause of the hypoxemia. The data suggest that feed deprivation results in an increase in parabronchial ventilation, possibly from improvement in aerodynamic valving, which would reduce pulmonary hypoxic vasoconstriction and right ventricular failure.

Animals↗

PubMed1998

The infusion rate dependent influence of acute metabolic acidosis on pulmonary vascular resistance in broilers.

Experiments were conducted to evaluate the pulmonary vascular responses of lightly anesthetized clinically healthy male broilers during acute metabolic acidosis induced by bolus i.v. injections or constant i.v. infusions of HCl. In Experiment 1, broilers received consecutive 1.5 mL i.v. bolus injections of 2.5% mannitol (volume control) and 0.4 N, 0.8 N, and 1.2 N HCl in 2.5% mannitol. Following each injection, equivalent concentrations of mannitol or HCl were infused i.v. at a rate of 0.05 mL/min.kg BW. In Experiment 2, repeated bolus injections of 2.5% mannitol and 1.2 N HCl were administered during ongoing constant infusion of 2.5% mannitol. The following variables were evaluated: pulmonary arterial pressure, pulmonary vascular resistance, mean arterial pressure, total peripheral resistance, cardiac output, stroke volume, heart rate, respiratory rate, hematocrit (HCT), and arterial blood gas (PaO2, PaCO2, pH, HCO3-). Mannitol alone did not alter any of the variables. The HCl loading protocols acidified the arterial blood to sustained (constant infusion) or transient (bolus injection) values averaging between pH 7.2 and 7.3. In both experiments, bolus injections of 1.2 N HCl caused transient increases in pulmonary vascular resistance and pulmonary arterial pressure, coincident with decreases in mean arterial pressure and cardiac output. When HCl was infused at a constant rate in Experiment 1, the arterial blood hydrogen ion concentration, [H+], was positively correlated with pulmonary arterial pressure and cardiac output, negatively correlated with mean arterial pressure and total peripheral resistance, and was not correlated with pulmonary vascular resistance. During constant i.v. infusion of mannitol or HCl in both experiments, pulmonary arterial pressure was positively correlated with pulmonary vascular resistance and cardiac output. Overall, bolus injections of 1.2 N HCl consistently triggered transient pulmonary vasoconstriction (increased pulmonary vascular resistance), leading to a transient increase in pulmonary arterial pressure in spite of opposing changes in cardiac output and mean arterial pressure. In contrast, equivalent or greater increases in [H+] during constant i.v. infusion of HCl caused a substantially lower increment in pulmonary arterial pressure, which, in, turn was primarily attributable to increases in cardiac output rather than pulmonary vascular resistance. Increments in either pulmonary vascular resistance or cardiac output induced by metabolic acidosis would be expected to contribute to the onset of pulmonary hypertension syndrome (PHS, ascites) in broilers.

Acidosis↗

PubMed1998

Flow-dependent pulmonary vasodilation during acute unilateral pulmonary artery occlusion in Jungle Fowl.

Giant Jungle Fowl previously were shown to be highly resistant to the onset of pulmonary hypertension syndrome (PHS, ascites) under conditions that induce a substantial incidence of PHS in broiler chickens. In the present study, lightly anesthetized, clinically healthy 12- to 13-wk-old male Giant Jungle Fowl maintained a lower respiratory rate, a similar hematocrit, and superior arterial blood gas values when compared with 6-wk-old male broilers. Giant Jungle Fowl weighed less than broilers (1,860 +/- 19 vs 2,788 +/- 63 g, respectively) and had equivalent absolute values for pulmonary arterial pressure, cardiac output, and pulmonary vascular resistance. Acute unilateral pulmonary artery occlusion in Giant Jungle Fowl doubled the pulmonary vascular resistance and forced the right ventricle to propel a sustained 60% increase in blood flow through the vasculature of the unoccluded lung. A transient increase in pulmonary arterial pressure initially was required to overcome the vascular resistance of the unoccluded lung; however, flow-dependent vasodilation gradually reduced the pulmonary vascular resistance and permitted pulmonary arterial pressure to return toward control levels. Unilateral pulmonary artery occlusion also triggered an immediate reduction in the partial pressure of oxygen in arterial blood, and the gradual return of pulmonary arterial pressure toward control levels did not eliminate this ventilation-perfusion mismatch, which has been attributed to blood flowing too rapidly through the unoccluded lung to permit diffusive gas equilibration. The inherent capacity for flow-dependent pulmonary vasodilation may reduce the susceptibility of Giant Jungle Fowl to PHS by reducing the increment in pulmonary arterial pressure required to propel an elevated blood flow through the lungs.

