Acute heat stress induces oxidative stress in broiler chickens

The stress responses and possible oxidative damage in plasma, liver and heart were investigated in broiler chickens acutely exposed to high temperature. Eighty 5-week old broiler chickens were exposed to 32 degrees C for 6h. The extent of lipid peroxidation, activities of superoxide dismutase and total antioxidant power in plasma, liver and heart tissues were investigated. Meanwhile, the blood metabolites such as glucose, urate, triiodothyronine, thyroxine, corticosterone, ceruloplasmin and creatine kinase were measured before and after 3 and 6h of heat exposure. The results showed that oxidative stress could be induced in 5-week old broiler chickens by acute heat exposure (32 degrees C, 6h). The results suggest that the elevated body temperature can induce the metabolic changes that are involved in the induction of oxidative stress. The liver is more susceptible to oxidative stress than heart during acute heat exposure in broiler chickens. The oxidative stress should be considered as part of the stress response of broiler chickens to heat exposure.     

Ambient temperature: a factor affecting performance and physiological response of broiler chickens

An experiment was conducted to elucidate the influence of four constant ambient temperatures (20°, 25°, 30° and 35°C) on the performance and physiological reactions of male commercial broiler chicks from 3 to 7 weeks of age. A 12 h light-dark cycle was operated, while relative humidity and air circulation were not controlled. Exposure of broiler chickens to the 20°, 25°, 30° and 35°C treatments showed highly significant (P<0.0001) depression in growth rate, food intake and efficiency of food utilization, and a significant increase in water consumption for the 30° and 35°C groups. Mortality was, however, not affected by the temperature treatments. Changes in physiological status, such as increased rectal temperatures, decreased concentration of red blood cells, haemoglobin, haematocrit, and total plasma protein were observed in birds housed in the higher temperature (30° and 35°C) environments. Moreover, in these broiler chickens, there was an increased blood glucose concentration and a decreased thyroid gland weight. These results indicate that continuous exposure of broiler chickens to high ambient temperatures markedly affects their performance and physiological response.     

Early age thermal manipulation on the performance and physiological response of broiler chickens under hot humid tropical climate

Initial brooding temperature is critical for post-hatch growth of broiler chickens. A study was conducted to investigate the early age thermal manipulation (EATM) on the performance and physiological responses broiler chickens under hot humid tropical climate. A total of 260 unsexed day-old Arbor-acre broiler chicks were assigned to five thermal treatments of brooding temperature regimens having 4 replicates of thirteen birds each. The heat treatments were: initial brooding temperature of 35 °C for the first 2 days, and then decreased subsequently, gradually to 22 °C at 21 d of age (CT), initial temperature of 35 °C, sustained for the first 4 days and then decreased gradually (conventionally) (FD), initial temperature of 35 °C for the first 7 days (SD), the birds in CT, but the brooding temperature was raised to 35 °C again for another 3 days from day 7 (SD3), initial brooding temperature of 35 °C for the first 10 days (TD). Data were collected on daily feed intake and weekly body weights. Blood samples were collected from 8 birds per treatment weekly for the determination of plasma uric acid, triglycerides, triiodothyronine (T₃) and creatinine kinase. Data obtained were laid out in a Completely Randomized Design (CRD). Results showed that the final weights of the birds in FD were higher (P < 0.05) than those of the other treatments at the finisher phase. Feed intake of the birds in FD was higher than those of SD3 and TD. FCR of broiler chickens in CT, SD, SD3 and TD was higher than that of FD. The rectal temperature, plasma MDA and blood glucose of the thermally challenged birds in FD was generally better (P < 0.05) than those of the other treatments. It was concluded that EATM can be used to improve performance and also protect broiler chickens from acute heat stress at market age.     

