Biomedical subjects

R F Wideman

Publications and source records attributed to R F Wideman.

At least 73 records · Page 4Linked to original sources

PubMed1996

Electrocardiographic evaluation of broilers during the onset of pulmonary hypertension initiated by unilateral pulmonary artery occlusion.

Electrocardiography previously has been used as a noninvasive method for detecting cardiac hypertrophy associated with pulmonary hypertension syndrome (PHS, ascites). In the present study, 36 of 100 male broiler chicks were selected for inclusion in the experiment based on their hatch weight (> or = 40 g), Day 1 to 14 BW gain (upper 50% of population distribution), and the normalcy of their Day 14 electrocardiogram (ECG). On day 16, 10 chicks were assigned to the unoperated control group (CONTROL), sham operations were performed on 10 chicks (SHAM), and pulmonary hypertension was initiated by clamping the left pulmonary artery in 16 chicks (PA-CLAMP). Electrocardiogram leads I, II, III, and aVF were recorded daily until Day 27, when 6 of the 12 birds surviving in the PA-CLAMP group had developed clinical ascites. The right: total ventricular weight ratio (RV:TV) was higher and BW was lower in the PA-CLAMP group than in the CONTROL and SHAM groups on Day 27. The RS, R, and S wave amplitudes in lead II for the CONTROL and SHAM groups did not change, whereas in lead II for the PA-CLAMP group the S wave attained a more negative amplitude by Day 21, the RS wave attained a more negative amplitude by Day 22, and the R wave declined to a less positive amplitude by Day 23 when compared with presurgery values. Similar differences were observed for the RS and S waves for leads III and aVF. The mean electrical axis (MEA) and mean resultant vector (MRV) of the CONTROL and SHAM groups did not change; however the PA-CLAMP group the MEA rotated significantly from +3 degrees to -72 degrees and to -88 degrees on Days 14, 22 and 27, respectively, and the MRV amplitude increased from 0.052 to 0.108 mV and then to 0.179 mV on Days 14, 22, and 27, respectively. When data from all treatment groups were combined, higher absolute and BW-normalized RV:TV ratios were inversely correlated (r = 0.859 to -0.880) with increasingly negative S wave amplitudes in leads II and aVF. Higher absolute and BW-normalized RV:TV ratios were directly correlated (r = 0.786 to 0.789) with increasing MRV amplitudes. These ECG characteristics constitute accurate, noninvasive predictive criteria suitable for detecting cardiac changes occurring early during the onset of primary pulmonary hypertension.

Animals↗

PubMed1996

Blood viscosity in broilers: influence on pulmonary hypertension syndrome.

Elevation in apparent blood viscosity may enhance the pulmonary hypertension that leads to pulmonary hypertension syndrome (PHS) and ascites in fast-growing broilers. We investigated the importance of packed cell volume (PCV) and shear rate in modifying apparent viscosity of the blood from broilers assigned to normal, preascites, and ascites groups. Apparent viscosity of broiler blood increased at all shear rates as PCV increased; the increase in apparent viscosity became greater as the shear rate decreased at PCV above 0.30. At the PCV of normal broilers (0.30 or below), apparent viscosity was nearly shear rate independent, at least down to 11.25 per second, the lowest shear rate studied. Apparent viscosity, at any given PCV and shear rate, was significantly lower in the blood of birds with ascites than in normal birds; however, the relative viscosity was not different between those groups, indicating that lower plasma viscosity in the birds with PHS was responsible for the finding. The results show that the principal factor responsible for increased apparent viscosity of blood in birds with PHS is the increase in PCV. The increased resistance to flow of blood as the result of higher blood viscosity may contribute to the pulmonary hypertension.

Animals↗

PubMed1996

Independent and simultaneous unilateral occlusion of the pulmonary artery and extra-pulmonary primary bronchus in broilers.

