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PHYSIOLOGY, ENDOCRINOLOGY, AND REPRODUCTION |
Department of Poultry Science, University of Arkansas, Fayetteville 72701
1 Corresponding author: alorenzo{at}uark.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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75% HbO2 were assigned to a "high O2" group, whereas those that initially averaged < 75% HbO2 were assigned to a "low O2" group. The HbO2 and heart rate (HR) were measured using a pulse oximeter before, during, and after broilers in both groups inhaled 100% O2. In experiment 3, HbO2 and HR were measured using a pulse oximeter before, during, and after broilers inhaled 100% O2, after i.v. MP injections, and during a second period of 100% O2 inhalation. The HbO2 rapidly decreased after i.v. MP injections, and subsequently providing 100% O2 to breathe increased the HbO2 above preinjection control levels in experiments 1 and 3. In experiment 2, inhaling 100% oxygen eliminated the initial spontaneous differences in HbO2 between the high O2 and low O2 groups, whereas the return to breathing ambient air restored the initial group differences in HbO2. These experiments indicate that MP-induced and spontaneous hypoxemia can be attributed to a diffusion limitation rather than to arterial-venous shunts, because the hypoxemia resulting from arterial-venous shunts cannot be wholly eliminated by providing 100% O2 to inhale.
Key Words: broiler • pulmonary hypertension • microparticle • hypoxemia
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The pathogenesis of PHS includes the development of systemic arterial hypoxemia characterized by reductions in the partial pressure of O2 in arterial blood (PaO2) and reductions in the saturation of hemoglobin with O2 (HbO2) in arterial blood (Julian, 1988, 1993; Peacock et al., 1989, 1990; Julian and Mirsalimi, 1992; Wideman and Bottje, 1993; Wideman, 2000, 2001; Wideman et al., 2007). Clinically healthy broilers injected i.v. with cellulose MP exhibit the acute onset of systemic arterial hypoxemia within 5 min postinjection (Wideman and Erf, 2002). This hypoxemic response has been attributed to the existence of a subclinical diffusion limitation that can be revealed whenever erythrocytes are forced to flow through gas-exchange capillaries too rapidly to permit full saturation of the hemoglobin with O2 (Wideman, 2000, 2001; Wideman and Erf, 2002). Recent studies demonstrated that the hypoxemic response to MP injections persists for 24 h but then spontaneously recovers toward preinjection (well-oxygenated) levels within 48 h postinjection (Wideman et al., 2005). Entrapped cellulose MP are not cleared from the pulmonary microvasculature for more than 10 d (Wideman et al., 2002; Wang et al., 2003); therefore, the rapid spontaneous recovery to relatively normal blood oxygenation cannot be attributed to a reversal of microvascular occlusion. These observations raise the possibility that factors other than a diffusion limitation may contribute to the hypoxemic response to MP. For example, the acute hemodynamic sequelae to microvascular occlusion might involve enhanced shunting of substantial quantities of deoxygenated pulmonary arterial blood directly into the pulmonary venous drainage without the blood being exposed to effectively ventilated gas-exchange surfaces. Arterial-venous (A-V) shunts were not detected during detailed microanatomical studies of the pulmonary circulation of domestic fowl (Abdalla and King, 1975; King et al., 1978).
Systemic arterial hypoxemia attributable to a diffusion limitation and hypoxemia due to A-V shunts can be differentiated by monitoring the responses of PaO2 or HbO2 while the subject is breathing 100% O2 (West, 1993). Inhaled 100% O2 gas greatly amplifies the driving force for O2 diffusion across the gas-exchange barrier, thereby eliminating systemic arterial hypoxemia when it is caused predominantly by a diffusion limitation. In contrast, when significant A-V shunts are present in the pulmonary circulation, the blood entering the pulmonary veins is a mixture of fully oxygenated blood from well-ventilated regions of the lungs combined with poorly oxygenated blood from unventilated or under-ventilated vascular conduits. Therefore, the hypoxemia resulting from A-V shunts cannot be wholly eliminated by providing 100% O2 to inhale because a substantial portion of the cardiac output is not exposed to effectively ventilated gas-exchange surfaces (West, 1993; Wideman et al., 2000).
