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Undernormoxic conditions in vitro, isolated pulmonary arteries from broilers exhibit reduced endothelium-dependent relaxation responses when compared with Leghorns. In vivo, hypoxia increases the susceptibility of broiler chickens to pulmonary hypertension syndrome (PHS), whereas Leghorns are considered resistant to PHS. Because L-arginine supplementation decreases the incidence of PHS in vivo and improves the relaxation responses of broiler isolated pulmonary arteries in vitro, we hypothesized that in vitro hypoxia would further reduce the relaxation responses of broilers to endothelium-derived nitric oxide (EDNO)-dependent vasodilators and that L-arginine supplementation would alleviate this impairment. As a test of this hypothesis, pulmonary arteries from broiler and Leghorn chickens were isolated and exposed to normoxia or hypoxia in the presence or absence of L-arginine while their constriction and relaxation responses to vasoactive compounds were recorded. In broilers, hypoxia did not affect the constriction responses of isolated pulmonary arteries but decreased EDNO-dependent acetylcholine-induced relaxation responses. In contrast, in Leghorns hypoxia increased endothelin-1-induced vasoconstriction responses only to the lowest concentration of acetylcholine used. L-Arginine supplementation augmented the relaxation responses to acetylcholine in broilers and Leghorns under normoxia but failed to augment them under hypoxia. Relaxation responses to the NO donor, sodium nitroprusside, were not affected by hypoxia in Leghorns but were increased by hypoxia in broilers. These results suggest that the increased incidence of PHS in broiler chickens reared under hypoxia may be associated with a hypoxia-induced reduction in the synthesis or activity of EDNO in the pulmonary circulation. [ABSTRACT FROM AUTHOR]

Vascular function plays a preponderant role in the pulmonary changes that occur with maturation, during birth, and in the development of pulmonary hypertension. This study was designed to characterize the changes in vasoactivity occurring in broiler and Leghorn chickens from late embryonic life to 5 wk of age. Pulmonary arteries were isolated from 19- and 20-d-old embryos, hatchlings, and 1-, 2-, 3-, 4- and 5-wk-old chickens of both lines and subjected to KCl (45.4 mM)- and endothelin-1 (10(-7.5) M)-induced vasoconstrictions followed by acetylcholine (ACh; 10(-5), 10(-6) and 10(-7) M)- and papaverine (10(-4) M)-induced vasodilations. Vasoconstrictions were greatest at hatch and rapidly declined thereafter, whereas vasodilations were greatest in 20-d-old embryos except with 10(-7) M ACh. Broilers grew faster than Leghorns and had lower vasodilation responses to all concentrations of ACh at 2 and 5 wk of age. Broilers also had greater right-to-total ventricular weight ratios at 5 wk of age, whereas ratios were greater in Leghorn embryos at 20 d of incubation and at hatch. Thus, for a brief period before hatch there is a significant increase in pulmonary endothelium-dependent vasodilation capacity in the chicken embryo, which may aid in the transition from chorioallantoic to pulmonary respiration. The absence of differences in vasodilator capacity between broilers and Leghorns before hatch suggests that the differences in pulmonary artery relaxation capacity and pulmonary hypertension observed after hatch in broilers are not necessarily acquired during incubation but may be related to rapid growth of the broiler chicken.

This study was conducted to validate echocardiography in chickens, and to compare cardiac structure and function between broiler and Leghorn chickens. Diameters of the right and left ventricles, and thicknesses of the left ventricular free wall and the interventricular septum were measured echocardiographically in 5- and 7-wk-old chickens from both lines. Images were obtained from minimally restrained, standing birds using a 7.5 MHz probe placed in a parasternal position. End-systolic and end-diastolic echocardiographic measurements were compared with post-mortem measurements of the same variables. Comparisons resulted in correlation coefficients greater than 0.70 between in vivo (echocardiographic) and post-mortem measurements of the same variables, with post-mortem measurements more closely resembling end-diastolic echocardiographic measurements. After being normalized to body weight, post-mortem myocardial thicknesses, aortic and left ventricular diameters, heart weight at 5 wk of age, and left ventricular weight at 7 wk of age were smaller in broiler than in Leghorn chickens. Echocardiographic parameters, including ventricular wall thicknesses, ventricular diameters, and left ventricular fractional shortening, were also smaller in the broiler chicken. Right ventricular fractional shortening did not differ between the chicken lines. These results indicate that echocardiography is a useful noninvasive technique for in vivo evaluation of cardiac structure and function in the chicken, and that broiler chickens have a relatively smaller structural and functional heart than Leghorn chickens.

An in vitro technique was developed whereby the carbon dioxide (CO2) tension of the buffer bathing the isolated shell gland could be altered without changing the pH. The isolated shell gland tissue showed a steady and linear transport of calcium. When the CO2 tension of the buffer bathing the serosal side of the shell gland tissue was increased, there was approximately an 80% enhancement (P less than .05) of the unidirectional flux of 45Ca from serosal to mucosal surfaces.

Two experiments were conducted to determine physiological responses in heat-stressed broilers fed a control diet or one containing 125 ppm Nicarbazin. Male birds were surgically implanted with a carotid catheter and fitted with a chest movement transducer and rectal probe. In Experiment 1, birds were exposed to an abrupt change from thermoneutral (22.5 C, 70% relative humidity [RH]) to heat stress (37 C and 40 to 50% RH) conditions within 10 min and maintained in this environment for 120 min. In Experiment 2, birds were exposed to a gradual change from thermoneutral to heat stress (38 C, 68% RH) conditions over 4 h and maintained in this environment for an additional 1 h. Heart rate (HR), respiration rate (RR), and body temperature (Tb) were monitored throughout each experiment, and arterial samples were obtained for determination of acid-base balance and lactate. Birds fed Nicarbazin had higher (P less than .05) Tb and lower (P less than .05) blood PCO2 and bicarbonate during heat stress than controls in both experiments. Thermal polypnea was observed in both experiments, but, although there were no treatment differences in Experiment 1, RR was lower (P less than .05) in the last hour of heat stress for Nicarbazin-fed birds in Experiment 2. In the second experiment, birds fed Nicarbazin exhibited higher (P less than .05) HR and blood lactate during heat stress than control-fed birds. The results of this study indicate that Nicarbazin, by an as yet unidentified mechanism, increases Tb in heat-stressed birds, which results in greater deviations in blood acid-base balance, blood lactate, and HR than in control-fed birds.

An experiment was conducted to determine the change with time in the blood ionized calcium concentration of hens exposed to an acute heat stress. Five hens were surgically fitted with carotid artery cannulae and placed in cages inside a temperature-controlled chamber. Blood samples were drawn before (23 C), during (35 C), and after (23 C), a 3-hr heat-stress exposure. Whole blood ionized calcium, blood gas, plasma pyruvate, and lactate were determined. Respiratory alkalosis developed 1 hr after the start of heat exposure (35 C). Approximately 1 hr later, there was a concomitant decline in blood pH as plasma lactate and pyruvate concentration increased (P less than .05). In addition, the blood ionized calcium level was reduced (P less than .05) by 19% and was negatively correlated (P less than .05) with plasma pyruvate (-.77) and lactate (-.81). These results suggest that changes in acid-base balance during heat stress reduce the blood ionized calcium level, which may in turn limit the availability of calcium for egg shell formation.