Test post-weaning duration for performance, feed intake and feed efficiency in Nellore cattle

O objetivo neste estudo foi determinar o melhor período de avaliação para medidas de desempenho, consumo e eficiência alimentar. Durante 112 dias, 60 machos da raça Nelore, recém-desmamados, submetidos à prova de ganho de peso, foram alimentados em baias individuais para determinação do consumo alimentar e do desempenho. O peso corporal dos animais foi determinado a cada 28 dias, depois de jejum de 16 horas de líquidos e sólidos. As alterações na variância, variância relativa e correlações de Pearson e Spearman entre os dados dos períodos de avaliação reduzidos (28, 56 e 84 dias) e período total (112 dias) foram usados para determinar a melhor duração do período de avaliação. A duração do período de avaliação para ganho médio diário, consumo de matéria seca, conversão alimentar e consumo alimentar residual pode ser reduzida para 84, 28, 84 e 84 dias, respectivamente, pois tal redução não diminui significativamente a confiabilidade das avaliações em animais alimentados em baias individuais.

Residual feed intake and relationships with performance of Nellore cattle selected for post weaning weight

Objetivou-se com este trabalho avaliar desempenho, parâmetros de eficiência e correlações fenotípicas entre medidas de eficiência energética de animais Nelore selecionados para peso pós-desmame e classificados quanto ao consumo alimentar residual, calculado pela diferença entre o consumo observado e o predito, com base no peso vivo médio metabólico e no ganho médio diário. Assim, os animais foram classificados em três grupos: alto (> média + 0,5 desvio-padrão; menos eficientes); médio (± 0,5 desvio-padrão da média); e baixo (< média - 0,5 desvio padrão; mais eficientes) consumo alimentar residual. Não foram observadas diferenças nos pesos vivos inicial e final, no ganho médio diário e no consumo de matéria seca entre os grupos. Animais com baixo consumo alimentar residual mostraram-se também com melhor eficiência alimentar, conversão alimentar e eficiência parcial de crescimento e não apresentaram diferenças em relação aos outros grupos quanto à taxa de crescimento relativo e taxa Kleiber. O consumo alimentar residual apresentou correlação significativa com eficiência alimentar (_0,25), conversão alimentar (0,25), eficiência parcial de crescimento (_0,37) e consumo de MS (0,16) e não apresentou correlação significativa com peso vivo (0,04), ganho médio diário (_0,02), taxa de crescimento relativo (_0,03) e taxa de Kleiber (_0,05). Foram encontradas correlações significativas entre conversão alimentar e peso vivo inicial (0,34) e ganho médio diário (_0,46). Eficiência parcial de crescimento apresentou correlação significativa comtodos os outros parâmetros de eficiência analisados. O consumo alimentar residual, em comparação às demais medidas de eficiência energética, apresenta grande potencial na eficiência produtiva, sendo independente de crescimento e tamanho dos animais.

ROLE OF CHOLINERGIC AND ADRENERGIC PATHWAYS OF THE MEDIAL SEPTAL AREA IN THE WATER-INTAKE AND PRESSOR-RESPONSE TO CENTRAL ANGIOTENSIN-II AND CARBACHOL IN RATS

In the present study, we investigated the effect of previous injection of either prazosin (alpha 1-adrenergic antagonist) or atropine (muscarinic cholinergic antagonist) into the medial septal area (MSA) on the presser and dipsogenic responses induced by intracerebroventricular (ICV) injection of carbachol (cholinergic agonist) and angiotensin II (ANGII) in rats. The presser and dipsogenic responses to ICV carbachol (7 nmol) were reduced after previous treatment of the MSA with atropine (0.5 to 5 nmol), but not prazosin (20 and 40 nmol). The dipsogenic response to ICV ANGII (25 ng) was reduced after prazosin (40 nmol) into the MSA. The presser response to ICV ANGII was not changed either by previous treatment of the MSA with prazosin or atropine. The present results suggest a dissociation among the pathways subserving the control of dipsogenic and presser responses to central cholinergic or angiotensinergic activation.