Acutely tightening a snare around one pulmonary artery previously was shown to trigger a reversible ventilation-perfusion (V/Q) mismatch in broilers, as reflected by decreases in the partial pressure of oxygen in arterial blood (hypoxemia), accompanied by increases in the hydrogen ion concentration (acidosis) and partial pressure of carbon dioxide (hypercapnia). In the present study, snares were loosely implanted around the right pulmonary artery and the right extrapulmonary primary bronchus in anesthetized male broilers. These snares were tightened and released independently and then simultaneously to evaluate the possibility that directing the entire respiratory minute volume toward the left lung might attenuate the V/Q mismatch caused by forcing the entire cardiac output (CO) through the left lung. Fully reversible arterial blood hypoxemia, acidosis, and hypercapnia occurred when either snare was tightened independently. Presumably, tightening the bronchial snare restricted ventilation but not blood flow to the right lung, thereby permitting blood to perfuse poorly ventilated gas exchange surfaces. Simultaneously tightening both snares triggered arterial blood hypoxemia, acidosis, and hypercapnia similar to or greater in magnitude than the responses obtained by tightening the pulmonary artery snare independently. Tightening either snare independently or both snares simultaneously caused pulmonary arterial pressure to increase (pulmonary hypertension), and permanent obstruction of one bronchus in a separate experiment caused an increase in the right:total ventricular weight ratio, which is indicative of chronic pulmonary hypertension. The mean systemic arterial pressure decreased when the pulmonary artery snare was tightened independently or in combination with the bronchial snare, but not when the bronchial snare was tightened independently. The respiratory rate increased and the heart rate decreased when the pulmonary artery snare was tightened independently, but not when the bronchial snare was tightened independently or in combination with the pulmonary artery snare. These results demonstrate that the V/Q mismatch caused by forcing all the CO to perfuse one lung cannot be attenuated by simultaneously directing the entire respiratory minute volume toward the same lung.

Acidosis↗

PubMed1996

Artificial neural network prediction of ascites in broilers.

An artificial neural network was trained to predict the presence or absence of ascites in broiler chickens. The neural network was a three-layer back-propagation neural network with an input layer of 15 neurons (defining 15 physiological variables), a hidden layer of 16 neurons, and an output layer of 2 neurons (the presence or absence of ascites). Male by-products of a breeder pullet line were brooded at 32 and 30 C during Weeks 1 and 2, respectively. The training set for the neural network consisted of data from birds subjected to cool temperatures (18 C) to induce ascites. After training, the predictive ability of the neural network was verified with two new data sets. The second data set was from birds subjected to cool temperatures (18 C). The third data set was from birds subjected to clamping of the pulmonary artery to simulate the physiological processes involved in ascites (the temperature was 24 C). A comparison was made between laboratory diagnostic results and the neural network predicted ascites incidence. The neural network accurately identified the presence or absence of ascites in the first (training) set. Two false positives and one false positive were identified in the second and third verification sets, respectively. The birds identified as false positives were determined to be in the developmental stages of ascites before the occurrence of fluid accumulation. Artificial neural networks were found to effectively identify broilers with and without ascites.

Animals↗

PubMed1996

Cardio-pulmonary function during acute unilateral occlusion of the pulmonary artery in broilers fed diets containing normal or high levels of arginine-HCl.

Cardio-pulmonary function was measured in male broilers reared on diets formulated to contain 1.5% arginine (NORMAL group) or 2.5% arginine (ARGININE group). A snare placed around the right pulmonary artery permitted acute shunting of the entire cardiac output (CO) through the left pulmonary artery, resulting in sustained increases in blood flow (BF) through the left lung in both groups. The unilateral increase in BF was accompanied by sustained increases in pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) in the NORMAL group. However, following initial transient increases in PAP and PVR in the ARGININE group, subsequent pulmonary vasodilation gradually reduced PVR, and thus PAP, in spite of the ongoing elevation of BF through the left lung. The capacity of the pulmonary vasculature in the ARGININE group to accommodate an increased BF at a normal PAP accounts for the previously reported lower incidence of pulmonary hypertension syndrome (PHS, ascites) in cold-stressed broilers fed supplemental dietary arginine. Hypoxemia and respiratory acidosis ensued rapidly in both groups after tightening the pulmonary artery snare, in spite of a compensatory increase in the respiratory rate. The gradual return of PVR and PAP to presnare levels in the ARGININE group did not eliminate the concurrent ventilation-perfusion mismatch caused by the increased rate of BF through the left lung. Tightening the pulmonary artery snare caused mean systemic arterial pressure (MAP) to drop from control levels of approximately 98 mm Hg to sustained hypotensive levels of approximately 65 mm Hg in both groups. This systemic hypotension was caused by decreases in CO and total peripheral resistance (TPR). The reduction in CO were caused by reduction in stroke volume (SV) rather than heart rate (HR), suggesting that acutely tightening the pulmonary artery snare increased PVR sufficiently to impede left ventricular filling. Accordingly, the maximum increment in PAP attainable by the right ventricle during acute increases in PVR apparently was inadequate to propel the entire CO through the pulmonary vasculature, setting the stage for the congestive right-sided pooling of blood routinely associated with PHS in broilers.