Previously it was demonstrated that inhaling 100% O2 fully restored the PaO2, HbO2, and associated cardiopulmonary hemodynamic parameters of preascitic (spontaneously hypoxemic) broilers to levels that did not differ from clinically healthy broilers (Wideman and Tackett, 2000; Wideman et al., 2000). The objective of the present study was to use blood gas analysis and noninvasive pulse oximetry to assess the response of broilers to 100% O2 inhalation before and during the acute hypoxemic responses to i.v. MP injections. It was our hypothesis that breathing pure O2 should eliminate the acute hypoxemia triggered by MP if the hypoxemia is predominantly attributable to a diffusion limitation, but not if the hypoxemia is caused by A-V shunts.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Experiment 1: Blood Gas Analysis
Thirteen broilers, 40 to 48 d of age, were anesthetized using i.m. injections of 1 mL of allobarbital (5, 5-diallyl-barbituric acid; 25 mg/mL, Sigma Chemical Co. St. Louis, MO) and 1 mL of ketamine HCl (100 mg/mL, Henry Schein Inc., Melville, NY). The birds were positioned in lateral recumbency on a surgical board with the head elevated. The left brachial artery was cannulated with heparinized PE-50 polyethylene tubing attached to a 3-mL syringe for arterial blood sampling. When birds were stable and calm 2 arterial blood samples were collected as control samples (control intervals C1 and C2) 6 and 3 min before microgranular CM-32 ion-exchange cellulose microparticles (MP; 30 µm average particle diameter) were administered. The MP were suspended at 0.02 g/mL in heparinized saline and maintained in uniform suspension by continuous stirring in a magnetic stirring plate. One milliliter of the MP suspension was injected into the left basilica vein, and arterial blood (0.5 mL) was withdrawn for blood gas analysis 3, 6, and 9 min later (microparticle MP1 to MP3). An inhalation mask was loosely placed over the chicken’s head to direct 100% O2 at 0.7032 kg/cm2 and a rate of 700 mL/min toward the nostrils while allowing sufficient open space for the excess gas to escape. Arterial blood was withdrawn 3, 6, and 9 min after the beginning of 100% O2 inhalation (oxygen intervals Ox1 to Ox3). The gas flow was shut off, the mask was removed, the birds were allowed to freely breathe ambient air for 3 min, and then recovery samples (R1 to R3) were withdrawn at 3-min intervals. Blood samples were withdrawn anaerobically and immediately injected into a ABL330 Acid-Base Laboratory (Radiometer, America Inc., Westlake, OH), which measured arterial blood values for pH, PaO2, partial pressure of CO2 (PaCO2), and percentage saturation of hemoglobin with O2 (HbO2). These arterial blood values were measured by the ABL330 analyzer operating at a sample chamber temperature of 37°C and recalculated for a temperature of 41°C to match the normal body temperature of the domestic fowl (Fedde, 1986). Appropriate function of the blood gas analyzer was assessed by periodically injecting Blood Gas Qualicheck (Henry Schein Inc.) reference standards. The pH values were converted to hydrogen ion (H+) concentrations for statistical analyses.
Experiment 2: Pulse Oximetry
Forty-five broilers, 31 to 49 d of age, were lightly anesthetized with 0.6 mL of ketamine HCl (100 mg/mL, Henry Schein Inc.). The sensor of a pulse oximeter (Vet/Ox Model 4403, using the universal C-sensor; Sensor Devices Inc., Milwaukee, WI) was positioned on the right wing to illuminate the tissue between the radius and the ulna to determine HbO2 and heart rate (HR; Wideman et al., 2000). When the birds were calm, the HbO2 and HR were recorded every 60 s during a 5-min period (control sample intervals C1 to C5). Oxygen was administered as described for experiment 1, and both HbO2 and HR were recorded during the ensuing 0.5, 1, 2, 3, 4, and 5 min (oxygen sample intervals Ox0.5 to Ox5). The mask was removed, the birds were allowed to breathe ambient air, and HbO2 and HR were recorded during the following 5 min (recovery sample intervals R0.5 to R5). At the end of the experiment the birds were euthanized with a 10-mL injection of 0.1 M KCl. Their hearts were removed and dissected to calculate the right:total ventricular weight ratio (RV:TV) as an index of pulmonary hypertension (Burton et al., 1968).