Central serotonergic and adrenergic/imidazoline inhibitory mechanisms on sodium and water intake

Recent studies have shown the existence of two important inhibitory mechanisms for the control of NaCl and water intake: one mechanism involves serotonin in the lateral parabrachial nucleus (LPBN) and the other depends on alpha(2)-adrenergic/imidazoline receptors probably in the forebrain areas. In the present study we investigated if alpha(2)-adrenergic/imidazoline and serotonergic inhibitory mechanisms interact to control NaCl and water intake. Male Holtzman rats with cannulas implanted simultaneously into the lateral ventricle (LV) and bilaterally into the LPBN were used. The ingestion of 0.3 M NaCl and water was induced by treatment with the diuretic furosemide (10 mg/kg of body weight)+the angiotensin converting enzyme inhibitor captopril (5 mg/kg) injected subcutaneously 1 h before the access of rats to water and 0.3 M NaCl. Intracerebroventricular (i.c.v.) injection of the alpha(1)-adrenergic/imidazoline agonist clonidine (20 nmol/l RI) almost abolished water (1.6 +/- 1.2, vs. vehicle: 7.5 +/- 2.2 ml/2 h) and 0.3 M NaCl intake (0.5 +/- 0.3, vs. vehicle: 2.2 0.8 ml/2 h). Similar effects were produced by bilateral injections of the 5HT(2a/2b) serotonergic agonist 2,5-dimetoxy-4-iodoamphetamine (DOI, 5 mug/0.2 mul each site) into the LPBN on water (3.6 +/- 0.9 ml/2 h) and 0.3 M NaCl intake (0.4 +/- 0.2 m1/2 h). Injection of the (alpha(2)-adrenergic/imidazoline antagonist idazoxan (320 nmol) i.c.v. completely blocked the effects of clonidine on water (8.4 +/- 1.5 ml/2 h) and NaCl intake (4.0 +/- 1.2 ml/2 h), but did not change the effects of LPBN injections of DOI on water (4.2 +/- 1.0 ml/2 h) and NaCl intake (0.7 +/- 0.2 ml/2 h). Bilateral injections of methysergide (4 mug/0.2 mul each site) into the LPBN increased 0.3 M NaCl intake (6.4 +/- 1.9 ml/2 h), not water intake. The inhibitory effect of i.c.v. clonidine on water and 0.3 M NaCl was still present after injections of methysergide into the LPBN (1.5 +/- 0.8 and 1.7 +/- 1.4 ml/2 h, respectively). The results show that the inhibitory effects of the activation of a,-adrenergic/imidazoline receptors in the forebrain are still present after blockade of the LPBN serotonergic mechanisms and vice versa for the activation of serotonergic mechanisms of the LPBN. Therefore, each system may act independently to inhibit NaCl and water intake. (C) 2002 Elsevier B.V. B.V. All rights reserved.

INFLUENCE OF DIETARY-PROTEIN INTAKE AND RECOMBINANT HUMAN SOMATOTROPIN ADMINISTRATION ON GROWTH AND BODY-COMPOSITION OF JUVENILE TAMBACU (A PIARACTUS-MESOPOTAMICUS X COLOSSOMA-MACROPOMUM CROSS)

This experiment was undertaken to study the interaction between level of dietary protein and recombinant human somatotropin (rhGH) administration on performance and body composition of juvenile tambacu (a crossbred Brazilian fish). A total of 72 juvenile tambacu, initially weighing and measuring (mean +/- s.e.m.) 23 +/- 2 g and 9 +/- 0.5 cm, respectively, were randomly divided into 18 groups of 4 fish each. Water temperature was 28 degrees C. Triplicate groups received one of two levels of dietary protein (15 and 30% as fed basis) and one of 3 doses of rhGH (0, 2 and 4 mu g/g) via intraperitoneal injection twice a week for 6 weeks, using a randomized complete block design. Somatotropin was noted to stimulate linear and body weight gain. The higher protein level supported increased growth in weight and length, but there was no interaction between protein level and rhGH dose for either parameter. Protein efficiency ratio and percentage protein deposited showed higher values on diets containing 15% protein. Somatotropin treatment did not significantly affect body composition, but there was a trend towards improved protein retention and reduced carcass lipid. In conclusion, the results of this experiment suggest that rhGH is able to stimulate linear gain in tambacu.

