Avaliação das dimensões da sede: revisão integrativa / Assessment of the thirst dimension: integrative review

A sede é um sintoma multifatorial e subjetivo cuja mensuração requer múltiplos instrumentos. O objetivo deste estudo foi identificar as dimensões de avaliação da sede e os instrumentos de mensuração utilizados. Incluíram-se artigos publicados entre 2005 a 2015 das bases de dados Lilacs, PubMed e SciELO. A amostra final foi de 18 artigos que evidenciaram as dimensões da sede: intensidade, frequência e desconforto. Também se avaliou a xerostomia e sua intensidade. Essas dimensões foram identificadas por Escalas Visuais Analógicas, Escalas Verbais Numéricas, Escalas de Faces e Escalas Likert, empregadas no Inventário de Sede, Inventário de Xerostomia e Escala de Desconforto da Sede. Avaliou-se a sede principalmente em pacientes dialíticos e internados em unidade de terapia intensiva. Embora a sede seja um sintoma, sua avaliação concentra-se sobretudo na intensidade e é realizada em populações específicas.

Thirst is a multifactorial and subjective symptom that request multiple measuring instruments. The objective of this study was to identify the assessment dimensions of thirst and the measurement tools used. We included studies published between 2005 and 2015 from the databases Lilacs, PubMed and SciELO. Eighteen articles composed the final sample that showed thirst dimensions: intensity, frequency, and discomfort. We also assessed the xerostomia and its intensity. These dimensions were identified by Visual Analogic Scales, Verbal Numeric Scales, Face's Scales and Likert-type Scales, used in the Thirst Inventory, Xerostomia Inventory, and Thirst Discomfort Scale. We assessed thirst especially in dialytic patients and the ones admitted to the intensive care unit. Although thirst is a symptom, in general, its assessment concentrates in its intensity, and it is conducted in specific populations

Histology and renal lipoperoxidation in rats exercised on a treadmill and submitted to water restriction / Histología y lipoperoxidación renal en ratas ejercitadas sobre una caminadora y sometidas a restricción de agua

Physical effort stimulates an increase in oxygen consumption in tissues, generating toxic chemical species derived from oxygen (ROS), which are considered the initiators of the lipid peroxidation process (LPO), the major mechanism of cellular injury. As the essential mechanism for maintaining the electrolyte balance depends on an effective kidney function, oxidative stress in this organ can be a key factor in the development and persistence of hypertension. This study aimed to determine the kidney changes induced by a combination of fluid restriction and exercise in rats. The study consisted of 24 male Wistar rats of 90 days of age, divided into four groups, two of which were submitted to water restriction and exercise on a treadmill.Twenty-four hours after the last training session, the animals were euthanized and the left kidney was removed.The upper part of the kidney was used for the histological procedures and the lower part for the quantification of membrane lipoperoxides.Analysis of variance was applied after testing the normality of data, and the comparison between groups was performed using the Bonferroni test, adopting a significance of p<0.05. The restriction had an influence on body weight; kidney weight; proximal tubule maximum diameter; and area, perimeter and diameter of glomeruli, whereas the exercise affected the weight and the minimum diameter of the proximal tubule. According to the TBARS (thiobarbituric acid reactive substances) method, there was a difference between the G1 (control) and G3 (sedentary with water restriction) and between the G2 (exercised with water) and G4 (exercised with water restriction) compared to G1. The treadmill exercise combined with the water restriction promoted structural changes in the glomeruli and promoted oxidative stress, although neither variable corroborated for the potentiating of lipid peroxidation.

El esfuerzo físico estimula un aumento en el consumo de oxígeno en los tejidos, generando variedades químicas tóxicas derivadas de oxígeno (ROS), que son considerados iniciadores del proceso de peroxidación lipídica (LPO), principal mecanismo de lesión celular. Como el mecanismo esencial para mantener el equilibrio de los electrolitos depende de una función renal eficaz, el estrés oxidativo en este órgano puede ser un factor clave en el desarrollo y persistencia de la hipertensión. Este estudio tuvo como objetivo determinar los cambios renales en ratas, inducidos por una combinación de restricción de líquidos y ejercicio. Esta investigación se realizó en 24 ratas Wistar machos de 90 días de edad, divididos en cuatro grupos, dos de los cuales fueron sometidos a restricción de agua, mientras que los dos grupos restantes fueron ejercitados en una caminadora. Veinticuatro horas después de la última sesión de entrenamiento, los animales fueron sacrificados y se realizó la extracción del riñón izquierdo. La parte superior del riñón se usó para los procedimientos histológicos y la parte inferior para la cuantificación de peróxidos lipídicos en la membrana. El análisis de varianza se aplicó después de probar la normalidad de los datos, y la comparación entre grupos se realizó mediante la prueba de Bonferroni, adoptando una significación de p<0,05. La restricción hídrica tuvo influencia sobre: el peso corporal, peso de los riñones, diámetro máximo del túbulo proximal, y área, perímetro y diámetro de los glomérulos. Mientras que el ejercicio afectó el peso y el diámetro mínimo del túbulo proximal de las ratas. Según el método SRAT (sustancias reactivas al ácido tiobarbitúrico), existió una diferencia entre el G1 (control) y G3 (sedentarismo con restricción de agua) y entre el G2 (ejercicio con agua) y G4 (ejercicio con restricción de agua) en comparación con G1. El ejercicio rodante combinado con la restricción de agua promovió cambios estructurales en los glomérulos y estimuló el desarrollo de estrés oxidativo, aunque ninguna variable fue corroborada para establecer la potenciación de la peroxidación lipídica.