Animal Feed↗

PubMed1995

Furosemide reduces the incidence of pulmonary hypertension syndrome (ascites) in broilers exposed to cool environmental temperatures.

The incidence of pulmonary hypertension syndrome (PHS; ascites) was evaluated in two experiments using broiler breeder male by-product chicks exposed after 3 wk of age to cool environmental temperatures (10 to 15 C). In Experiment 1, 3- to 6-wk-old birds were fed a grower diet to which 0 (Control), .001, .005, .010, or .015% furosemide had been added. All groups in Experiment 1 were fed a finisher ration containing no furosemide during Weeks 7 to 8. In Experiment 2, the Control group received no furosemide, a second group received .015% furosemide during the grower phase only (Weeks 3 to 6), and the third group received .015% furosemide during the grower and finisher phases (Weeks 3 to 8). Cumulative PHS mortality was significantly reduced by furosemide in both experiments. Compared with Controls, birds fed .015% furosemide did not have lower (P = .077) final body weights in Experiment 1 but did have significantly lower final body weights in Experiment 2. Lower levels of furosemide significantly reduced PHS mortality without reducing body weights. Furosemide did not improve feed conversion in either experiment. Neither body weight on Day 1 or 21 nor net Day 1 to 21 weight gain were predictive of susceptibility to PHS during the subsequent grower and finisher intervals in either experiment. On Day 55 of Experiment 2, large healthy birds fed .015% furosemide had significantly lower right:total ventricular weight ratios than control birds, indicating that furosemide reduced right ventricular hypertrophy, presumably by reducing pulmonary arterial pressure.

Animals↗

PubMed1995

Supplemental L-arginine attenuates pulmonary hypertension syndrome (ascites) in broilers.

The incidence of pulmonary hypertension syndrome (PHS; ascites) was evaluated in two experiments using broiler breeder male by-product chicks exposed after 3 wk of age to cool environmental temperatures (10 to 15 C). In Experiment 1, 3- to 6-wk-old birds were fed a grower diet to which 0 (Control), .25, .5, or 1% supplemental L-arginine HCl had been added. During Weeks 7 to 8, all groups in Experiment 1 were fed a finisher diet containing no supplemental arginine. In Experiment 2, the Control group received no supplemental arginine, a second group was fed a grower diet supplemented with 1% L-arginine HCl (Weeks 3 to 6), and a third group was fed grower and finisher diets supplemented with 1% L-arginine HCl (Weeks 3 to 8). Cumulative PHS mortality was significantly reduced by 1% L-arginine HCl on Days 34 to 46 in Experiment 1. When data from all birds fed grower or finisher diets supplemented with 1% L-arginine HCl were pooled in Experiment 2, cumulative PHS mortality was marginally lower (P = .065) than for the Control group. Supplemental L-arginine HCl had no effect on final body weights, weight gain, or feed conversion in either experiment. Neither body weight on Day 1 or 21 nor net weight gain from Days 1 to 21 determined susceptibility to PHS during the subsequent grower and finisher intervals in either experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Changes in pulmonary arterial and femoral arterial blood pressure upon acute exposure to hypobaric hypoxia in broiler chickens.