Effects of central alpha-adrenergic agonists on hormone-induced 3% NaCl and water intake

Male rats received intracerebroventricular (ICV) renin (600 ng) or daily subcutaneous injections of deoxycorticosterone (5 mg) to induce 3% NaCl and water intake. Noradrenaline (NOR; 40-160 nmol) and clonidine (CLO; 5-20 nmol) injected ICV. induced 70 to 100% inhibition of the intakes. Phenylephrine (PHE; 40-160 nmol) injected ICV induced 60 to 95% inhibition of the intakes. NOR and PHE induced a stronger inhibition on the 3% NaCl intake induced by renin than on the intake induced by deoxycorticosterone (DOC), and CLO did the opposite. CLO was always more effective than PHE to induce inhibition of the intakes. The results suggest that NOR inhibits hormone (angiotensin II, aldosterone)-induced NaCl intake by acting mainly on alpha(2)-adrenergic receptors.

Receptor-mediated effects of clonidine on need-induced 3% NaCl and water intake

Clonidine combined with adrenergic antagonists were injected in the medial septal area in order to characterize the type of receptors involved with its inhibitory effect on 3% NaCl and water intake of sodium-depleted (furosemide + 24 h of removal of ambient sodium) and 30-h water-deprived rats, respectively. The inhibitory effect of clonidine (20 nmol) on need-induced water intake was reduced 50% by an 80-nmol dose of either idazoxan, yohimbine or prazosin. The inhibitory effect of clonidine (30 nmol) on need-induced 3% NaCl intake was completely antagonized by idazoxan (80, 160 nmol), not altered by yohimbine (40-160 nmol), and partially potentiated (40 nmol) or inhibited (160 nmol) by prazosin. Propranolol did not alter the effects of clonidine on either water (80 nmol) or 3% NaCl (40-160 nmol) intake. The results suggest that the inhibitory effects of clonidine on 3% NaCl and water intake are mediated by different types of alpha2-adrenergic receptors. Copyright (C) 1997 Elsevier B.V.

Idazoxan and the effect of intracerebroventricular oxytocin or vasopressin on sodium intake of sodium-depleted rats

The alpha(2)-adrenergic agonist clonidine and the neuropeptide oxytocin, inhibit sodium intake when injected intracerebroventricularly (i.c.v.). The present work investigates whether (1) vasopressin also inhibits sodium intake when injected i.c.v., and (2) the effect of oxytocin and of vasopressin on sodium intake is affected by i.c.v. injection of idazoxan, an alpha(2)-adrenergic antagonist. Clonidine (30 nmol), oxytocin (40, 80 nmol) and vasopressin (40, 80 nmol) were injected i.c.v. 20 min prior to a 1.5% NaCl appetite test, in rats depleted of sodium for 24 h by a combination of a single s.c. injection of furosemide (10 mg/rat) and removal of ambient sodium. Every dose of clonidine, oxytocin and vasopressin inhibited the 1.5% NaCl intake. Seizures were observed with the higher dose of vasopressin, but not with either dose of oxytocin. The effect of i.c.v. injection of clonidine (30 nmol), oxytocin (80 nmol) or vasopressin (40 nmol) was partially inhibited by prior i.c.v. injection of idazoxan (160, 320 nmol). The results suggest that the inhibition of 1.5% NaCl intake induced by i.c.v. injection of neuropeptides in sodium-depleted rats depends, in part, on the activation of central alpha(2)-adrenoceptors. (C) 1997 Elsevier B.V. B.V. All rights reserved.

Paraventricular nucleus administration of DuP753 or PD123319 inhibits the effects of angiotensin on water and sodium intake

We determined the effects of DuP753 and PD123319 (both nonpeptides and selective antagonists of the AT(1) and AT(2) angiotensin receptors, respectively), and [Sar(1), Ala(8)]ANG II (a non-selective peptide antagonist of angiotensin receptors) on water and 3%NaCl intake induced by administration of angiotensin II (ANG II) into the paraventricular nucleus (PVN) of sodium-depleted Holtzman rats weighing 250-300 g. Twenty hours before the experiments, the rats were depleted of sodium using furosemide (10 ng/rat, sc). The volume of drug solution injected was 0.5 mu l over a period of 10-15 sec. Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Pre-treatment with DuP753 (14 rats) at a dose of 60 ng completely abolished the water intake induced by injection of 12 ng of ANG II (15 rats) (6.4 +/- 0.6 vs 1.4 +/- 0.3 ml/2 h), where [Sar(1), Ala(8)]ANG II (12 rats) and PD123319 (10 rats) at the doses of 60 ng partially blocked water intake (6.4 +/- 0.6 vs 2.9 +/- 0.5 and 2.7 +/- 0.2 ml/2 h, respectively). In the same animals, [Sar(1), Ala(8)]ANG II, DuP753, and PD123319 blocked the sodium intake induced by ANG II (9.2 +/- 1.6 vs 3.3 +/- 0.6, 1.8 +/- 0.3, and 1.4 +/- 0.2 ml/2 h, respectively). These results indicate that both DuP753 and PD123319, administered into the PVN, blocked the water and sodium intake induced by administration of ANG II into the same site.