Breast muscle and plasma metabolomics profile of broiler chickens exposed to chronic heat stress conditions

Understanding the variations of muscle and plasma metabolites in response to high environmental temperature can provide important information on the molecular mechanisms related to body energy homeostasis in heat-stressed broiler chickens. In this study, we investigated the effect of chronic heat stress conditions on the breast muscle (Pectoralis major) and plasma metabolomics profile of broiler chickens by means of an innovative, high-throughput analytical approach such as the proton nuclear magnetic resonance (¹H NMR) spectrometry. A total of 300 Ross 308 male chicks were split into two experimental groups and raised in either thermoneutral conditions for the entire rearing cycle (0–41 days) (TNT group; six replicates of 25 birds/each) or exposed to chronic heat stress conditions (30 °C for 24 h/day) from 35 to 41 days (CHS group; six replicates of 25 birds/each). At processing (41 days), plasma and breast muscle samples were obtained from 12 birds/experimental group and then subjected to ¹H NMR analysis. The reduction of BW and feed intake as well as the increase in rectal temperature and heterophil: lymphocyte ratio confirmed that our experimental model was able to stimulate a thermal stress response without significantly affecting mortality. The ¹H NMR analysis revealed that a total of 26 and 19 molecules, mostly related to energy and protein metabolism as well as antioxidant response, showed significantly different concentrations respectively in the breast muscle and plasma in response to the thermal challenge. In conclusion, the results obtained in this study indicated that chronic heat stress significantly modulates the breast muscle and plasma metabolome in fast-growing broiler chickens, allowing to delineate potential metabolic changes that can have important implications in terms of body energy homeostasis, growth performance and product quality.     

Effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration,ROS production and lipid peroxidation in broiler chickens

In order to investigate the effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, production of reactive oxygen species (ROS) and lipid peroxidation in broiler chickens, 128 six-week-old broiler chickens were kept in a controlled-environment chamber. The broiler chickens were initially kept at 25 °C (relative humidity, RH, 70 ± 5%) for 6 d and subsequently exposed to 35 °C (RH, 70 ± 5%) for 3 h, then the heat stress was removed and the temperature returned to 25 °C (RH, 70 ± 5%). Blood and liver samples were obtained before heat exposure and at 0 (at the end of the three-hour heating episode, this group is also abbreviated as the HT group), 1, 2, 4, 8, 12 h after the stress was removed. The results showed that acute heat stress induced a significant production of ROS, function of the mitochondrial respiratory chain, antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activity, and formation of malondialdehybe (MDA). Within the first 12 h after removal of the heat stress, the acute modification of the above parameters induced by heat stress gradually approached to pre-heat levels. The results of the present study suggest that acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This leads to over-production of ROS, which ultimately results in lipid peroxidation and oxidative stress. When the high temperature was removed, the production of ROS, mitochondrial respiratory function and oxidative injury that were induced by acute heat exposure gradually approached the levels observed before heating, in a time-dependent manner.     

The effect of heat stress on intestinal integrity and Salmonella invasion in broiler birds

The intestinal mucosa works as a barrier to protect the internal environment of the animal from bacteria and bacterial toxins found in the gut lumen. Heat stress may harm this function. Therefore, we designed the current experiment to investigate the effect of heat stress on intestinal integrity, physiological and immunological responses and Salmonella invasion in broiler chickens. At 26 days of age, 72 birds were randomly distributed into 3 treatments, with 8 replicates per treatment and 3 birds per replicate. The three treatments were control treatment; kept at thermoneutral environmental conditions (20 ± 2 °C), chronic heat stress treatment (exposed to 30 ± 2 °C; 24 h/day) and acute heat stress treatment (exposed to 35 ±2 °C from 09:00 to 13:00 and kept at 20 ± 1 °C from 13:00 to 09:00). The heat stress exposure was conducted for 10 successive days. Compared with the control treatment, birds subject to chronic and acute heat stress had reduced (P < 0.05) body weight and body gain and increased (P < 0.05) feed conversion ratio. However, feed intake and mortality rate were only increased (P < 0.05) in the acute heat stress treatment. Rectal temperature and Δ rectal temperature (°C/h) increased (P < 0.05) sharply during the first 2 days of exposure followed by gradual decreases until a plateau was achieved. Heat-stressed birds had increased (P < 0.05) serum concentrations of corticosterone, endotoxin lipopolysaccharide and the systemic inflammatory cytokine: TNF-α and IL-2, as well as a higher (P < 0.05) prevalence of Salmonella spp. in meat and livers, as compared with control treatment. It can be concluded that heat stress impaired intestinal integrity which resulted in increased intestinal permeability to endotoxin, translocation of intestinal pathogens (Salmonella spp.) and serum inflammatory cytokines. Therefore, avoiding thermal dysfunction of intestinal barrier is a significant factor in maintaining welfare, immune status and meat safety of broiler birds.     