An experiment was conducted to investigate the pulmonary arterial and femoral arterial pressure responses to acute hypobaric hypoxia. Twenty-four, 7-wk-old Hubbard x Hubbard male chickens were lightly anesthetized and catheters were introduced into the right femoral artery and the pulmonary artery. The birds were then placed in a hypobaric chamber, and blood pressure responses were monitored during acute (15 min) exposures to simulated altitudes of 2,000 and 4,000 m. The pulmonary artery pressure increased .7 and 4% during the first and second exposures to a simulated altitude of 2,000 m, whereas the femoral artery pressure decreased 6 and 8% during exposures to this altitude. The pulmonary artery pressure increased 7% on the first exposure and 23% (P < .05) on the second exposure to a simulated altitude of 4,000 m. The femoral arterial pressure decreased (P < .05) on both exposures to this altitude (29 and 24%, respectively). The initial femoral and pulmonary artery pressures and changes in these pressures upon exposure to hypobaric hypoxia were not consistently correlated with the characteristics of the electrocardiogram, packed cell volume, body weight, or the right:total ventricular weight ratio. These results indicate that acute hypobaric hypoxia elicits a hypotensive response in the systemic arterial circulation and a hypertensive response in the pulmonary arterial circulation of broiler chickens.(ABSTRACT TRUNCATED AT 250 WORDS)

Altitude↗

PubMed1995

A pulmonary artery clamp model for inducing pulmonary hypertension syndrome (ascites) in broilers.

Two experiments were conducted to test the hypothesis that a primary increase in pulmonary vascular resistance can initiate a pathophysiological progression leading to pulmonary hypertension syndrome (PHS, ascites). Pulmonary vascular resistance was increased by surgically clamping the left pulmonary artery when male broiler chicks were 15 to 19 d of age, resulting in a 90% incidence of PHS in Experiment 1, and a 68% incidence of PHS in Experiment 2. The incidence of PHS was 8% for control or sham-operated broilers in Experiment 1, whereas in Experiment 2 no (0%) PHS occurred in sham-operated broilers or in individuals with a pulmonary artery that only was partially occluded. Broilers with a fully occluded left pulmonary artery developed pulmonary hypertension, as demonstrated by increased right:total ventricular weight ratios (right ventricular hypertrophy) and by increased electrocardiogram lead II R-S wave amplitudes (generalized ventricular dilation and hypertrophy). Forcing the entire cardiac output through the right lung resulted in a lower percentage saturation of hemoglobin with oxygen and an elevated hematocrit, reflecting generalized systemic hypoxemia. Pulmonary hypertension and hypoxemia also were specifically characteristic of all birds that developed ascites, regardless of treatment group. These observations demonstrate for the first time that PHS (ascites) can be directly induced by a primary increase in pulmonary vascular resistance. The observed changes in percentage saturation of hemoglobin with oxygen suggest that the lungs of broilers may be unable to efficiently oxygenate the blood when forced to receive an increased cardiac output at an elevated pulmonary arterial pressure.

Animals↗

PubMed1995

Growth of broiler chickens in response to feed restriction regimens to reduce ascites.

A trial was conducted to investigate the impact of early feed restriction on ascites induced by cold temperatures and the subsequent effect on the whole body and breast muscle growth of broilers. Two feed restriction regimens were tested, consisting of limiting daily feed intake of the birds to 75% of the ME required for normal growth from either 4 to 11 d or from 7 to 14 d. At 21 d, half of the birds were moved to a cold house (17.8 C) to induce ascites. Five birds from each pen were killed for the breast muscle growth, Pectoralis major and Pectoralis minor, and heart and abdominal fat pad weights at 4, 7, 11, 14, 21, 35, and 49 d of the experiment. Birds in the cold house were heavier and had better feed conversion than birds in the control house at 49 d of age. This could be attributed to the high ambient temperatures (27 to 33 C) in the control house. The ad libitum birds had a significantly greater percentage of P. major than the feed-restricted birds. Exposure to cold temperatures caused significantly higher percentage of ascites from 21 to 49 d. Cold temperatures also increased the percentage of total heart and the right ventricle weight relative to total heart weight ratio at 35 and 49 d of age, suggesting that the surviving birds were more likely to develop ascites. Although catch-up growth was observed, the final body weight of feed-restricted birds was not the same as ad libitum birds. Early feed restriction reduced the incidence of ascites, but at the cost of breast muscle growth.