Antagonism of clonidine injected intracerebroventricularly in different models of salt intake

Clonidine, an alpha 2-adrenergic agonist, injected into the brain inhibits salt intake of animals treated by the diuretic model of sodium depletion. In the present study, we address the question of whether central injection of clonidine also inhibits salt intake in animals deprived of water or in the need-free state. Saline or clonidine (30 nmol) was injected into the anterior third ventricle of 24-h sodium-depleted (furosemide + removal of ambient sodium), of 24-h water-deprived and of normovolemic (need-free state) adult male rats, Clonidine injected intracerebroventricularly (icv) inhibited the 1.5% NaCl intake for 120 min by 50 to 90% in every model tested. Therefore, different models of salt intake are inhibited by icv injection of clonidine, Idazoxan, an alpha 2-adrenergic antagonist, injected icy at a dose of 160 nmol, inhibited the effect of clonidine only in the furosemide + removal of ambient sodium model of salt intake. This indicates that the antagonism of this effect by idazoxan is dependent on the body fluid/sodium status of the animal.

Toxic effects of alcohol intake on prostate of rats

BACKGROUND. The present report was carried out to determine whether alcohol intake could induce prostate lesions.METHODS. We tested male rats for 300 days. Animals were divided into three groups: controls received only tap water as liquid diet; the chronic alcohol intake group received only ethanol solution in semivoluntary research; and the withdrawal group received the same treatment as chronic alcohol intake until 240 days, after which they reverted to drinking water.RESULTS. Chronic alcohol intake increased lipoperoxide concentrations and acid phosphatase activities. Cu-Zn superoxide dismutase (SOD) was decreased at 60 days, but approached controls values at 300 days following treatment. The serum increased alkaline phosphatase, and alanine transaminase activities reflected the chronic toxic effect of ethanol.CONCLUSIONS. Since SOD activity was unable to scavenge superoxide radical and lipoperoxide formation, we can conclude that superoxide is an important intermediate in prostate damage of chronic alcohol intake. (C) 1997 Wiley-Liss, Inc.

Effects of digitonin on hyperglycaemia and dyslipidemia induced by high-sucrose intake

This study examined whether high-sucrose intake effects on lipid profile and oral glucose tolerance may be inhibited by a single administration of digitonin, a saponin from the seeds of Digitalis purpurea Male Wistar 24 rats were initially divided into two groups (n = 12): (C) was given standard chow and water; (S) received standard chow and 30% sucrose in its drinking water. After 30 days of treatments, C rats were divided into two groups (n = 6): (CC) given an intra-gastric dose 0.5 mL saline, (CD) given a single intragastric dose of 15 mg/kg digitonin. S rats were also divided into two groups (n = 6): (SC) given intra-gastric saline and (SD) given digitonin. Rats were sacrificed after the oral glucose tolerance test (OGTT) at 2 h after the digitonin administration. S rats had higher total energy intake and final body weight than C. SC rats had fasting hyperglycaemia and impaired OGTT. Digitonin in SD group improved the glucose tolerance. Triacylglycerol (TG), very-low-density lipoprotein (VLDL-C) and free fatty acid (FFA) serum concentrations were increased in SD rats from CC. Digitonin in SD rats decreased FFA and led TG and VLDL-C concentrations at the levels observed in the CC group. Despite the enhanced cholesterol in CD group from CC., the high-density lipoprotein (HDL-C) was increased in these animals. HDL-C/TG ratio was higher in CD and SD than in CC and SC, respectively. No significant differences were observed in lipid hydroperoxide(LH) between the groups. VLDL-C/LH ratio and gamma-glutamyl transferase (GGT) activity were increased in SC group and were decreased in SD rats from the SC. In conclusion digitonin enhanced glucose tolerance and had beneficial effects on serum lipids by improve antioxidant activity. (c) 2005 Elsevier Ltd. All rights reserved.