Experiment 3. Pulse Oximetry During the MP Response
Eighteen broilers, 51 to 54 d of age, were anesthetized using i.m. injections of 1 mL of allobarbital (5, 5-diallyl-barbituric acid; 25 mg/mL, Sigma Chemical Co.) and 1 mL of ketamine HCl (100 mg/mL, Henry Schein Inc.). Birds were placed in lateral recumbency, and the pulse oximeter was used to record HbO2 and HR as described in experiment 2. Control intervals for HbO2 and HR were recorded every 60 s during a 3-min period (sample intervals C1 to C3). Oxygen was administered as described in experiment 1, and HbO2 and HR were recorded during the ensuing 0.5, 1, 2, 3, 4, and 5 min (sample intervals Ox0.5 to Ox5). The mask was removed and HbO2 and HR were recorded during the ensuing 0.5, 1, 2, 3, 4, and 5 min (recovery sample intervals R0.5 to R5). Next, 1 mL of MP suspension (0.02 g of MP/mL) was injected in the basilica vein, and the HbO2 and HR were monitored every 60 s for 5 min (sample intervals MP1 to MP5). After the MP administration, the birds underwent a second period of 100% O2 breathing, and HR and HbO2 were recorded during the ensuing 0.5, 1, 2, 3, 4, and 5 min (MP-Ox0.5 to MP-Ox5). The mask was removed, the birds were allowed to breathe ambient air, and HbO2 and HR were recorded during the ensuing 0.5, 1, 2, 3, 4, and 5 min (recovery sample intervals MP-R0.5 to MP-R5).
Statistical Analysis
Data were analyzed within a group over time using the SigmaStat (Jandel Scientific, San Rafael, CA) repeated-measures, 1-way ANOVA procedure. The control interval preceding the beginning of O2 exposure was used as the basis for comparing changes during subsequent sample intervals. Means were differentiated by the Tukey method (Jandel Scientific, 1994). In experiment 2 the birds were sorted into high and low O2 groups based on their initial control HbO2 values, thereby differentiating between normoxemic (high O2) and hypoxemic (low O2) broilers. Data from the same birds also were sorted into "low RV:TV" and "high RV:TV" groups to differentiate between clinically healthy broilers (low RV:TV) vs. those with sustained pulmonary hypertension (high RV:TV; Wideman and Tackett, 2000; Wideman et al., 2000). The groups resulting from each sorting of the data were compared within a single sample interval using the SigmaStat t-test to assess differences among means. In experiment 3, the HbO2 values recorded during the first and second periods of 100% O2 inhalation were compared using 1-way ANOVA. In all experiments significant differences were declared when P 
0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The initial control values for broilers breathing ambient air averaged (sample intervals C1 and C2 combined) 95.18 ± 4.8 mmHg for PaO2, 95.2 ± 1.4% for HbO2, 33.5 ± 2.6 mmHg for PaCO2, and 3.07 x 10–08 Eq/L for H+ concentration (Figure 1
). The PaO2 and HbO2 decreased within 3 and 6 min after the MP injection, respectively, whereas PaCO2 and H+ concentrations did not differ from control levels. Throughout the 100% O2 inhalation period, PaO2 increased to values 232 mmHg and HbO2 increased to 100% saturation. The H+ concentration in the arterial blood also increased within 3 min after the beginning of 100% O2 inhalation but then subsided to values not different from control levels within 9 min (sample interval Ox3). Within 3 min after returning to breathing ambient air, PaO2, HbO2, and H+ concentrations did not differ from initial control values, whereas PaCO2 decreased and remained below initial control values during the entire recovery interval. Within 6 min after returning to breathing ambient air, PaO2 decreased and remained lower than initial control levels during the last 2 consecutive recovery intervals, whereas HbO2 did not differ from initial control values (P = 0.09; R2 to R3). The H+ concentration did not differ from initial control values during the first 6 min after the return to breathing ambient air, but did increase during the final sample interval.
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Average HbO2 values during the control intervals (sample intervals C1 to C5) were used to sort the birds into 2 categories. Birds averaging 75% HbO2 were assigned to the high O2 group whereas birds averaging <75% HbO2 were assigned to the low O2 group (Figure 2). Within high and low O2 groups, the HbO2 increased and the HR decreased compared with their control levels throughout the 100% O2 inhalation period (sample intervals Ox0.5 to Ox5 compared with control intervals C1 to C5). The HbO2 returned to values no different from the control intervals within 1 and 2 min after the end of 100% O2 inhalation period for high and low O2 groups, respectively (recovery sample intervals R1 and R2). The HR followed a similar tendency, returning to values no different from the control intervals 2 and 3 min after the end of the 100% O2 inhalation period for high and low O2 groups, respectively (recovery sample intervals R2 and R3).