Supplemental ascorbic acid does not affect inferred heat loss in broiler chickens exposed to elevated temperature

The provision of supplemental ascorbic acid has been reported to lower the body temperature of chickens maintained at elevated environmental temperatures. Since body temperature is the net effect of heat production and heat loss, it is not known if the reductions in body temperature were due to a lower heat production or an increase in heat loss. The purpose of this work was to determine if supplemental ascorbic acid facilitates heat loss in chickens exposed to an elevated temperature. On day 12 post-hatch broiler chickens were implanted intra-abdominally with a thermo-sensitive radio transmitter. The following day, birds were placed inside an indirect calorimeter maintained at 34 C for 24 h and provided water containing 0 or 400 ppm ascorbic acid. Oxygen consumption, carbon dioxide production, heat production, respiratory exchange ratio, and body core temperature were measured for 3 h; beginning 21 h after the birds were placed inside the calorimeter. No differences were observed in heat production or body core temperature between birds provided or not and 400 ppm ascorbic acid. This suggests that ascorbic acid has no effect on heat loss. Birds provided ascorbic acid did exhibit a significantly lower respiratory exchange ratio suggesting a greater utilization of lipid for energy production. Although lipid has a lower heat increment compared with protein and carbohydrate, the significance of this finding to birds exposed to elevated temperature is not known. In conclusion, under the conditions of this study the provision of supplemental ascorbic acid to broiler chickens maintained at an elevated temperature did not affect heat loss as inferred from measured heat production and body core temperature.     

Combined Effects of Muscular Dystrophy,Ecological Stress,and Selenium on Blood Antioxidant Status in Broiler Chickens

The results obtained in this study demonstrated that experimentally induced alimentary muscular dystrophy (MD) in Cobb 500 broiler chickens resulted in increased plasma concentrations of malondialdehyde (MDA), deviations in activities of erythrocyte antioxidant enzymes Cu,Zn-SOD (decrease), and CAT (increase) as well as reduction in plasma concentrations of trace elements Cu, Zn, and Se in affected birds. These data evidenced the presence of oxidative stress in birds with MD, reared both under conditions of ecological comfort and ecological stress. The increased MDA and САТ levels and the reduced Cu,Zn-SOD, Cu, Zn, and Se concentrations in healthy chickens reared under unfavorable microclimatic conditions such as higher air temperature and humidity, higher ammonia concentrations, and lower light intensity were indicative about an induced ecological stress. After the 10-day oral treatment with a selenium-containing preparation, the levels of MDA, Cu,Zn-SOD, CAT, Cu, Zn, and Se attained their normal values in chickens with MD, reared under ecologically comfortable conditions. According to our results, ecological stress was shown to exert independently a significant adverse effect upon the levels of the studied parameters and possibly to be a cause for their slower and not complete normalization despite the selenium therapy in experimental broiler chickens.     