Animals↗

PubMed1997

Probabilistic neural network prediction of ascites in broilers based on minimally invasive physiological factors.

A Probabilistic Neural Network (PNN) was trained to predict ascites in broilers based on minimally invasive inputs (i.e., physiological factors that do not require the death of the bird). A PNN is a supervised, three-layer, artificial neural network that classifies input patterns (e.g., physiological data) into specific output categories (e.g., ascites or no ascites). The PNN inputs were O2 level in the blood, body weight, electrocardiogram (ECG), hematocrit, S wave, and heart rate of individual birds. These data were from three experiments that have been described previously (Roush et al., 1996a,b). The three data sets were pooled into a combined data set for a total of 170 observations. From the pooled data, a training set (117 birds), a calibration set (17 birds), and a verification set (36 birds) were extracted. The PNN was trained on the training data set. To prevent the PNN from overfitting the training data, the neural network was evaluated on its ability to make correct predictions of the calibration data set. At the point at which the neural network made the highest number of correct classifications for the calibration data set, the trained neural network was saved on the computer. When the PNN was applied to the complete data set, the sensitivity or proportion of the birds with ascites that the PNN correctly diagnosed was 0.97 (75/77 birds). The specificity or proportion of birds that the PNN made a correct diagnosis of not having ascites was 0.98 (91/93 birds). When the PNN was applied to the verification data set, which was not subjected to neural network training, the sensitivity was 0.95 (19/20) and the specificity was 0.88 (14/16 birds). Use of models developed with artificial neural networks may enhance the diagnosis of ascites in broilers. The results may be useful in choosing and developing broiler strains that do not have a propensity for ascites.

Animals↗

PubMed1997

Evaluation of logistic versus linear regression models for predicting pulmonary hypertension syndrome (ascites) using cold exposure or pulmonary artery clamp models in broilers.

Syndromes such as ascites (pulmonary hypertension syndrome) present difficulties both in the interpretation of associated physiological observations and in their analyses. The ability to predict which physiological variables have the greatest influence on survival or, more importantly, which individuals are most susceptible or resistant to ascites would be very useful selection tools. When addressed in this manner, ascites data become binary data sets (healthy or affected). Binary data can be problematic in that they do not meet all of the assumptions necessary for more traditional analyses such as ANOVA and linear regression. Binary data are discrete and do not have normally distributed errors, which violates a fundamental assumption of linear models. The predictive abilities of linear and logistic regression were evaluated in two replicated experiments using two methods to induce ascites, cold exposure (COLD) and surgical clamping of one pulmonary artery (PAC). The logistic and linear predictive models were derived using the same data and variables. The first data set from PAC and COLD were used to develop the predictive models and the replicate data sets of PAC and COLD were used as "test data sets" for the prediction of ascites. The linear models developed were complex, using four or five variables and requiring up to seven different measurements. On average, the linear models predicted ascites correctly 87.6% of the time. The logistic models were simple (single variable) models that predicted ascites correctly 92.0% of the time. The variables used in the logistic models were derivations of the ratio of right ventricular weight to total ventricular weight, either corrected for age or the body weight of the bird. Although linear regression predicted the incidence of ascites almost as well as logistic regression did, logistic regression is the more appropriate test statistic to use.

Analysis of Variance↗

PubMed1997

Chronic unilateral occlusion of an extrapulmonary primary bronchus induces pulmonary hypertension syndrome (ascites) in male and female broilers.

