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PubMed2000

Effect of age and testosterone on the vasopressin and aquaporin responses to dehydration in Fischer 344/Brown-Norway F1 rats.

To determine if the aging-associated decline in testosterone results in attenuated vasopressin (VP) responses to dehydration, testosterone implants were given to aged male Fischer 344Brown-Norway F1(F344BNF1) rats. Water deprivation caused comparable dehydration, increased plasma VP (pVP), and decreased posterior pituitary (PP) VP content in 4-, 15-, and 28-month-old rats. Dehydration increased VP mRNA content of supraoptic nuclei only at 4 months, whereas VP mRNA length was increased at both 4 and 15 months of age. The elevated pVP in the water-deprived aged rats indicates that even without an increase in VP mRNA content, PP VP storage was adequate to maintain elevated pVP. Dehydration increased aquaporin-2 content at 4, but not at 15 or 28 months of age, suggesting decreased renal responsiveness to VP. Testosterone replacement did not produce dehydration-induced increases in VP mRNA or aquaporin-2. Therefore, testosterone deficiency does not result in altered VP responses to dehydration in aged F344BNF1 rats.

Aging↗
PubMed2003

Investigation into the ability of roots of the poikilohydric plant Craterostigma plantagineum to survive dehydration stress.

The ability of the root system of the poikilohydric plant Craterostigma plantagineum to survive dehydration was investigated. The data presented here reveal that the root system is capable of surviving dehydration, but shortly after rehydration the root system senesces. Two weeks after rehydration the growth of a complete new root system is initiated. During dehydration sucrose accumulates from 36 to a maximum of 111 micromol g-1 DW in the roots. It is suggested that the accumulation of sucrose protects the root system during dehydration. There are major stores of stachyose in the roots of Craterostigma (making up over 40% of the dry weight of the tissue) and during dehydration these stores are metabolized. It is suggested that these stachyose stores act as carbohydrate reserves for the synthesis of sucrose. However, over 350 micromol g-1 DW stachyose is metabolized in the roots, which is well in excess of that required for the accumulation of sucrose observed. It is likely that the stachyose reserves in the root system are translocated to other regions of the plant to support carbohydrate metabolism during dehydration of the tissue. During rehydration, the stachyose reserves return to their original level within 96 h. There is no change in the elevated sucrose content of the roots over this period. Thus the roots maintain the protective properties of sucrose much longer than they are needed. The maintenance of high sucrose contents in rehydrating roots is discussed as a possible survival strategy against recurrent desiccation events.

Carbohydrate Metabolism↗
PubMed1992

The ability of dehydrated hamster and human sperm nuclei to develop into pronuclei.

To determine whether the nuclei of mature mammalian spermatozoa are resistant to dehydrated conditions, nuclei of hamster and human spermatozoa were freeze-dried or treated with various dehydrating agents before injection into hamster oocytes. Freeze-dried nuclei remained capable of developing into pronuclei even after 12 mo of storage at 4 degrees C. The level of DNA synthetic activity in the sperm (male) pronucleus was comparable to that in the egg (female) pronucleus. Sperm nuclei that had been stored in 100% ethanol, 100% methanol, or chloroform-methanol (2:1) mixture for 20 days were also capable of developing into pronuclei. Even the nuclei that had been dehydrated ("fixed") with Carnoy's fluid could develop into morphologically normal pronuclei. However, the level of DNA synthesis in the pronuclei derived from these chemically dehydrated nuclei was generally lower than that in the female pronuclei. Although the genetic integrity of the dehydrated sperm nuclei is yet to be determined, nuclei of mature hamster and human spermatozoa appear to be fairly resistant to dehydrated conditions.

Animals↗
PubMedDate not supplied

The effect of dehydration on the elimination of aqueous contrast media from the subarachnoid space.

