The physiological and metabolic impacts on sheep and cattle of feed and water deprivation before and during transport

Sheep and cattle are frequently subjected to feed and water deprivation (FWD) for about 12 h before, and then during, transport to reduce digesta load in the gastrointestinal tract. This FWD is marked by weight loss as urine and faeces mainly in the first 24 h but continuing at a reduced rate subsequently. The weight of rumen contents falls although water loss is to some extent masked by saliva inflow. FWD is associated with some stress, particularly when transportation is added. This is indicated by increased levels of plasma cortisol that may be partly responsible for an observed increase in the output of water and N in urine and faeces. Loss of body water induces dehydration that may induce feelings of thirst by effects on the hypothalamus structures through the renin-angiotensin-aldosterone system. There are suggestions that elevated cortisol levels depress angiotensin activity and prevent sensations of thirst in dehydrated animals, but further research in this area is needed. Dehydration coupled with the discharge of Na in urine challenges the maintenance of homeostasis. In FWD, Na excretion in urine is reduced and, with the reduction in digesta load, Na is gradually returned from the digestive tract to the extracellular fluid space. Control of enteropathogenic bacteria by normal rumen microbes is weakened by FWD and resulting infections may threaten animal health and meat safety. Recovery time is required after transport to restore full feed intake and to ensure that adequate glycogen is present in muscle pre-slaughter to maintain meat quality.

Effects of twenty-four hour transport or twenty-four hour feed and water deprivation on physiologic and performance responses of feeder cattle

The objective of this study was to compare the effects of 24-h road transport or 24-h feed and water deprivation on acute-phase and performance responses of feeder cattle. Angus x Hereford steers (n = 30) and heifers (n = 15) were ranked by gender and BW (217 +/- 3 kg initial BW; 185 +/- 2 d initial age) and randomly assigned to 15 pens on d -12 of the experiment (3 animals/pen; 2 steers and 1 heifer). Cattle were fed alfalfa-grass hay ad libitum and 2.3 kg/animal daily (DM basis) of a corn-based concentrate throughout the experiment (d -12 to 28). on d 0, pens were randomly assigned to 1 of 3 treatments: 1) transport for 24 h in a livestock trailer for 1,200 km (TRANS), 2) no transport but feed and water deprivation for 24 h (REST), or 3) no transport and full access to feed and water (CON). Treatments were concurrently applied from d 0 to d 1. Total DMI was evaluated daily from d -12 to d 28. Full BW was recorded before treatment application (d -1 and 0) and at the end of experiment (d 28 and 29). Blood samples were collected on d 0, 1, 4, 7, 10, 14, 21, and 28. Mean ADG was greater (P < 0.01) in CON vs. TRANS and REST cattle but similar (P = 0.46) between TRANS and REST cattle (1.27, 0.91, and 0.97 kg/d, respectively; SEM = 0.05). No treatment effects were detected for DMI (P >= 0.25), but CON had greater G: F vs. TRANS (P < 0.01) and REST cattle (P = 0.08) whereas G: F was similar (P = 0.21) between TRANS and REST cattle. Plasma cortisol concentrations were greater (P <= 0.05) in REST vs. CON and TRANS cattle on d 1, 7, 14, and 28 and also greater (P = 0.02) in TRANS vs. CON cattle on d 1. Serum NEFA concentrations were greater (P < 0.01) in REST and TRANS vs. CON cattle on d 1 and greater (P < 0.01) in REST vs. TRANS cattle on d 1. Plasma ceruloplasmin concentrations were greater (P = 0.04) in TRANS vs. CON cattle on d 1, greater (P = 0.05) in REST vs. CON on d 4, and greater (P <= 0.05) in REST vs. TRANS and CON on d 14. Plasma haptoglobin concentrations were greater (P < 0.01) in TRANS vs. CON and REST cattle on d 1 and greater (P <= 0.05) for REST vs. TRANS and CON cattle on d 7. In conclusion, 24-h transport and 24-h nutrient deprivation elicited acute-phase protein reactions and similarly reduced feedlot receiving performance of feeder cattle. These results suggest that feed and water deprivation are major contributors to the acute-phase response and reduced feedlot receiving performance detected in feeder cattle transported for long distances.