Antidipsogenic effects of central adenosine-5'-triphosphate

Besides other physiological functions, adenosine-5'-triphosphate (ATP) is also a neurotransmitter that acts on purinergic receptors. In spite of the presence of purinergic receptors in forebrain areas involved with fluid-electrolyte balance, the effect of ATP on water intake has not been investigated. Therefore, we studied the effects of intracerebroventricular (icv) injections of ATP (100, 200 and 300 nmol/µL) alone or combined with DPCPX or PPADS (P1 and P2 purinergic antagonists, respectively, 25 nmol/µL) on water intake induced by water deprivation. In addition, the effect of icv ATP was also tested on water intake induced by intragastric load of 12 percent NaCl (2 mL/rat), acute treatment with the diuretic/natriuretic furosemide (20 mg/kg), icv angiotensin II (50 ng/µL) or icv carbachol (a cholinergic agonist, 4 nmol/µL), on sodium depletion-induced 1.8 percent NaCl intake, and on food intake induced by food deprivation. Male Holtzman rats (280-320 g, N = 7-11) had cannulas implanted into the lateral ventricle. Icv ATP (300 nmol/µL) reduced water intake induced by water deprivation (13.1 ± 1.9 vs saline: 19.0 ± 1.4 mL/2 h; P < 0.05), an effect blocked by pre-treatment with PPADS, but not DPCPX. Icv ATP also reduced water intake induced by NaCl intragastric load (5.6 ± 0.9 vs saline: 10.3 ± 1.4 mL/2 h; P < 0.05), acute furosemide treatment (0.5 ± 0.2 vs saline: 2.3 ± 0.6 mL/15 min; P < 0.05), and icv angiotensin II (2.2 ± 0.8 vs saline: 10.4 ± 2.0 mL/2 h; P < 0.05), without changing icv carbachol-induced water intake, sodium depletion-induced 1.8 percent NaCl intake and food deprivation-induced food intake. These data suggest that central ATP, acting on purinergic P2 receptors, reduces water intake induced by intracellular and extracellular dehydration.

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.

Evaluation of vasopressin mediated effects on hemostatic mechanisms: relationship with aquaporins and caveolin proteins.

With a view to evaluate the role of AQP-1 and caveolin proteins in the hemostatic actions of vasopressin, hemostasis was evaluated by bleeding and clotting time respectively.Groups of mice and guinea pigs were treated with arginine vasopressin (AVP) and 1-deamino-8D-AVP (DDAVP) to evaluate their effects on the hemostasis. DDAVP and AVP were able to appreciably reduce the bleeding and clotting time after sodium thiopentone, but not effectively after TEA treatment. Animal groups were pretreated with aquaporin-1 (AQP-1) blockers or water deprived to enhance the expression of AQP-1 water channels. Another group of animals were treated with caveolin protein modulators, cholera toxin (CTX) and the effect of vasopressin analogues evaluated. The results suggest that AQP-1 water channels and caveolin proteins contribute to modulate the hemostatic mechanisms of vasopressin.

Ultrastructural changes in Spirodela intermedia in response to osmotically-induced water shortage

The ultrastructural changes produced in the upper mesophyl cells of Spirodela intermedia W. Koch, by the inclusion of polyethylene glycol (PEG) in the nutrient solution, are related to the degree of the osmotically-induced water shortage. The ultrastructural characteristics of the -0.08 MPa treated fronds differed from the untreated ones in the form of the chloroplasts. PEG up to -0.20 MPa induced considerable cell structural disorganization as the swelling, breaking and disappearance of the outer membrane of the chloroplasts and the breakdown of the tonoplast into small vesicles.