The frequency of side effects and complications from aqueous myelography is increased by dehydration. To study the effect of dehydration on the elimination of water-soluble contrast medium from the lumbar subarachnoid space, we measured iodine concentrations in the cerebrospinal fluid, serum, and urine for 24 hours after myelography in "hydrated" and "dehydrated" monkeys. Dehydrated animals were fasted for 12 hours prior to and 24 hours after myelography; hydrated animals received oral fluids ad libitum and 300 ml of intravenous fluids. Dehydrated animals had a lower concentration of contrast medium in the blood than hydrated animals. Dehydration slows the elimination of aqueous contrast medium from the lumbar subarachnoid space.

Animals↗
PubMed1996

Hypertonic saline/dextran treatment for severe pressure-driven hemorrhage in dehydrated conscious swine.

Although dehydration impairs the response to a fixed volume hemorrhage, both 7.5% hypertonic saline/6% dextran 70 (HSD: 4 mL/kg) and standard Ringer's lactate (33 mL/kg) are effective resuscitation fluids. However, the efficacy of resuscitation during continuing hemorrhage remains in question. Using a conscious swine model of continuous pressure-driven hemorrhage, we evaluated the effects of dehydration and HSD resuscitation on survival time, hemorrhage volume, regional blood flows, and central hemodynamics. Three groups of pigs were compared: euhydrated control (EC), dehydrated control (48 h water deprived) (DC); and dehydrated and resuscitated with HSD (D + HSD). All pigs were subjected to an initial 37% blood volume hemorrhage for 60 min followed by a continuous hemorrhage proportional to the instantaneous mean arterial pressure. The D + HSD pigs were resuscitated at the end of the 37% blood volume hemorrhage. Dehydration reduced body weight (-6.5 +/- .3%) and increased hematocrit (8.9 +/- 1.8%), serum osmolality (11.6 +/- .9%), serum sodium (11.9 +/- .9%), and serum total protein (9.4 +/- 1.8%). Compared with the EC group, DC had a greater increase in heart rate and arterial base deficit in response to the pressure-driven hemorrhage and a reduced pH and survival time (159 vs. 107 min). In contrast to the DC group, D + HSD had increased mean arterial pressure, cardiac output, oxygen delivery, and regional blood flows to the gut (superior mesenteric artery), kidneys, liver (hepatic artery), and adrenals at 5 min after HSD resuscitation. The HSD did not increase blood loss but tended to prolong survival (+26 min; p = .1079). thus, dehydration compromises survival time (-33%) and the hemodynamic and metabolic responses to pressure-driven hemorrhage, while treatment with HSD improves the hemodynamic responses.

Acid-Base Equilibrium↗
PubMed2003

Sickle cell disease: from membrane pathophysiology to novel therapies for prevention of erythrocyte dehydration.

Sickle cell anemia is characterized by the presence of dense dehydrated erythrocytes that have lost most of their K content. Due to the unique dependence of Hb S polymerization on intracellular Hb S concentration, preventing this dehydration should markedly reduce polymerization. The erythrocyte intermediate conductance Ca-activated K channel (hSK4 or KCNN4), first described by Gardos, has been shown to be a major pathway for sickle cell dehydration. Studies with the imidazole antimycotic clotrimazole have shown reduction of sickle cell dehydration in vivo in a small number of patients with sickle cell disease; dose-limiting gastrointestinal and liver toxicities were observed. Based on the chemical structure of clotrimazole metabolites, a novel Gardos channel inhibitor, ICA-17043, has been developed. It has shown substantial activity both in vitro and in vivo in transgenic sickle mice. ICA-17043 is currently in phase 2 human trials. Another potential therapeutic target is the K-Cl cotransport. When sickle erythrocytes are exposed to relatively acidic conditions, they undergo cell shrinkage via activation of this pathway. K-Cl cotransport can be blocked by increasing the abnormally low erythrocyte Mg content of sickle erythrocytes. Oral Mg supplementation has been shown to reduce sickle cell dehydration in vivo in transgenic sickle mice and in patients in two separate clinical trials. Oral Mg pidolate is being tested in clinical trials in homozygous sickle cell disease and in Hb S/HbC (SC) disease, either as a single agent or in combination with hydroxyurea. The ongoing trials will determine the clinical effectiveness of therapies aimed at preventing sickle erythrocyte dehydration.