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

Adult rats deprived of water for 24-30 h were allowed to rehydrate by ingesting only water for 1-2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 +/- 0.8 ml/2 h; n = 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na+; 2) decreased blood volume; and 3) reduced total body Na+; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na+ concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.

Water deprivation-induced sodium appetite and differential expression of encephalic c-Fos immunoreactivity in the spontaneously hypertensive rat

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Water deprivation-induced thirst is explained by the double-depletion hypothesis, which predicts that dehydration of the two major body fluid compartments, the extracellular and intracellular compartments, activates signals that combine centrally to induce water intake. However, sodium appetite is also elicited by water deprivation. In this brief review, we stress the importance of the water-depletion and partial extracellular fluid-repletion protocol which permits the distinction between sodium appetite and thirst. Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Water deprivation has physiological and health effects in humans that might be related to the salt craving shown by our species.

Episodes of water deprivation enhance daily hypertonic NaCl intake in rats

Water and 1.8% NaCl intake was recorded daily in adult male rats (N = 6) submitted to four water deprivations plus four sodium appetite tests, each at the end of each 7-day interval, or in controls (non-deprived, N = 6). Water deprivation was achieved by removing water and 1.8% NaCl for 24 h. Water was then offered for 2 h. At the end of this period, 1.8% NaCl was also offered in addition to water (sodium appetite test). Average daily 1.8% NaCl intake was enhanced from 5.2 ± 1.0 to 15.7 ± 2.5 ml from the first to the fifth week in the experimental group and was unchanged in the control group. Daily water intake was not altered in either group. Thus, repeated episodes of water deprivation enhance daily NaCl intake.

Damage to the central amygdala produces differential encephalic c-fos expression in the water deprivation-partial rehydration protocol

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Water deprivation-induced sodium appetite

A water deprived animal that ingests only water efficiently corrects its intracellular dehydration, but remains hypovolemic, in negative sodium balance, and with high plasma renin activity and angiotensin II. Therefore, it is not surprising that it also ingests sodium. However, separation between thirst and sodium appetite is necessary to use water deprivation as a method to understand the mechanisms subserving sodium appetite. For this purpose, we may use the water deprivation-partial repletion protocol, or WD-PR. This protocol allows performing a sodium appetite test after the rat has quenched its thirst; thus, the sodium intake during this test cannot be confounded with a response to thirst. This is confirmed by hedonic shift and selective ingestion of sodium solutions in the sodium appetite test that follows a WD-PR. The separation between thirst and sodium appetite induced by water deprivation permits the identification of brain states associated with sodium intake in the appetite test. One of these states relates to the activation of angiotensin II All receptors. Other states relate to cell activity in key areas, e.g. subfornical organ and central amygdala, as revealed by immediate early gene c-Fos immunoreactivity or focal lesions. Angiotensin II apparently sensitizes the brain of the water deprived rat to produce an enhanced sodium intake, as that expressed by spontaneously hypertensive and by young normotensive rat. The enhancement in sodium intake produced by history of water deprivation is perhaps a clue to understand the putative salt addiction in humans.The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009. (C) 2010 Published by Elsevier B.V.

Physiological diversity in tolerance to water deprivation among species of South American desert rodents

Rodents from and and semi-arid deserts are faced with the problem of water conservation. The physiological responses of small rodents to such conditions have been intensively investigated over broad geographically disjunct areas. Despite the presence of xeric habitats in South America since the late Tertiary, some studies suggest that sigmodontine South-American desert rodents do not display the same diversity of physiological responses at the species level as those observed in other desert-dwelling species of rodents. In this paper, we analyzed the physiological responses to water deprivation, at the interespecific and interindividual level, among eight species of sigmodontine desert-dwelling rodents from different geographical areas within South-American deserts. Using randomization tests, we found no significant phylogenetic signal for resistance to water deprivation or for individual variability in this response. Contrary to our initial predictions, we observed that sigmodontine rodents from arid/semi-arid habitats (Monte Desert) had significantly lower rates of body mass loss per day (higher tolerances to water deprivation) than species from the hyperarid deserts. We showed that sigmodontine rodents from South America showed a remarkable diversity of physiological mechanisms for coping with water shortage resulting from different evolutionary adaptive strategies. This diversity, however, displays a rather unexpected pattern in terms of its geographical distribution. (c) 2007 Elsevier Ltd. All rights reserved.