Ascorbic acid decreases heat shock protein 70 and plasma corticosterone response in broilers (Gallus gallus domesticus) subjected to cyclic heat stress

It is known that ascorbic acid (AA) supplementation can ameliorate the chicken's responses to heat stress. The influence of AA on heart heat shock protein 70 (hsp70) and plasma corticosterone (CS) was evaluated in young male broiler chickens fed either no AA (N-AA) or 500 mg AA /kg (AA) and exposed to cyclic high temperatures (21 to 30 to 21 degrees C) over a 3.5 h period on three consecutive days. Dietary AA supplementation elevated plasma AA and maintained it at high levels after heating, but in N-AA birds, only heat elevated plasma AA. In N-AA fed chickens, plasma CS was elevated and was further increased by heat stress as compared with AA-fed birds. Heart hsp70 expression was greater in N-AA-fed chickens compared to AA-fed chickens, and heat stress further elevated hsp70 in both N-AA- and AA-fed birds. The hsp70 increase after heat was two-fold greater in N-AA- vs. AA-fed birds. Plasma CS and heart hsp70 were positively correlated, plasma AA and heart hsp70 were negatively correlated, and plasma CS and AA were negatively correlated. It was concluded that chickens experience a less severe stress response after exposure to high temperatures when they are provided dietary AA.     

A role for gastrointestinal endotoxins in enhancement of heat tolerance by physical fitness

Sakurada, Sotaro, and J. Robert S. Hales. A role forgastrointestinal endotoxins in enhancement of heat tolerance by physical fitness. J. Appl. Physiol.84(1): 207-214, 1998.To further elucidate mechanisms underlyingthe higher heat tolerance of physically fit compared with sedentarypeople, we have investigated the possibility that endotoxins (ofgastrointestinal origin) act, as in the normal development of fever, toraise body temperature and therefore reduce heat tolerance. In aninitial series of experiments, five physically fit and four sedentarysheep were exposed twice at rest to an environment of 42/35°C(dry/wet bulb temperature). When animals were given normal saline iv,rectal temperature (T_re) rose at a significantly higherrate in sedentary than in fit animals; this confirms that heattolerance is improved by physical fitness. Treatment withiv indomethacin did not affect the rate of rise of T_re infit animals. In sedentary animals, however, T_re was loweredto approximate that of fit animals. Because indomethacin blocksprostaglandin pathways involved in endotoxin-induced fever, theindomethacin-induced improvement of heat tolerance of sedentary but notfit animals supports the contention that endotoxins play a role indetermining that difference in heat tolerance. In a second series ofexperiments, quantitative cardiovascular measurements were made byusing radioactive microspheres. Under normothermic conditions, bloodflows in the brain, ileum, and diaphragm were higher in fit than insedentary animals. During hyperthermia up to T_re of42°C (in a 42/39°C environment), fit compared with sedentary animals exhibited 1) a greaterincrease in cardiac output, 2) anincrease in blood flow through arteriovenous anastomoses to higher andbetter maintained levels, 3) lessreduction in blood flow to the ileum, and4) greater increase in blood flowsto the myocardium, turbinates, nasal mucosa, and respiratorymuscles. Endotoxins are likely to come from the gut lumen,because reduction of gut blood flow forms part of the normal responseto heat stress. We suggest that improvement of heat tolerance byphysical fitness is caused by a greater cardiovascular capacity thatpermits not only greater perfusion of heat-loss tissues but themaintenance of a better gastrointestinal tract blood supply, therebybetter maintaining the normal barrier to movement of endotoxins from gut lumen to plasma. Sedentary people, with their lower cardiovascular capacity, redistribute more blood flow away from the gut during environmentally induced hyperthermia, thus allowing endotoxin-induced fever to aggravate hyperthermia.