Anemia, Sickle Cell↗
PubMed1996

The bioavailability of febantel in dehydrated camels.

In the present study the bioavailability of febantel paste and febantel suspension was investigated in the fully hydrated and the dehydrated camel. The serum concentrations of febantel and its metabolites, fenbendazole, oxfendazole and fenbendazole sulfone were determined by high performance liquid chromatography following extraction with ether. The exposure to febantel and its metabolites in fully hydrated camels was significantly higher in camels dosed with febantel paste compared to febantel suspension, as measured by AUC and Cmax. The AUC and Cmax of fenbendazole and oxfendazole were significantly lower in dehydrated camels as compared to control camels dosed with febantel paste. The systemic availability of febantel suspension in control and dehydrated camels was very low and differences between dehydration and control phases were insignificant. The low systemic availability of febantel in camels dosed with febantel suspension may cause nematodes to become resistant to this anthelmintic. It is, thus, suggested to increase the dose of febantel paste in dehydrated camels in order to increase the exposure to febantel and its metabolites. The binding of febantel, fenbendazole, oxfendazole and fenbendazole sulfone to camels' serum proteins was over 85%. Oxfendazole was only about 70% bound. Dehydration of 10 days did not affect the binding of these benzimidazole derivatives to serum proteins.

Administration, Oral↗
PubMed1999

Metabolic and thermodynamic responses to dehydration-induced reductions in muscle blood flow in exercising humans.

1. The present study examined whether reductions in muscle blood flow with exercise-induced dehydration would reduce substrate delivery and metabolite and heat removal to and from active skeletal muscles during prolonged exercise in the heat. A second aim was to examine the effects of dehydration on fuel utilisation across the exercising leg and identify factors related to fatigue. 2. Seven cyclists performed two cycle ergometer exercise trials in the heat (35 C; 61 +/- 2 % of maximal oxygen consumption rate, VO2,max), separated by 1 week. During the first trial (dehydration, DE), they cycled until volitional exhaustion (135 +/- 4 min, mean +/- s.e.m.), while developing progressive DE and hyperthermia (3.9 +/- 0.3 % body weight loss and 39.7 +/- 0.2 C oesophageal temperature, Toes). On the second trial (control), they cycled for the same period of time maintaining euhydration by ingesting fluids and stabilising Toes at 38.2 +/- 0.1 degrees C. 3. After 20 min of exercise in both trials, leg blood flow (LBF) and leg exchange of lactate, glucose, free fatty acids (FFA) and glycerol were similar. During the 20 to 135 +/- 4 min period of exercise, LBF declined significantly in DE but tended to increase in control. Therefore, after 120 and 135 +/- 4 min of DE, LBF was 0.6 +/- 0.2 and 1.0 +/- 0.3 l min-1 lower (P < 0.05), respectively, compared with control. 4. The lower LBF after 2 h in DE did not alter glucose or FFA delivery compared with control. However, DE resulted in lower (P < 0.05) net FFA uptake and higher (P < 0.05) muscle glycogen utilisation (45 %), muscle lactate accumulation (4.6-fold) and net lactate release (52 %), without altering net glycerol release or net glucose uptake. 5. In both trials, the mean convective heat transfer from the exercising legs to the body core ranged from 6.3 +/- 1.7 to 7.2 +/- 1.3 kJ min-1, thereby accounting for 35-40 % of the estimated rate of heat production ( approximately 18 kJ min-1). 6. At exhaustion in DE, blood lactate values were low whereas blood glucose and muscle glycogen levels were still high. Exhaustion coincided with high body temperature ( approximately 40 C). 7. In conclusion, the present results demonstrate that reductions in exercising muscle blood flow with dehydration do not impair either the delivery of glucose and FFA or the removal of lactate during moderately intense prolonged exercise in the heat. However, dehydration during exercise in the heat elevates carbohydrate oxidation and lactate production. A major finding is that more than one-half of the metabolic heat liberated in the contracting leg muscles is dissipated directly to the surrounding environment. The present results indicate that hyperthermia, rather than altered metabolism, is the main factor underlying the early fatigue with dehydration during prolonged exercise in the heat.