Age Factors↗

PubMed1995

Evidence of a ventilation-perfusion mismatch during acute unilateral pulmonary artery occlusion in broilers.

A ventilation-perfusion (V/Q) mismatch can be diagnosed when a moderate increase in cardiac output (CO) causes systemic hypoxemia, thereby exposing a pulmonary incapacity to fully oxygenate the additional blood flowing through the pulmonary vasculature. The susceptibility of broiler chickens to hypoxemia was evaluated in lightly anesthetized, clinically healthy, 40- to 49-d-old males. A snare placed around one pulmonary artery permitted acute, reversible shunting of the entire CO through the unobstructed lung. Blood samples were withdrawn from arterial and venous cannulas for blood gas analysis, and a pulse oximeter was used for noninvasive measurements of the percentage saturation of hemoglobin with oxygen in arterialized capillary beds. The partial pressure of oxygen in arterial blood averaged 103 mm Hg during control periods, 79 mm Hg (hypoxemia) when the pulmonary artery snare was tightened for 12 min, and 101 mm Hg within 5 min after releasing the snare. The percentage saturation of hemoglobin with oxygen before, during, and after tightening the snare averaged, respectively, 96, 91, and 96% for arterial blood, 81, 55, and 78% for venous blood, and 87, 67, and 88% for arterialized capillary beds. Tightening the snare increased the partial pressure of carbon dioxide and the hydrogen ion concentration above control levels in both arterial and venous blood, and these variables returned to control levels upon release of the snare. The combined data constitute direct evidence that clinically healthy broiler chickens are susceptible to hypoxemia during an acute moderate (approximately twofold) increase in pulmonary blood flow.

Animals↗

PubMed1995

Does pulmonary hypertension syndrome (ascites) occur more frequently in broilers medicated with monensin?

The performance of broilers reared in floor pens and given monensin in the feed at 121 ppm was compared with that of birds given no drug. Feed intake and BW gain of medicated birds was significantly lower than that of unmedicated birds from 0 to 22 d of age. Feed intake and feed conversion of medicated birds was significantly reduced, compared with unmedicated birds, from 22 to 53 and 0 to 60 d of age. Total mortality, and mortality due to leg abnormalities from 22 to 53 and 0 to 60 d, was significantly lower in birds given monensin. There was no difference in the incidence of tibial dyschondroplasia (TD) by 60 d. No differences in mortality due to pulmonary hypertension syndrome (PHS) were observed for any age period. Birds removed from pens at 28 d that had received monensin had lower hematocrit and percentage saturation of hemoglobin with oxygen in the blood than unmedicated birds. No differences in these variables were found at 54 d. There were no differences in the right ventricle weight: total ventricular weight ratios or electrocardiogram lead II values at 28 or 54 d. The results indicate that PHS does not occur more frequently in broilers medicated with monensin.

Animals↗

PubMed1994

Hypercalciuric response to dietary supplementation with DL-methionine and ammonium sulfate.

Renal Ca and inorganic P (Pi) excretion were evaluated in Single Comb White Leghorn pullets reared on diets containing 1 or 3.5% Ca alone or supplemented with .6% DL-methionine or .53% ammonium sulfate. Plasma and urine samples were collected during a CONTROL period, and while 200 mM Ca was infused intravenously (Ca-LOADING). Excess Ca, whether supplied chronically in the feed or infused acutely into birds fed 1% Ca diets, significantly reduced glomerular filtration rates, effective renal plasma flow rates, and Pi excretion rates and significantly increased Ca excretion rates and urine pH. Birds fed diets supplemented with DL-methionine and ammonium sulfate maintained significantly lower plasma Ca concentrations during the CONTROL and Ca-LOADING periods than birds fed the respective 1 or 3.5% Ca basal diets. When compared with birds fed the respective 1 or 3.5% Ca basal diets, birds fed the 1% Ca diet supplemented with ammonium sulfate or the 3.5% Ca diet supplemented with DL-methionine had significantly higher absolute urinary Ca excretion rates during Ca-LOADING. Fractional Ca excretion during Ca-LOADING was significantly higher in birds fed 3.5% Ca supplemented with DL-methionine or ammonium sulfate than in birds fed the 3.5% Ca basal diet. These results indicate that DL-methionine and ammonium sulfate accelerated urinary Ca excretion and reduced Ca retention in the extracellular fluid. The hypercalciuric efficacies of DL-methionine and ammonium sulfate were revealed only when the filtered load of Ca was increased through intravenous Ca infusions.