     

Thermal acclimation of broiler birds by intermittent heat exposure

Heat stress impairs the performance of broilers which increases the economic losses. Effect of duration of heat exposure on performance and acclimatory responses in broiler birds was investigated. At 21 d of age 160 Hubbard birds (80 males+80 females) were equally distributed into 5 treatments (T). The T1, T2, T3 and T4 were acclimated by daily exposure to heat (38±1 °C, 62±2% RH) for 1, 2, 3 and 4 h/d, respectively, for 14 d. T0 was the non-acclimated control (kept at 22±2 °C, 65±2% RH). At 36 d of age the thermotolerance of all birds was evaluated under simulated heat wave conditions by exposing them to an acute heat stress (43±1 °C, 55±3% RH) for 4 h. Body weight (BW), average daily gain (ADG) and average daily feed intake (ADFI) were not affected in T2 and T3, while T3 and T4 showed significant reductions in BW, ADG and ADFI compared to the control. Daily changes in ADFI/kg of metabolic BW (ADFI/BW^0.75), rectal temperature (Tr), rate of increase in rectal temperature (RITr) and evaporative water loss (EWL) showed biphasic patterns of acclimatory responses. The 2 phases were distinctly differentiated by plateau days. Phase 1 characterized by a sharp decline in ADFI/BW^0.75 followed by a gradual increase until the plateau, while Tr, RITr and EWL increased sharply followed by gradual decreases until the plateau. Beyond the plateau (phase 2), homeostatic responses in ADFI/BW^0.75, Tr, RITr and EWL were observed toward the end of the study. Acclimated birds were able to withstand the simulated heat wave with 0% mortality, lower Tr, and longer survival time compared to the control. In conclusion, acclimation could protect birds from acute heat waves and associated heat stress mortality until marketing age. However, applicability of these results towards the industry needs further investigations.     

Metabolic characteristics and oxidative damage to skeletal muscle in broiler chickens exposed to chronic heat stress

Emerging evidence has shown that acute heat exposure affects metabolic characteristics and causes oxidative damage to skeletal muscle in birds. Little is known, however, about such phenomena under chronic heat stress conditions. To address this, we designed the present study to determine the influence of cyclic (32 to 24 to 32 °C: 32 °C for 8 h/d, 32–24–32HS ), and constant (32 and 34 °C, 32HS and 34HS, respectively) heat exposure on the metabolic and peroxide status in skeletal muscle of 4-wk-old male broiler chickens. Heat stress, particularly in the 32HS and 34HS groups, depressed feed intake and growth, while cyclic high temperature gave rise to a less severe stress response in performance terms. Malondialdehyde (MDA) levels in skeletal muscle were enhanced (P < 0.05) by constant heat treatment; the degree of enhancement was not as large as the changes observed in our previous ‘acute’ heat stress model. The 3HADH (3-hydroxyacyl CoA dehydrogenase related to fatty acid oxidation) and CS (citrate synthase) enzyme activities were lowered (P < 0.05) by both the cyclic and constant 34HS treatments, and constant 34HS group, respectively. These results suggest that chronic heat exposure decreases metabolic oxidation capacity in skeletal muscle of broiler chickens. On exposure to chronic heat stress, GPx activity remained relatively constant, though a temperature-dependent elevation in Cu/Zn-SOD activity was observed, implying that anti-oxidation ability was disturbed by the chronic stress condition. From these results it can be concluded that chronic heat stress did not induce oxidative damage to a major extent. This may probably be due to a decrease in metabolic oxidation capacity or due to a self-propagating scavenging system, though the system was not fully activated.     

Cyclic variations in incubation conditions induce adaptive responses to later heat exposure in chickens: a review

Selection programs have enabled broiler chickens to gain muscle mass without similar enlargement of the cardiovascular and respiratory systems that are essential for thermoregulatory efficiency. Meat-type chickens cope with high ambient temperature by reducing feed intake and growth during chronic and moderate heat exposure. In case of acute heat exposure, a dramatic increase in morbidity and mortality can occur. In order to alleviate heat stress in the long term, research has recently focused on early thermal manipulation. Aimed at stimulation of long-term thermotolerance, the thermal manipulation of embryos is a method based on fine tuning of incubation conditions, taking into account the level and duration of increases in temperature and relative humidity during a critical period of embryogenesis. The consequences of thermal manipulation on the performance and meat quality of broiler chickens have been explored to ensure the potential application of this strategy. The physiological basis of the method is the induction of epigenetic and metabolic mechanisms that control body temperature in the long term. Early thermal manipulation can enhance poultry resistance to environmental changes without much effect on growth performance. This review presents the main strategies of early heat exposure and the physiological concepts on which these methods were based. The cellular mechanisms potentially underlying the adaptive response are discussed as well as the potential interest of thermal manipulation of embryos for poultry production.     