Adult↗
PubMedDate not supplied

Dehydration and hydration in the terminally ill: care considerations.

Debate continues about whether to withhold or withdraw intravenous, subcutaneous, or nasogastric hydration in the terminally ill. Nurses may be confronted with situations where the terminally ill patient or family must make a decision regarding hydration. Therefore, nurses must be knowledgeable about terminal dehydration literature and research. This article is a review of the literature on terminal dehydration. The focus is on the definition of terminal dehydration, physiological benefits and disadvantages of terminal dehydration, rationale for hydrating, review of research in terminal dehydration, physiological basis for comfort in the terminally dehydrated, and suggestions for research and practice.

Cost of Illness↗
PubMed1983

Hydrostatic and oncotic pressures in the interstitium of dehydrated and volume expanded rats.

The pressures in the renal interstitial space seem to have important influence on the setting of the sensitivity of the tubuloglomerular feedback that controls the glomerular filtration rate (GFR), and on the rate of proximal tubular fluid reabsorption. Measurements were made of interstitial pressure conditions, GFR, renal plasma flow (RPF), urinary excretion of sodium and potassium, and plasma renin activities in dehydrated animals and normopenic controls, before and after saline volume expansion (5% of body weight and hour). Colloid osmotic pressure, estimated from the protein concentration in renal hilar lymph, was 7.5 mmHg in the dehydrated animals (controls 2.8 mmHg) and decreased to 3.1 (controls 1.7 mmHg) after volume expansion. The lymph flow rate was increased in both groups of animals after volume expansion. Interstitial hydrostatic pressure, measured in the subcapsular space, was 2-3 mmHg in dehydrated and control animals and increased to 3-4 mmHg after volume expansion. In dehydrated rats GFR and RPF was reduced to 60% of the control values, but after volume expansion they regained control values. After volume expansion, urinary excretion of fluid and electrolytes increased more in controls than in dehydrated rats. Plasma renin activity was decreased in both groups of rats after volume expansion. Thus, in dehydrated animals there was a high colloid osmotic pressure and a low hydrostatic pressure in the renal interstitium, while after volume expansion the oncotic pressure fell and the hydrostatic pressure rose. The effect of volume expansion was found to be dependent on the preceding volume balance situation in the animal.

Animals↗
PubMed1983

Activation of the tubuloglomerular feedback mechanism in dehydrated rats.

To study the influence of the tubuloglomerular feedback control (TGF) on the regulation of glomerular filtration rate (GFR) during dehydration, micropuncture experiments were performed on surface nephrons of dehydrated rats. Dehydration was achieved by withdrawal of food and water for 24 h. The urine flow rate decreased to 1.5 microliters/min (controls 2.9 microliters/min) and GFR decreased in these rats to 0.80 ml/min (controls 1.22). TGF was studied by two different micropuncture procedures. With the first technique the changes in proximal stop-flow pressure in response to changes of the late proximal microperfusion rate were measured. With this technique the perfusion rate necessary to induce a half maximal stop-flow pressure response, the turning point, was also determined. An increased TGF sensitivity was found in dehydrated rats, as indicated by increased stop-flow pressure responses (35 versus 26%) and decreased turning points (16 versus 21 nl/min). With the second micropuncture technique the single nephron GFR (SNGFR) was measured at distal and proximal tubular sites, in the same nephron. Distal SNGFR was decreased during dehydration to 32.2 nl/min, versus 42.7 nl/min in controls. A significant difference between paired SNGFR measurements in the same nephron was observed during dehydration, the proximal value being 5.3 nl/min higher than the distal, whereas this difference was not seen in control rats. This finding indicates that activation of the feedback mechanism takes place to reduce SNGFR. It is concluded that the decrease in whole kidney GFR is partly caused by the observed increase in feedback activity. The present results are also in agreement with our earlier hypothesis that the hydrostatic and oncotic pressure conditions within the interstitial space surrounding the macula densa cells modulate the sensitivity of the tubuloglomerular feedback mechanism.