Ammonium Sulfate↗

PubMed1994

Acute heat acclimation and kidney function in broilers.

Broilers previously exposed to high environmental temperatures (heat-acclimated) are more resistant to heat stress and consume more water during heat stress than nonacclimated controls. Two experiments were conducted to determine whether heat-acclimated broilers conserve body water by reducing urine and solute (Na) excretion. In the first experiment, renal function studies were conducted at an ambient temperature (Ta) of approximately 21 C using anesthetized 7-wk-old male broilers. Control birds reared at a constant Ta of 24 C (Group N: noncycled Ta) were compared with birds that had been heat-acclimated by exposure for 3 to 6 d to a daily sinusoidal cycle of 24 to 35 to 24 C (Group C: cycled Ta). In the second experiment, renal function studies were conducted on anesthetized 5-wk-old control and heat-acclimated male broilers while they were exposed to a Ta of 21 C (Ambient Ta: Groups NA, CA), or to a Ta of 32 C (High Ta: Groups NH, CH). When high intravenous infusion rates (.37 mL/kg body mass per min) were used to simulate the volume expansion caused by thermogenic polydipsia, urine flow rates were significantly lower in Groups C and CA than in Groups N and NA, osmolal clearances were lower in Groups CA and CH than in Groups NA and NH, and all heat-acclimated groups in both experiments (Groups C, CA, CH) had significantly lower glomerular filtration rates (GFR), filtered loads of Na, and tubular Na reabsorption rates than the respective control groups (Groups N, NA, NH). These changes in kidney function potentially would minimize urinary fluid and solute loss when heat-acclimated broilers consume large quantities of water to support evaporative cooling. Reductions in GFR, filtered loads of Na, and tubular Na reabsorption rates also may help heat-acclimated broilers reduce the metabolic heat load associated with active (energy requiring) recovery of solute (Na) from the glomerular ultrafiltrate.

Acclimatization↗

PubMed1994

Responses of laying hens to diets containing up to 2% DL-methionine or equimolar (2.25%) 2-hydroxy-4-(methylthio)butanoic acid.

Diets supplemented with up to .6% DL-Met (DLM) or .68% 2-hydroxy-4-(methylthio)butanoic acid (HMB, Alimet) acidify the urine and reduce the incidence of urolithiasis in pullets and laying hens. Excessive acidification potentially may reduce eggshell quality and bone mineralization by interfering with Ca metabolism and may severely challenge the liver and kidneys, which are the primary organs responsible for attenuating metabolic acidosis. To evaluate these possibilities, 30-wk-old Single Comb White Leghorn hens in full production (five hens per replicate, six replicates per diet treatment) were fed for 30 d a 15.7% CP corn and soybean meal-based control layer ration alone or supplemented with DLM (.5, 1, 1.5, or 2%) or equimolar HMB (.56, 1.13, 1.69, or 2.25%). None of the diets caused mortality or gross hepatic or renal damage. Hens fed diets supplemented with the highest levels of DLM and HMB exhibited significant reductions in feed intake, hen-day egg production, and liver mass and had lower plasma concentrations of alanine amino-transferase and isocitrate dehydrogenase when compared with hens fed the control diet. Kidney mass was not significantly affected by high levels of DLM or HMB, but plasma uric acid was significantly higher in hens fed 2% DLM compared with hens fed the control diet. The highest levels of DLM and HMB did not significantly alter total plasma Ca or inorganic phosphate concentrations, nor were percentage eggshell or femur mineralization (femur ash mass:defatted bone mass, femur ash mass:bone volume) significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗

PubMed1993

Reduced renal arterial perfusion pressure stimulates renin release from domestic fowl kidneys.