The aversion of broiler chickens to concurrent vibrational and thermal stressors

The requirement for assessing the effects of multiple concurrent stressors in improving the welfare of broiler chickens during transport has not been widely recognised. A discrete-choice technique was used to investigate the aversion of broiler chickens to concurrent vibrational and thermal transport stressors. In experiment 1, 12 female broiler chickens, aged 42+/-3 days were studied individually using two choice-chambers. Each chamber had four compartments connected via a central zone and offered four treatments; thermal (T: air temperature; 40 degrees C, 21% RH), vibrational (V: frequency; 2Hz, acceleration; 1ms(-2)), concurrent vibrational and thermal (VT) and no applied stressors (N). Coloured compartment wall panels, allocated at random, assisted chickens' identification of compartments. Birds were fasted overnight and were required to make five consecutive choices on each of four consecutive days. A choice was defined as entering a compartment and feeding (5g pellets), whereupon confinement for 60min was initiated. Choices were totalled over all birds and analysed using a log-linear generalised linear model. The vibration was significantly avoided (V and VT versus N and T; P<0.05) but the thermal stressor was not (T and VT versus N and V; P>0.05) and there was no interaction. In experiment 2, the procedure was repeated with 12 more birds and modifications to increase method sensitivity and maximise bird learning. Choices were more disparate than before with vibration avoided to a greater extent (V and VT versus T and N; P<0.01) but there was still no main effect of the thermal treatment or a significant interaction. Substantial differences between individuals were observed in both experiments. The overall response to vibration supported previous findings for short-term exposure, however, non-avoidance of the thermal treatment was unexpected. Possibly, the birds were unable to associate the delayed heat stress with the compartment. Alternatively, the thermal conditions were not perceived as aversive either initially or throughout the 60min confinement. The preference method provides a useful starting point for assessing combinations of stressors which affect broiler welfare, allowing relative ranking of treatments from an animal-centred perspective.     

Response of mice to continuous 5-day passive hyperthermia resembles human heat acclimation

Chronic repeated exposure to hyperthermia in humans results in heat acclimation (HA), an adaptive process that is attained in humans by repeated exposure to hyperthermia and is characterized by improved heat elimination and increased exercise capacity, and acquired thermal tolerance (ATT), a cellular response characterized by increased baseline heat shock protein (HSP) expression and blunting of the acute increase in HSP expression stimulated by re-exposure to thermal stress. Epidemiologic studies in military personnel operating in hot environments and elite athletes suggest that repeated exposure to hyperthermia may also exert long-term health effects. Animal models demonstrate that coincident exposure to mild hyperthermia or prior exposure to severe hyperthermia can profoundly affect the course of experimental infection and injury, but these models do not represent HA. In this study, we demonstrate that CD-1 mice continuously exposed to mild hyperthermia (ambient temperature ~37°C causing ~2°C increase in core temperature) for 5 days and then exposed to a thermal stress (42°C ambient temperature for 40 min) exhibited some of the salient features of human HA, including (1) slower warming during thermal stress and more rapid cooling during recovery and (2) increased activity during thermal stress, as well as some of the features of ATT, including (1) increased baseline expression of HSP72 and HSP90 in lung, heart, spleen, liver, and brain; and (2) blunted incremental increase in HSP72 expression following acute thermal stress. This study suggests that continuous 5-day exposure of CD-1 mice to mild hyperthermia induces a state that resembles the physiologic and cellular responses of human HA. This model may be useful for analyzing the molecular mechanisms of HA and its consequences on host responsiveness to subsequent stresses.     