Animals↗
PubMed1988

Subcutaneous interstitial fluid colloid osmotic pressure in dehydrated rats.

We collected interstitial fluid for measurement of colloid osmotic pressure (COPi) of normally hydrated and dehydrated rats with two methods: (1) saline-soaked nylon-wicks implanted in vivo for 1 h; and (2) the crossover method, i.e. titration with wicks pre-loaded with serial dilutions of rat plasma implanted post mortem for 15-20 min. All wicks were implanted in subcutis on the back. Dehydration was induced by injection of 40 mg furosemide followed by 24 h water deprivation. The saline-soaked wick method gave an average control COPi of 10.8 mmHg, 2-3 mmHg lower than the corresponding pressure obtained with the crossover method. This discrepancy between the methods increased to 10-11 mmHg in dehydrated animals, indicating that the saline-soaked wick method underestimates COPi even more during dehydration than during control conditions. The mean COPi of 22.8 mmHg (SD = 3.7, n = 9) obtained in dehydrated rats using the crossover method corresponds well with what is to be expected from the reduction in interstitial fluid volume. The present study suggests that the frequently used implantation period for saline-soaked wicks of 60 min should be prolonged to 90-120 min. It further shows that the rise in COPi is about 3 times more important than the fall in interstitial fluid hydrostatic pressure in restricting mobilization of interstitial fluid during dehydration.

Animals↗
PubMedDate not supplied

The effect of dehydration on parotid salivary gland function.

Dehydration is common in the elderly, and has been traditionally linked with salivary hypofunction. This study examined the effect of dehydration on parotid salivary flow rates. Twelve young and 12 older healthy subjects abstained from food and fluid intake for 24 hrs (dehydration) and then underwent i.v. rehydration proportional to the amount of weight lost. Unstimulated and stimulated parotid flow rates, weight, hematocrit and hemoglobin values were assessed at baseline and 24 hrs, and 1 hr after completion of rehydration. All subjects experienced decreases in weight and increases in hematocrit and hemoglobin during dehydration. I.v. fluids caused weight gain and decreased hematocrit and hemoglobin, demonstrating that subjects were metabolically rehydrated. During dehydration, unstimulated flow rates decreased in young (p < 0.001) and older (p < 0.001) subjects, and stimulated flow rates decreased in young (p > 0.05) and older (p = 0.03) subjects. While flow rates increased with rehydration, they remained lower than baseline levels. No age or gender differences were detected for salivary data. These findings suggest that dehydration may cause decreased parotid flow rates, independent of age in healthy adults.

Adult↗
PubMed2001

Sapid solutions and food intake in repeated dehydration and rehydration periods in rats.