Inhibitory effect of DUP-753 on the drinking responses of rats to central administration of noradrenaline and angiotensin II and to dehydration

We investigated the effect of losartan (DUP-753) on the dipsogenic responses produced by intracerebroventricular (icv) injection of noradrenaline (40 nmol/mul) and angiotensin II (ANG II (2 ng/mul) in male Holtzman rats weighing 250-300g. The effect of DUP-753 was also studied in animals submitted to water deprivation for 30 h. After control injections of isotonic saline (0.15 M NaCl, 1 mul) into the lateral ventricle (LV) the water intake was 0.2 ñ 0.01 ml/h. DUP-753 (50 nmol/mul) when injected alone into the LV of satiated animals had no significant effect on drinking (0.4 ñ 0.02 ml/h) (N = 8). DUP-753 (50 nmol/mul) injected into the LV prior to noradrenaline reduced the water intake from 2.4 ñ 0.8 to 0.8 ñ 0.2 ml/h (N = 8). The water intake induced by injection of ANG II and water deprivation was also reduced from 9.2+ 1.4 and 12.7 ñ 1.4 ml/h to 0.8 ñ 0.2 and 1.7 ñ 0.3 ml/h (N = 6 and N=8), respectively. These data indicate a correlation between noradrenergic pathways and angiotensinergic receptors and lead us to conclude that noradrenaline-induced water intake may be due to the release of ANG II by the brain. The finding that water intake was reduced by DUP-753 in water-deprived animals suggests that dehydration releases ANG II and, that AT1 receptors of the brain play an important role in the regulation of water intake induced by deprivation.

Effects of water deprivation on renal hydroelectrolytic excretion in chronically Trypanosoma cruzi-infected rats

The effect of an 8 hour-period of water deprivation on fluid and electrolyte renal excretion was investigated in male Wistar rats infected with the strain Sao Felipe (12SF) of Trypanosoma cruzi, in comparison with age and sex matched non-infected controls. The median percent reductions in the urinary flow (-40 per cent v -63 per cent) and excretion of sodium (-57 per cent v - 79 per cent) were smaller in chagasic than in control rats, respectively. So, chagasic rats excereted more than controls. On the other hand, the median percent decrement in the clearance of creatinine was higher in chagasic (-51 per cent) than in controls (-39 per cent). Thus, chagasic rats showed some disturbed renal hydroelectrolytic responses to water deprivation, expressed by smaller conservation, or higher excretion of water and sodium in association with smallerglotmerular filtration rate. This fact denoted an elevation in the fractional excretion of sodium and water.

Developmental toxicity of lithium treatment at prophylactic levels

Lithium (Li+) salts are frequently used in psychiatry and may be administered to women in theirreproductive years. We have investigated the influence of chronic Li+ administration on rat offspring. Pregnant Wistar rats drank either tap water ad libitum or 10 mM LiCl, or were water restricted (paired to rats receiving LiCl) until pup weaning. Following birth, pups were fostered to form five experimetnal groups (N = numbers of litters): a) Control-S, stressed by water restriction (N = 21), b) Li+ during the prenatal and lactating periods (N=18),c) Li+ during the prenatal period only (N=22), d) Li+ during the lactating period only (N = 15), and e) Control-NS no treatment (N = 13). Prenatal water restriction of Li+ treatment impaired the performance of the righting reflex, altered the number of males born and delayed the final date of eye opening. Postnatal water restriction or Li+ treatment of the dams reduced body growth and the date of eye opening of pups. No difference was found in the time to pup earflap opening, or in the motor coordination test. The specific effect of lithium on pups included impairment of the righting reflex, an increase in the number of males born, a reduction in body weight at weaning and a delay in the eye opening date. The serum Li+ levels of the dams were maintained at approximately 0.5 mEq/l. Ther was an increase in serum potassium, but not sodium, concentrations. We conclude that chronic treatment of dams with Li+ in amounts similar to those used in the prophylaxis of bipolar disorders aggravated the delay in physical and behavioral development of pups produced by stress associated with limited water intake and handling

Injection of ramipril into the lateral ventricle interferes with the drinking response induced by pharmacological and natural thirst stimuli

We investigated the effects of ramipril, an angiotensin I-converting enzyme (ACE) inhibitor, on water intake by male Holtzman rats (250-300 g) with cannulae implanted into the lateral ventricle. Intracerebroventricular (icv) injection of ramipril (1 µg/µl) significantly reduced drinking in response to subcutaneous (sc) injection of isoprenaline (100 µg/kg) from 8.49 + or - 0.69 to 2.96 + or - 0.36 ml/2 h, polyenthyleneglycol (PEG) (30 percent w/v, 10 ml/kg) from 9.51 + or - 2.20 to 1.6 + - 0.34 ml/2 h or water deprivation for 24 h from 12.61 + or - 0.83 to 5.10 + or - 1.37 ml/2 h. Ramipril had no effect on water intake induced by cellular dehydration produced by sc injection of hypertonic saline (2 M NaCl). These results are consistent with the hypothesis that ramipril acts as an ACE-blocking agent in the brain. The possibility that ramipril is transformed to ramiprilat, the active drug, by the brain is suggested