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The birds used for experiment 2 were also sorted based on their RV:TV ratios; birds with RV:TV 0.28 or <0.28 were included in the high and low RV:TV groups, respectively (Figure 3). The high and low RV:TV ratio groups exhibited the same statistical differences for HbO2 (within and between groups) as described above for the low and high O2 groups, respectively. Within the high and low RV:TV groups, the HR decreased 0.5 and 1 min after the beginning of 100% O2 inhalation, respectively (sample intervals Ox0.5 and Ox1), and remained lower than their respective control values during the subsequent samples of the 100% O2 inhalation period (Figure 3). During the recovery period, HR returned to values no different from control within 2 min after the end of 100% O2 administration in both groups (recovery sample interval R2). The HR values between the high and low RV:TV groups did not differ throughout the experiment, with the exception of the sample interval C2.
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Birds inhaling ambient air had average values of 84.1% ± 1.5 for HbO2 and 338 ± 6 beats/min for HR during control sample intervals C1 to C3 (Figure 4). Inhaling 100% O2 increased HbO2 to 95.5% ± 0.5 and reduced HR to 322 ± 6 beats/min (average for sample intervals Ox0.5 to Ox5). The HbO2 and HR returned to control levels 2 and 1 min after the birds returned to breathing ambient air, respectively (recovery sample intervals R2 and R1). The MP injection reduced HbO2 and HR within 1 and 3 min, respectively (sample intervals MP1 and MP3 compared with control intervals C1 to C3), and both HbO2 and HR remained depressed until the ensuing inhalation of 100% O2. The second 100% O2 inhalation period (sample intervals MP-Ox0.5 to MP-Ox5) increased HbO2 to levels that did not differ from the levels attained during the first 100% O2 inhalation period (sample intervals Ox0.5 to Ox5). During sample intervals MP-Ox1 to Mp-Ox3, the HR remained lower than control sample intervals C1 to C3, after which the HR increased to levels that did not differ from control values for the remainder of the experiment. The return to breathing ambient air sharply reduced (within 2 min) the HbO2 during the final recovery intervals MP-R0.5 to MP-R5.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The modest differences in HbO2 values during O2 inhalation in experiment 1 (100% HbO2) vs. experiments 2 (94 to 96.5% HbO2) and 3 (95.5% HbO2) likely reflect the different approaches used to measure HbO2. In experiment 1 arterial blood was withdrawn directly from a catheter and injected into a blood gas analyzer to measure PaO2 and HbO2, whereas in experiments 2 and 3 a pulse oximeter was used to record HbO2. The probe of the pulse oximeter measures the HbO2 of blood as it exits a pulsating wing artery and begins to donate O2 to the surrounding tissues (Peacock et al., 1990; Wideman and Kirby, 1995).
Susceptibility to ascites syndrome is highly variable among members of the same broiler flock (Wideman and Bottje., 1993; Wideman et al., 2002; Wideman and Erf, 2002; Lorenzoni 2006). In experiment 2 pulse oximetry was used to quantify the impact of 100% O2 inhalation on broilers that ranged in general appearance from clinically healthy to obviously preascitic (visibly cyanotic). The resulting HbO2 and HR data were sorted into groups having the well-documented characteristics of clinically healthy individuals (e.g., high initial HbO2 values, low RV:TV ratios) or preascitic individuals (e.g., low initial HbO2 values, high RV:TV ratios; Burton et al., 1968; Peacock et al., 1989, 1990; Julian, 1993; Wideman, 2000, 2001). Birds from the high HbO2 and low RV:TV groups had greater control values for HbO2 and lower HR compared with birds from the low HbO2 and high RV:TV groups. The responses observed during inhalation of 100% O2 reproduced the results of previous studies in which inhaling pure O2 fully restored the PaO2 and HbO2 of spontaneously hypoxemic and preascitic broilers to levels that did not differ from clinically healthy controls (Wideman and Tackett, 2000; Wideman et al., 2000). Therefore, these and previous observations indicate that the onset of a diffusion limitation predominantly accounts for the systemic arterial hypoxemia in broilers developing PHS.
Cardiac output is the volume of blood pumped by a single ventricle over a given time and is the product of the HR and stroke volume. In birds acute adjustments in cardiac output are primarily associated with proportional changes in HR, whereas chronically sustained increments in cardiac output generally reflect increases in heart size and stroke volume. The magnitude of the cardiac output directly reflects the whole-body demand for oxygen (Jones and Johansen, 1972; Grubb, 1983; Sturkie 1986; Faraci, 1991; Wideman, 1999; Smith et al., 2000). In experiments 2 and 3 of the present study, HR declined when the broilers were provided 100% O2 to breathe, presumably indicating that the heart was required to pump a lower cardiac output as long as the hemoglobin was fully saturated with O2. Reductions in cardiac out-put and PAP in preascitic and hypoxemic broilers breathing pure O2 had been proposed previously to contribute to reducing their pulmonary diffusion limitation by permitting the erythrocytes to reside longer at the gas-exchange surfaces (Wideman and Tackett, 2000; Wideman et al., 2000). Indeed, in experiment 2 the reduction in HR and corresponding elimination of the diffusion limitation during 100% O2 inhalation were most pronounced in hypoxemic (low O2 group) and preascitic (high RV:TV group) broilers.