NATRIURESIS, NOT SEIZURES, INDUCED BY CHOLINERGIC STIMULATION OF THE LOCUS-CERULEUS IS AFFECTED BY FOREBRAIN LESIONS AND WATER-DEPRIVATION

Two groups of rats with electrolytic lesions of the medial and upper septal area (MUL) or, alternatively, of the anteroventral portion of the third ventricle (AV3V) and a third group of sham-operated rats were water loaded and received three carbachol injections into the locus coeruleus according to the following schedule: 1) prelesion, 2) on the second postlesion day and 3) on the seventh postlesion day. Both MUL and AV3V lesions inhibited the carbachol-induced natriuresis on the second postlesion day. Recovery was almost complete after MUL but not after AV3V lesion on the seventh day. Water deprivation also reduced the carbachol-induced natriuresis but passive hydration of AV3V animals did not avoid the impairment induced by the lesion. Transient seizure phenomena such as clonic convulsions, salivation and analgesia subsequent to carbachol injection were not altered by the lesions.

Antagonism of the renin-angiotensin system and water deprivation-induced NaCl intake in rats

Adult male rats (n = 5-7 per group) were water deprived for 24 h with only food available. Then they had access to water for 2 h. At the end of the 2 h, 1.5% NaCl was offered to the animals and the intake was measured for another 2 h. The rats drank an average of 9.8 +/- 3.0 ml/120 min of 1.5% NaCl; water intake during this time was negligible (not more than 1.0 ml/120 min). Captopril injected IP at the doses of 12 and 24 mg/kg induced 60-90% inhibition of the intake. Losartan or PD123319 injected ICV induced 50-80% inhibition of the intake. Losartan (80 nmol) inhibited the intake at a lower dose than PD123319 (160 nmol). Neither losartan nor PD123319 inhibited 10% sucrose intake. The inhibition of 1.5% NaCl intake was not related to alterations in arterial pressure. The results show that the antagonism of the renin-angiotensin system inhibits the 1.5% NaCl intake induced by water deprivation. The inhibition induced by the angiotensin II antagonists suggest that this peptide is important for the control of salt intake induced by water deprivation.

Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: influence of sodium intake

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Enhanced Expression of Heme Oxygenase-1 and Carbon Monoxide Excitatory Effects in Oxytocin and Vasopressin Neurones During Water Deprivation

A growing body of evidence indiates that carbon monoxide (CO) acts as a gas neurotransmitter within the central nervous system. Although CO has been shown to affect neurohypophyseal hormone release in response to osmotic stimuli, the precise sources, targets and mechanisms underlying the actions of CO within the magnocellular neurosecretory system remain largely unknown. In the present study, we combined immunohistochemistry and patch-clamp electrophysiology to study the cellular distribution of the CO-synthase enzyme heme oxygenase type 1 (HO-1), as well as the actions of CO on oxytocin (OT) and vasopressin (VP) magnocellular neurosecretory cells (MNCs), in euhydrated (EU) and 48-h water-deprived rats (48WD). Our results show the expression of HO-1 immunoreactivity both in OT and VP neurones, as well as in a small proportion of astrocytes, both in supraoptic (SON) and paraventricular (PVN) nuclei. HO-1 expression, and its colocalisation with OT and VP neurones within the SON and PVN, was significantly enhanced in 48WD rats. Inhibition of HO activity with chromium mesoporphyrin IX chloride (CrMP; 20 mu m) resulted in a slight membrane hyperpolarisation in SON neurones from EU rats, without significantly affecting their firing activity. In 48WD rats, on the other hand, CrMP resulted in a more robust membrane hyperpolarisation, significantly decreasing neuronal firing discharge. Taken together, our results indicate that magnocellular SON and PVN neurones express HO-1, and that CO acts as an excitatory gas neurotransmitter in this system. Moreover, we found that the expression and actions of CO were enhanced in water-deprived rats, suggesting that the state-dependent up-regulation of the HO-1/CO signalling pathway contributes to enhance MNCs firing activity during an osmotic challenge.