The effects of chronic exposure to elevated environmental temperature on intestinal morphology and nutrient absorption in the domestic fowl (Gallus domesticus).

1. Exposure of growing broiler chickens to elevated environmental temperature (35 degrees C) for two weeks, markedly reduced food intake (29%) and growth rate (37%) compared to birds maintained at 22 degrees C. 2. These changes in growth were accompanied by increased in vivo jejunal uptakes of galactose (36%) and methionine (50%) measured per unit intestinal dry weight. 3. Both the electrogenic (phloridzin sensitive) and non-electrogenic (phloridzin insensitive) components of galactose absorption were increased by 24 and 52% respectively during the chronic heat stress. 4. The size of the absorptive compartment may be reduced by the heat stress as reflected by decreased villus heights (19%) and wet (26%) and dry (31%) weights per unit length of jejunum. 5. It is suggested that the changes in hexose and amino acid during chronic exposure to elevated ambient temperature may reflect adaptations to optimise nutrient absorption in the face of reduced nutrition and decreases in the size of the absorptive compartment. A functional hypothyroidism (plasma luminal T3 decreased by 66%) associated with heat stress may contribute to the observed alterations in jejunal structure and function.     

The effects of DL-AP5 and glutamate on ghrelin-induced feeding behavior in 3-h food-deprived broiler cockerels

This study was designed to examine the effects of intracerebroventricular injection of DL-AP5 (N-methyl-D-aspartate (NMDA) receptor antagonist) and glutamate on ghrelin-induced feeding behavior in 3-h food-deprived (FD3) broiler cockerels. At first, guide cannula was surgically implanted in the right lateral ventricle of chickens. In experiment 1, birds were intracerebroventricularly injected with 0, 2.5, 5, and 10 nmol of DL-AP5. In experiment 2, chickens received 5 nmol DL-AP5 prior to the injection of 0.6 nmol ghrelin. In experiment 3, birds were administered with 0.6 nmol ghrelin after 300 nmol glutamate, and the cumulative feed intake was determined at 3-h postinjection. The results of this study showed that the intracerebroventricular injection of DL-AP5 increased food consumption in FD3 broiler cockerels (P ≤ 0.05), and this increase occurs in a dose-dependent manner. Moreover, the decreased food intake induced with the intracerebroventricular injection of ghrelin was additively enhanced by pretreatment with glutamate, and this effect was attenuated by DL-AP5 administration(P ≤ 0.05).These results suggest that there is an interaction between ghrelin and glutamatergic system (through NMDA receptor) on food intake in broiler cockerels.     

Growth performance and concentrations of thyroid hormones and growth hormone in plasma of broilers at high temperatures

Responses of broiler chickens to a high ambient temperature (35 degrees C) were measured in two experiments. In one experiment temperatures were increased abruptly from 21 degrees C to a daily range of 21-35 degrees C whereas, in the other, temperatures were increased more gradually over 6 days. The high temperatures were maintained for 5 h/day. In both experiments, birds exposed to the high temperatures ate less food and gained less liveweight than birds maintained at 21 degrees C. Efficiency of food conversion to liveweight gain and body composition were not affected by high temperature but there was a tendency for thyroid weight to decrease. Overall, the plasma concentration of triiodothyronine (T3) decreased and the plasma concentration of thyroxine (T4) increased, resulting in a decreased T3/T4 molar ratio, during exposure to high temperature. The concentration of plasma growth hormone, but not plasma reverse T3, was increased by high temperature. The initial responses to increased temperature were variable, with birds exposed more gradually adjusting relatively well until the maximum temperature was increased to 35 degrees C. All heated birds readjusted quickly to the daily reduction in temperature to 21 degrees C.