Diffusion limitations can be attributed to hemodynamic, anatomical, and pathological contributions to pulmonary function. When the pulmonary vascular capacity is marginally inadequate, increases in PAP and cardiac output accelerate the rate of blood flow through pulmonary capillaries, reducing the residence time during which the erythrocytes are able to acquire O2 at the gas-exchange surfaces (Wideman and Kirby, 1995; Wideman, 2000). In addition, increases in PAP can promote the transudation of edema fluid from blood capillaries into the pulmonary interstitial spaces. Pulmonary edema increases the thickness of the blood gas barrier and can further aggravate an incipient diffusion limitation. Pulmonary edema is accelerated by increased capillary permeability caused by reactive oxygen species generated by responding lymphocytes during chronic pulmonary inflammation (Rahman and MacNee, 2000). Microparticles entrapped in the pulmonary vasculature of broilers rapidly elicit focal intrapulmonary inflammatory responses that, when combined with microvascular obstruction, can rapidly lead to edema of the surrounding parenchyma (Wideman and Erf, 2002; Wideman et al., 2002, Wang et al., 2003). Therefore, it is possible that rapidly developing and gradually subsiding focal edema may contribute to the somewhat transient (48 h) diffusion limitation evoked after MP are injected i.v. in broilers.
Broilers increase their respiratory rate after MP are injected, presumably reflecting a chemoreceptor-mediated response to compensate for reductions in arterial PaO2 (Wang et al., 2002). Conversely, inhaling 100% O2 attenuates the respiratory drive and reduces the respiratory rate (Wideman and Tackett, 2000). Hyperventilation increases the PaO2 and reduces the PaCO2 of air entering the pulmonary gas exchange surfaces, whereas hypoventilation has the opposite effect (Leech et al., 1991). Accordingly, MP-induced hyperventilation increases the PaO2 gradient favoring O2 diffusion from the air into the blood, and amplifies the PaCO2 gradient favoring CO2 diffusion from the blood into the air. Indeed, injecting MP in experiment 1 caused numerical reductions in PaCO2 and H+ that most likely are attributable to + hyperventilation, whereas tendencies for PaCO2 and H to increase during 100% O2 inhalation most likely can be attributed to hypoventilation. However, PaO2 did not increase during the period of MP-induced hyperventilation. Carbon dioxide is 20 times more soluble than O2 in plasma (Sturkie, 1986; Powell, 2000), which may facilitate CO2 exchange when blood is flowing at an increased velocity. The small amount of dissolved O2 in plasma may be inadequate to overcome the MP-induced diffusion limitation within the pulmonary capillaries, explaining the reduction of PaO2 despite the MP-induced hyperventilation in experiment 1. Nevertheless, the reduction in HR (probably reducing the blood velocity) plus the increment in PaO2 allowed the full saturation of HbO2 during the 100% O2 inhalation period.
In conclusion, these experiments proved that blood flowing through the pulmonary circulation of preascitic and clinically healthy broilers injected with i.v. MP is effectively exposed to ventilated gas-exchange surfaces. Consequently, the distinctive arterial hypoxemia found in birds undergoing PHS or in normal birds injected with MP can be attributed to a diffusion limitation rather than to A-V shunts, because the hypoxemia resulting from A-V shunts cannot be wholly eliminated by providing 100% O2 to inhale.
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ACKNOWLEDGMENTS |
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Received for publication August 29, 2007. Accepted for publication September 29, 2007.
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REFERENCES |
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) denote values greater and lower (P 
; mean ± SEM; n = 29) or low (<75%; •; mean ± SEM; n = 16) HbO2 during 5 min while breathing ambient air (control intervals; C1 to C5); 0.5, 1, 2, 3, 4, and 5 min after the beginning of 100% O2 inhalation (Ox0.5 to Ox5); and 0.5, 1, 2, 3, 4, and 5 min after the 100% O2 breathing period ceased (recovery sampling intervals; R0.5 to R5). Asterisks (*) and daggers (