In a previous report, it has been shown that water deprivation significantly affects the two-bottle taste preferences and one-bottle taste acceptance in rats when no food was available during tests. Since no food was available, the course of drinking was never interrupted by eating. Theoretically, if a rat faces a simultaneous choice between food and fluid, and if the course of drinking is interrupted by eating, these conditions might interfere with taste preferences, total fluid intake and eating in thirsty rats. The aims of the present experiments were: to ascertain whether food intake during both two-bottle preference and one-bottle acceptance tests in thirsty rats might be influenced by the palatability of the solutions; to verify whether the availability of food during tests influences taste preference and acceptance, and total fluid intake; to detect variations induced by dehydration on body weight and some plasma and urinary parameters that might interfere with food and fluid intake, taste preference and acceptance. Using naive rats, five groups of rats showing the same taste preferences for one of four prototypical tastes and water were selected. Then, both two-bottle preference (Expt 1) and one-bottle acceptance tests (Expt 2) were performed in rats deprived of water for either 12, 24, 36 or 48 h. The results showed that in both Expt 1 and Expt 2, inhibition of feeding and decrease of body weight during dehydration was very similar in all rats. The presence of food during the tests did not affect taste preference and acceptance. During Expt 1, after severe water deprivation (36 and 48 h), food intake was related to the palatability of the solution paired with water. When rats drank either NaCl or sucrose, they ate less food than rats drinking HCl, quinine, or water. In Expt 2, rats drinking NaCl solution as the only source of fluid ate significantly less food than all other groups. The intake of sucrose and/or NaCl solutions be may explained by two different post-ingestion effects (energetic and osmotic). Since rats drinking either sucrose or NaCl ate less food but drank more fluid, they had a significantly higher fluid/food intake ratio than that of rats who drank water, quinine, or HCl, who ate more food but drank less fluid. The increase of the fluid/food intake ratio in rats drinking sucrose or NaCl was directly correlated with the length of dehydration. Self-denial of food during dehydration may be responsible for overeating and overdrinking during the recovery period after tests. After dehydration lasting for 24 and 48 h, plasma [Na(+)], [protein], osmolality and haematocrit values increased but [K(+)] decreased. Urinary volume decreased but urinary [Na(+)] increased. These results are related to food and fluid intake, taste preference and acceptance after dehydration periods. Experimental Physiology (2001) 86.4, 489-498.

Animals↗
PubMed1994

The struggle to maintain hydration and osmoregulation in animals experiencing severe dehydration and rapid rehydration: the story of ruminants.

Ruminants in tropical and desert areas routinely experience cycles of severe dehydration and rapid rehydration. These animals can withstand severe dehydration (18-40% of initial body weight), which exceeds considerably the capacity of most monogastric mammals. This capacity is related to their ability to use, during the course of dehydration, their large water reservoir in the rumen, which contributes 50-70% of the total water loss. As rumen fluid is in approximate isotonicity with systemic fluid, the utilization of gut water during the course of dehydration involves a considerable load of sodium and potassium. Consequently, the effectiveness of utilization of rumen fluid during dehydration depends on the capacity of the kidney to 'desalt' the water absorbed from the gut and on maintenance of salivary flow to the rumen. Following rehydration, ruminants can imbibe their entire water deficit in one drinking and the entire amount ingested is first retained in the rumen. The rumen volume at this stage may exceed the extracellular fluid volume and the sudden drop in rumen osmolality creates a huge osmotic gradient (200-300 mosmol kg-1) between the rumen and systemic fluid. Ruminant animals are confronted at this stage by two opposing tasks, each of them of vital importance: (i) the need to prevent the osmotic hazard leading to water intoxication; and (ii) the need to retain the ingested water, so that it is not missing for the next dehydration cycle. The most prevalent view until recently was a theory which attributes an osmotic protective mechanism to the rumen wall. However, such a capacity has not yet been demonstrated and is challenged by contradictory observations that large amounts of water are absorbed from the rumen following rehydration. The view that is most consistent with available information is that gustatory-alimentary and hepatoportal signals regarding the presence of large amounts of water in the rumen and the absorption of water from the gut activate a range of homeostatic responses involved in fluid and sodium restitution. The efferent elements, presumably activated by the CNS, include: a dramatic increase in secretion of hypotonic saliva and, reciprocally, a dramatic drop in urine flow. The enhanced saliva secretion recycles a considerable portion of the water absorbed from the gut back to the rumen, which allows effective retention of water while avoiding the danger of osmotic threat to the red blood cells. The enhanced saliva secretion also drains large amounts of sodium and bicarbonate from the blood. Accompanying responses are marked retention of sodium and carbonic acid in the kidney.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Breast feeding and oral rehydration at home during diarrhoea to prevent dehydration.