Systemic hypovolemia and hypotension increase plasma renin activity (PRA) in fowl, but it is not clear whether this response is mediated directly by reduced renal arterial perfusion pressure (RAPP) or indirectly via renal nerves activated when systemic baroreceptors detect hypotension. To evaluate the influence of RAPP on renin release, arterial and renal venous blood samples were collected as RAPP was reduced step-wise from 108 mm Hg (control) to 71 and 47 mm Hg. PRA in systemic arterial (aPRA) and renal venous (vPRA) plasma was measured as the rate of fowl angiotensin I (ANG I) generation. Basal vPRA (2.47 +/- 0.6 ng x ml-1 x min-1) tended to be higher than aPRA (1.24 +/- 0.3 ng x ml-1 x min-1). When RAPP was reduced to 47 mm Hg both vPRA (4.35 +/- 0.6 ng x ml-1 x min-1) and aPRA (1.91 +/- 0.3 ng x ml-1 x min-1) increased significantly. Significant negative slopes (P = 0.01) were obtained when changes in aPRA or vPRA were regressed on RAPP. Mean systemic arterial pressure did not change during reductions in RAPP, nor did angiotensinogen concentrations differ when systemic arterial (472 +/- 30 ng/ml) and renal venous (460 +/- 27 ng/ml) plasma values were compared. Renal plasma flow was fully autoregulated as RAPP was reduced from 108 to 47 mm Hg; consequently, RAPP-induced increases in vPRA cannot be attributed to hemoconcentration of secreted renin. These results demonstrate that reductions in RAPP directly stimulate renin release from domestic fowl kidneys.

Angiotensin I↗

PubMed1993

Susceptibility of two commercial single comb White Leghorn strains to calcium-induced urolithiasis: efficacy of dietary supplementation with DL-methionine and ammonium sulphate.

1. Susceptibility to calcium-induced urolithiasis was assessed in pullets of two commercial SCWL strains (A and B) reared together from 5 to 18 weeks of age on diets containing 10 g/kg calcium (normal calcium: NC) or 35 g/kg calcium (high calcium: HC). 2. Kidney damage was not observed in pullets reared on NC diets. For pullets fed on HC diets, strain A developed significantly greater kidney asymmetry, a higher incidence of gross kidney damage and a higher incidence of uroliths than strain B. 3. Supplementing the HC diet with 6 g/kg DL-methionine significantly reduced the incidence of calcium-induced gross kidney damage and urolith formation in both strains. Ammonium sulphate (5.3 g/kg) was significantly more effective than DL-methionine in reducing calcium-induced kidney damage. 4. Neither DL-methionine nor ammonium sulphate caused a measurable metabolic acidosis. Neither supplement consistently affected water consumption or manure moisture.

Ammonium Sulfate↗

PubMed1993

Response of the avian kidney to acute changes in arterial perfusion pressure and portal blood supply.

Domestic fowl kidneys autoregulate total renal blood flow and glomerular filtration rate (GFR) over a wide range of renal arterial perfusion pressure (RAPP). Sustained (approximately 2-4 h) restriction of renal portal blood flow attenuates the autoregulatory responses. The present study was designed to assess the effects of acute (approximately 10 min) alterations of renal portal blood flow on renal function, and to dissociate the renal responses to altered renal portal blood flow from the renal responses to reductions in RAPP. The thermal pulse decay (TPD) technique and p-aminohippuric acid clearance (CPAH) were used to measure blood flow. During acute increases and decreases in renal portal blood flow, regional renal blood flow as measured by the TPD system (RBFTPD) was significantly positively correlated with total kidney blood flow represented by CPAH (RBFPAH). These results indicate that changes in total kidney blood flow induced by alteration of portal perfusion were reflected in the regional measurement of renal blood flow. Changes in renal portal blood flow did not affect the urine flow rate (UFR), GFR, or fractional excretion of sodium (FENa). Reducing RAPP from 120 to 50 mmHg significantly reduced UFR, GFR, and FENa. Overall, these results indicate that large acute changes in renal portal blood flow can significantly alter total renal blood flow without significantly affecting parameters (UFR, GFR, and FENa) primarily influenced by the renal arterial vasculature.

Animals↗