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FLUID REPLACEMENT AND HEAT STRESS Fluid Replacement and Heat Stress, 1993 Pp. 215-227. Washington, D.C. National Academy Press 16 Changes in Plasma Volume During Heat Exposure in Young and Older Men Suzanne M. Fortney1 and Elizabeth Miescher INTRODUCTION Dilation of blood vessels during exposure to high ambient heat was noted in 1795 by a physician accompanying British soldiers during their occupation of colonial India. The observations of this physician were quoted in 1955 in a review article on heat acclimation, “In passing from a cold to a hot climate the first thing that occurs is the effect produced by the simple increase of heat on the human frame. Expansion of the fluids and consequent fullness of the vessels is constantly observed to take place.” (Bass et al., 1955, p. 323). This farsighted physician denounced the concept that European peoples could not safely perform exertions in the heat and said that “ while exertions of a single day have often been harmful, bad effects from the greatest exertions in the hottest weather were extremely rare after the campaign had been continued for a few days.” (Bass et al., 1955, p. 323). Hemodilution after a sudden increase in climatic temperature was reported by Barcroft in his fellow passengers during a voyage from England to Peru (Barcroft et al., 1922). Glickman et al. (1941) found that heat- 1 Suzanne M. Forntney, NASA Johnson Space Center, Mail Code SD/5, Houston, TX 77058.
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FLUID REPLACEMENT AND HEAT STRESS induced hemodilution occurs within the first few hours of a controlled laboratory heat exposure. The time course of the changes in plasma volume of men quietly sitting in the heat were described in detail by Bass and Henschel (1956). The hemodilution usually is weak (less than a 5% increase in plasma volume) and transient. Without fluid replacement, it disappears after approximately 30-45 min. It may not appear in subjects who have been dehydrated before the heat exposure (Sawka et al., 1984) or in subjects who have been anesthetized or have suffered transection of the spinal cord below the level of the medulla (Bass and Henschel, 1956). The transient increase in plasma volume during acute heat exposure provides a fluid reservoir for sweat production and attenuates the decrease in central blood volume as sweating continues and as blood flow is redistributed from the core to the skin. Without this initial increase of plasma volume, body temperature would increase more rapidly and heat tolerance would be reduced. With adequate fluid and electrolyte replacement, the expansion of plasma volume persists and plays a key role in reducing cardiovascular strain during the early stages of heat acclimation (Wyndham et al., 1968). Figure 16-1 illustrates the dynamic plasma volume responses of hydrated healthy young subjects to an acute 3-h heat exposure without fluid replacement. The plasma volume responses can be divided into three stages: initial hemodilution (stage 1), rapid hemoconcentration (stage 2), and slower hemoconcentration (stage 3). Several theories have been offered to explain these plasma volume responses. FIGURE 16-1 Pattern of plasma volume response of healthy young men during a 3-h passive heat exposure. See text for explanation of the stages of plasma volume response.
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FLUID REPLACEMENT AND HEAT STRESS Stage 1 The initial increase in plasma volume, which occurs within minutes of heat exposure, is most likely due to a direct effect of heat, which causes venodilation. Dilation of blood vessels was first noted by Jackson (1795). Later, Bass and Henschel (1956) theorized that expansion of the vascular bed without an increase in blood volume results in the rapid displacement of fluids from the interstitial compartment to the plasma. More recently, Harrison (1986) elaborated on this theory. According to Harrison, acute heat exposure initially results in venodilation without an accompanying vasodilation. As the veins dilate, pressure in the venous end of the capillaries decreases, reducing capillary filtration and increasing fluid reabsorption. Plasma volume expansion occurs rapidly and continues until the balance between the arteriolar and venous tone is restored or reversed by vasodilation. Stage 2 Active sweating and cutaneous vasodilation begin after approximately 4-6 min of heat exposure, depending on changes in core and skin temperatures, the hydration state, and the degree of heat acclimation of the subject (Nadel, 1985). As the sweat rate increases, the plasma volume decreases, since sweat is formed from fluid in the capillaries that perfuse the sweat glands. Cutaneous vasodilation has opposing effects on plasma volume. Vasodilation restores and possibly reverses the balance of arteriolar to venous constriction. This slows and possibly reverses the reabsorption of extracellular fluid across the cutaneous capillaries. However, a sudden increase in cutaneous perfusion stimulates lymph flow. According to Wasserman and Mayerson (1952), and later Senay (1970), a sudden increase in cutaneous perfusion increases protein transport from the lymph vessels to the vascular compartment. As the plasma protein content increases, the water-binding capacity of the plasma increases in a ratio of approximately 15 ml of serum water for each 1 g of protein added to the plasma (Rocker et al., 1976). Therefore, the initial effect of vasodilation may be to further increase plasma volume (this may contribute to the stage 1 hemodilution). However, after the priming action on lymph protein is completed, vasodilation increases the capillary surface area for fluid exchange, counteracts the effect of the venodilation, and causes a rapid decrease in the plasma volume.