In a case-control study we evaluated the role of maternal behaviour, as reflected in maintenance of breast feeding and the use of oral rehydration therapy (ORT) at home during acute diarrhoea, in preventing dehydration in infants and young children. A systematic 5% sample was taken of all children aged 1-35 months attending the treatment centre of the International Centre for Diarrhoeal Disease Research, Bangladesh, with acute watery diarrhoea of six days or less between August 1988 and September 1989. There were 285 children with moderate or severe dehydration as cases and 728 with no dehydration as controls in the study. In a multivariate analysis using a logistic regression model we showed that withdrawal of breast feeding during diarrhoea was associated with a five times higher risk of dehydration compared with continuation of breast feeding during diarrhoea at home. Lack of ORT with either complete formula or a salt and sugar solution at home was associated with 57% higher risk of dehydration compared with receipt of a reasonable amount of ORT after controlling for several confounders. The confounding variables--that is, lack of maternal education, history of vomiting, high stool frequency, young age and infection with Vibrio cholerae 01--were also shown to be risk factors of dehydration. Health education programmes should promote continued breast feeding and adequate oral rehydration therapy for infants with acute diarrhoea at home.

Bangladesh↗
PubMed1996

Case-control study of risk of dehydrating diarrhoea in infants in vulnerable period after full weaning.

OBJECTIVES: To investigate risk factors for dehydrating diarrhoea in infants, with special interest in the weaning period. DESIGN: Case-control study. SETTING: Metropolitan area of Porto Alegre, Brazil. SUBJECTS: Cases were 192 children aged 0-23 months hospitalised with acute diarrhoea and moderate to severe dehydration. Controls were 192 children matched for age and neighbourhood who did not have diarrhoea in the previous week. MAIN OUTCOME MEASURES: Associations between dehydrating diarrhoea and child's age, type of milk consumed, time since breast feeding stopped, and breast feeding status. RESULTS: In infants aged < 12 months the risk of dehydrating diarrhoea was significantly higher in the first 9 months of life (P < 0.001), and in those aged 12-23 months the risk was again greater in younger children (12-17 months) (P = 0.03). The type of milk consumed before start of diarrhoea episode was strongly associated with dehydration independent of socioeconomic, environmental, maternal reproductive, demographic, and health services factors. Compared with infants exclusively breast fed, bottle fed infants were at higher risk (odds ratio (95% confidence interval) for cow's milk 6.0 (1.8 to 19.8), for formula milk 6.9 (1.4 to 33.3)). Compared with those still breast feeding, children who stopped in the previous two months were more likely to develop dehydrating diarrhoea (odds ratio 8.4 (2.4 to 29.6)). This risk decreased with time since breast feeding stopped. CONCLUSION: These results confirm the protective effect of breast feeding and suggest there is a vulnerable period soon after breast feeding is stopped, which may be of relevance for developing preventive strategies.

Acute Disease↗
PubMed1999

Effects of dehydration on exercise performance.

Dehydration refers both to hypohydration (dehydration induced prior to exercise) and to exercise-induced dehydration (dehydration that develops during exercise). The latter reduces aerobic endurance performance and results in increased body temperature, heart rate, perceived exertion, and possibly increased reliance on carbohydrate as a fuel source. Although the negative effects of exercise-induced dehydration on exercise performance were clearly demonstrated in the 1940s, athletes continued to believe for years thereafter that fluid intake was not beneficial. More recently, negative effects on performance have been demonstrated with modest (<2%) dehydration, and these effects are exacerbated when the exercise is performed in a hot environment. The effects of hypohydration may vary, depending on whether it is induced through diuretics or sauna exposure, which substantially reduce plasma volume, or prior exercise, which has much less impact on plasma volume. Hypohydration reduces aerobic endurance, but its effects on muscle strength and endurance are not consistent and require further study.

Body Temperature↗