Sedation and need-free salt intake in rats treated with clonidine

The effect of intraperitoneal injection of clonidine (9-72 mu g/kg) on need-free 1.5% NaCl intake and on performance (defined as percent of a complete trial) in the rotarod test, was studied in normovolemic adult male rats. Clonidine (18 and 36 mu g/kg) inhibited the 1.5% NaCl intake in a 2-h test at doses that did not alter the performance in the rotarod test. The dose of 36 mu g/kg did not inhibit 10% sucrose intake. Only the highest dose (72 mu g/kg) of clonidine inhibited the 1.5% NaCl intake and the performance in the rotarod test, and produced signs of sedation. Sedation was determined either by change in posture (immobility or lack of postural tonus) of the animals during the ingestive test or by their performance in the rotarod test. The results suggest that sedation is not a determinant effect on the inhibition of 1.5% NaCl intake induced by clonidine. (C) 1999 Elsevier B.V.

PROGESTERONE ADMINISTRATION TO OVARIECTOMIZED RATS REDUCES WATER AND SALT INTAKE INDUCED BY CENTRAL ADMINISTRATION OF ANGIOTENSIN-II

We tested the effects of estradiol, progesterone and testosterone on water and salt intake induced by angiotensin II (ANG II) injected into the third ventricle of female Holtzman rats weighing 250-300 g. The water and salt ingestion observed after 120 min in the control experiments (injection of 0.5 mu l of 0.15 M NaCl into the third ventricle) was 1.6 +/- 0.3 ml (N = 10) and 0.3 +/- 0.1 ml (N = 8) in intact rats, respectively, and 1.4 +/- 0.3 ml (N = 10) and 0.2 +/- 0.1 (N = 8) in ovariectomized rats, respectively. ANG II injected in intact rats (4, 6, 12, 25, and 50 ng, icv, in 0.5 mu l saline) induced an increase in water intake (4.3 +/- 0.6, 5.4 +/- 0.7. 7.8 +/- 0.8, 10.4 +/- 1.2, 11.2 +/- 1.4 ml/120 min, respectively) (N = 43). The same doses of icv ANG II in intact rats increased the 3% NaCl intake (0.9 +/- 0.2; 1.4 +/- 0.3, 2.3 +/- 0.4, 2.2 +/- 0.3. and 2.5 +/- 0.4 ml/120 min, respectively) (N = 42). When administered to ovariectomized rats ANG II induced comparable amounts of water intake (4.0 +/- 0.5, 4.8 +/- 0.6, 6.9 +/- 0.7. 9.6 +/- 0.8, and 10.9 +/- 1.2 ml/120 min, respectively) (N = 43) but there was a significant decrease of 3% NaCl solution ingestion (0.3 +/- 0.1, 0.4 +/- 0.1, 0.8 +/- 0.2, 0.7 +/- 0.2, and 0.6 +/- 0.2 ml/120 min, respectively) (N = 44). Estrogen (50 mu g), progesterone (25 ng), and testosterone (300 mu g) were injected daily into ovariectomized rats for 21 days. Treatment with estrogen decreased the water intake and abolished the saline ingestion induced by icy injection of ANG II (12 ng (2.8 +/- 1.2 and 0.3 +/- 0.1 ml/120 min, respectively) (N = 8). Treatment with progesterone also reduced the water intake (3.3 +/- 0.6 ml/120 min) (N = 8) and abolished the ANG II-induced saline ingestion (0.4 +/- 0.1 ml/120 min) (N = 8), but these effects were not observed with testosterone (6.4 +/- 0.8 and 2.2 +/- 0.3 ml/120 min, respectively) (N = 8). These results indicate that ANG II induces a greater increase in sodium intake in intact female rats than in ovariectomized rats and that estrogen and progesterone impair water and sodium intake in ovariectomized rats.

Ibotenate lesion of the medial hypothalamus alters the salt intake and pressor responses to activation of the median preoptic nucleus in rats

We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and presser responses induced by the concomitant angiotensinergic, alpha(2) and beta adrenergic activation of the MnPO, whereas alpha(1) activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.