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FLUID REPLACEMENT AND HEAT STRESS Stage 3 The rapid decrease in plasma volume during stage 2 compromises cardiac filling, stimulating cardiopulmonary volume receptors, which attenuate the vasodilatory reflex and inhibit sweating (Nadel, 1985). Stimulation of the cardiopulmonary receptors also stimulates secretion of antidiuretic hormone (ADH) (Moore, 1971; Segar and Moore, 1968), which reduces free-water clearance and conserves plasma water (Khokhar et al., 1976). ADH may also affect the sweat glands directly, to inhibit sweating (Nadel, 1985). When central blood volume is decreased, arterial blood pressure may fall, stimulating the sinoaortic baroreceptors and thereby causing a redistribution of blood flow away from splanchnic vascular beds (Abboud et al., 1979). This reduction in splanchnic blood volume may be important in conserving plasma water. Horowitz (1984) has demonstrated the importance of restricting splanchnic perfusion for conserving body fluids by comparing the heat stress responses of various species of rats. Since the splanchnic capillaries are among the most porous capillaries of the body to proteins and fluids, a species that can significantly reduce splanchnic blood flow will be most successful in conserving plasma volume and surviving during severe water restriction. Horowitz (1984) reported that the desert rat species Psammomys obesus withstood dehydration for over 48 h at least partly because of its ability to almost completely reduce splanchnic vascular permeability. If such findings can be extrapolated to man, then, reducing splanchnic blood flow during heat exposure is a positive step toward conserving plasma proteins and water. The increase in plasma osmolality also reduces the rate of plasma volume loss during heat exposure. Sweat is a hypotonic secretion, and therefore, as sweat production continues, the plasma becomes more and more hypertonic. This increase in plasma osmolality inhibits sweating (Fortney et al., 1984) and attenuates the rate of water loss from the vascular compartment. EFFECT OF AGE ON BODY FLUIDS Aging has been defined as an inability to adapt to changing environmental conditions (Piscopo, 1985). Several investigators (Leaf, 1984; Miller, 1987; Phillips et al., 1984) have observed that elderly individuals have difficulty maintaining body fluid balance. Physiological alterations in water and sodium regulation result in an increased danger of both dehydration and overhydration in the elderly (Crowe et al., 1987). Leaf (1984) observed that nursing home patients have an increased susceptibility to dehydration, and
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FLUID REPLACEMENT AND HEAT STRESS Spangler et al. (1984) reported that as many as 25% of nursing home patients may be chronically dehydrated. However, these findings do not prove that there is an age-related change in fluid regulation, since the results may have been complicated by a restricted access to fluids or by the prevalent use of medications that alter body fluids. The extent of dehydration in healthy, active older individuals has been debated. One study by Phillips et al. (1984) reported normal hydration in elderly subjects, while another study by the same group found elevated baseline sodium concentrations and plasma osmolalities in healthy older subjects (Crowe et al., 1987). Miller (1987) recently reviewed potential mechanisms for the occurrence of body fluid disturbances during the normal aging process. Lindeman et al. (1960) found that renal concentrating capacity in response to dehydration decreases with age, becoming evident between approximately 45 and 50 years of age. Rowe et al. (1976) substantiated this observation in men after 12 h of dehydration. The regulation of plasma sodium also appears to be affected by the normal aging process. Epstein and Hollenberg (1976) studied the renal response to sodium restriction in individuals from 18 to 76 years of age. Renal sodium excretion decreased by 50% after 18 h in subjects younger than 30 years, after 24 h in subjects between 30 and 60 years of age, and after 31 h in subjects older than 60. Impaired fluid and electrolyte balance in the elderly also may be due to an inability to detect changes in body hydration. Phillips et al. (1984) compared thirst perception between a group of young men and a group of men 67 to 75 years of age. The subjects were dehydrated for approximately 24 h, until both groups had a similar decrease in body weight. Following dehydration, the older subjects were not as thirsty as the younger subjects, based on their responses to a visual analog thirst scale, despite a greater increase in plasma osmolality. Increased secretion of ADH in response to osmotic stimuli and decreased secretion in response to hypovolemic stimuli occur with aging (Bevilacqua et al., 1987; Ledingham et al., 1987). During water restriction, Phillips et al. (1984) found a greater increase in ADH in older subjects, despite a similar loss of plasma volume. Helderman et al. (1978) infused hypertonic saline into young and older individuals and found a greater release of ADH into the plasma of older subjects compared with that in the plasma of the young subjects. This increased responsiveness of ADH is believed to compensate for the reduced sensitivity of the kidneys of older subjects to ADH. Baseline concentrations of atrial natriuretic factor (ANF) increase with increasing age (Wambach and Kaufmann, 1988; Yamasaki et al., 1988). The consequences of these changes in ANF regulation on body fluid responses