Previously, it was demonstrated that acute (4 min) and chronic (12 d) occlusion of an extrapulmonary primary bronchus triggers pulmonary hypertension but not pulmonary hypertension syndrome (PHS, ascites) in broilers. The present study was conducted to determine whether a more prolonged period of bronchus occlusion causes PHS similar to that induced by clamping one pulmonary artery. Male and female broiler chicks, 14 to 18 d old, were anesthetized, the thoracic inlet was opened, and a silver clip was positioned to fully obstruct the left extrapulmonary primary bronchus (BRONCHUS CLAMP group) or the left pulmonary artery (PA-CLAMP group). Sham-operated chicks were anesthetized and the thoracic inlet was opened; however, neither the pulmonary artery nor the bronchus was clamped (SHAM group). An electrocardiogram (ECG) was obtained whenever clinical ascites became apparent in individual broilers, or prior to the final necropsy for broilers surviving to the end (Day 36) of the experiment. The right:total ventricular weight ratio (RV:TV) was evaluated as an index of pulmonary arterial pressure. Early post-surgical mortality (up to 21 d of age) was higher in the PA-CLAMP group (27% for males and females combined) than in the BRONCHUS CLAMP (10%) and SHAM (2%) groups. Cumulative ascites mortality (Days 22 to 36) also was higher in the PA-CLAMP group (86% for males, 77% for females) than in the BRONCHUS CLAMP (69% for males, 41% for females) and SHAM (23% for males, 0% for females) groups. Ascitic birds in all treatment groups had higher RV:TV ratios and more negative ECG Lead II S-wave amplitudes than nonascitic birds, reflecting the right ventricular hypertrophy and generalized ventricular dilation typically associated with PHS. These results demonstrate that unilateral bronchus occlusion is an effective experimental model for triggering ascites at a lower incidence than that obtained by occluding one pulmonary artery. Following the onset of pulmonary hypertension, the pathophysiological progression leading to ascites appears to be similar for broilers with either unilateral bronchus or pulmonary artery occlusion.

Animals↗

PubMed1996

Age and regulation of fluid and electrolyte balance during repeated exercise sessions.

A common response after only 3-4 days of repeated exercise in younger individuals is an expansion of plasma volume (PV); however, it is not known if older individuals have a similar response. In this study, six older (O) (67 +/- 1 yr) and six younger (Y) men (24 +/- 2 yr) cycled for 4 successive days at 50% maximal oxygen consumption (Vo2max) for 90 min in a warm environment [30 degrees C temperature dry bulb (Tdb), 24 degrees C temperature wet bulb (Twb)]. On day 4, PV was increased (P < 0.05) in Y (10.0 +/- 1%) but not (P > 0.05) in O (1.7 +/- 2%). The increased PV was associated with a greater (P < 0.05) daily fluid intake during the exercise period in Y (45 +/- 3 ml. day-1.kg body wt-1) compared with O (32 +/- 2 ml.day-1.kg body wt-1) and an increase (P < 0.05) in the total circulating protein (TCP) content in Y (0.23 +/- 0.1 g/kg body wt) but not in O (0.10 +/- 0.1 g/kg body wt). Throughout the 4-day exercise period there were similar reductions in 24-h urine flow rate (UV) and urinary sodium excretion (UNaV) in Y and O. Additionally, acute renal clearance measures made during exercise on days 1 and 4 showed similar (P > 0.05) reductions in UNaV between Y (-55 +/- 10%) and O (-44 +/- 6%). However, during exercise in O there were no changes (P > 0.05) in UV (2 +/- 12%) and urine osmolality (UOsm) (-12 +/- 6%) from resting values compared with Y, where UV was decreased (P < 0.05) by 41 +/- 9% and UOsm was increased (P < 0.05) by 39 +/- 8%. Therefore, the inability of the older subjects to increase PV after repeated days of exercise is not related to an impaired renal fluid and Na+ conservation ability, despite a reduced urine concentrating ability during exercise, but to other factors (e.g., fluid intake and TCP) that appear necessary for the hypervolemic response.

Acclimatization↗