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FLUID REPLACEMENT AND HEAT STRESS are not known. Specific high-affinity binding sites for ANF have been found in many areas of the body, including the kidneys, the adrenal gland, smooth muscles of blood vessels, and the hypothalamus. Increases in plasma ANF have been shown to inhibit aldosterone production in the adrenal zona glomerulosa (Laragh and Atlas, 1988) and thus might contribute to the altered sodium regulation that occurs with aging. ANF also has an antagonist role to many of the actions of angiotensin II. It inhibits water intake induced by the administration of angiotensin II to the central nervous system. It has the potential to block the formation and secretion of both ADH and angiotensin II (Kramer, 1988; Laragh and Atlas, 1988), and it modulates sympathetic activity by inhibiting epinephrine release and reducing baroreceptor responsiveness. We are just beginning to understand the role of ANF in the regulation of body fluids and electrolytes. HYPOTHESIS On the basis of two facts, that (1) acute heat exposure provokes rapid changes in body fluids and (2) older individuals have an impaired ability to regulate body fluids, we hypothesized that older subjects would have difficulty maintaining plasma volume and osmolality during prolonged heat exposure. By comparing the time courses of body fluid responses to heat exposure of young and older individuals, the mechanisms for altered body fluid regulation in older healthy men may become apparent. Study Description The experiment outlined below is described in more detail in Miescher and Fortney (1989). The plasma volume, protein, and osmolality responses of six young men (age, 24-29 years) were compared with those of five older men (age, 61-67 years). The subjects were normotensive, non-smokers who were not taking any medications. The subjects had an average level of aerobic fitness for their age (Astrand, 1960). Each subject had an active life-style but did not participate in routine exercise training or sports. The two groups were matched for height, body surface area, and surface area/weight ratio (Table 16-1). The tests were performed in the winter months in Baltimore. The subjects reported to our laboratory at 8 a.m. after a light breakfast and after
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FLUID REPLACEMENT AND HEAT STRESS Table 16-1 Age and anthropometric characteristics of older and younger mena Subjects Age (yr) Weight (kg) SAb (m2) SA/Wt (m2/kg) VO2maxc (ml/kg/min) Older men (n = 5) 64.0d 73.0 1.9 0.026 38.8e ±SEM ± 1.0 ± 2.3 ± 0.04 ± 0.000 ± 2.3 Younger men (n = 6) 26.0 69.3 1.8 0.027 52.1 ±SEM ± 0.7 ± 3.1 ± 0.05 ± 0.000 ± 2.2 a All values are mean ±SEM. b Surface area. c maximal oxygen consumption. d p < 0.05, older versus younger. e p < 0.01, older versus younger. abstaining from caffeine beverages for at least 10 h. They were given 200 ml of water to drink when they arrived. They changed into shorts and were provided with a rectal thermistor, an Exersentry heart rate monitor, and venous catheter. They rested for 30 min in a cool room (25°C) before moving to a hot, dry heat chamber (45°C, 25%) for 180 min of heat exposure without fluid replacement. The subjects reclined to a sitting position in a webbed chair, and blood samples were drawn by a free-flowing technique just before they entered the heat chamber and every 30 min during the heat exposure. From each blood sample, hematocrit (microhematocrit technique), hemoglobin concentration (cyanomethemoglobin method), and total protein concentration (refractometry) were determined. Also, measurements of body weight, rectal temperature, and heart rate were obtained at 30-min intervals. Following 30 min of baseline rest, the older men had significantly lower rectal temperatures (Figure 16-2) and higher plasma osmolalities, despite similar hematocrits, hemoglobin concentrations, and plasma protein concentrations (Figure 16-3). During the 180-min heat challenge, rectal temperatures rose in both groups, but the rise was significantly greater in the older men ( Figure 16-2). The decreases in body mean weight were similar in both groups (1.52% in the older subjects and 1.55% in the younger subjects), yet the change in xxxxxx
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FLUID REPLACEMENT AND HEAT STRESS FIGURE 16-2 Rectal temperature responses and changes in rectal temperature for young (n = 6) and older (n = 5) men during a 3-h passive heat exposure. Values are the means ± standard errors of the mean.
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FLUID REPLACEMENT AND HEAT STRESS FIGURE 16-3 Plasma osmolality, percent changes in plasma volume, and absolute changes in plasma proteins in young (n = 6) and older (n = 5) men during a passive 3-h heat exposure. Values shown are the means ± standard errors of the mean.
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FLUID REPLACEMENT AND HEAT STRESS plasma volume in the older subjects was significantly greater during the heat exposure (Figure 16-3). Every young subject hemodiluted during the first 30 min of heat exposure, while only one older subject hemodiluted. The increases in plasma osmolality were similar in both groups during the heat exposure, although the older group maintained significantly higher plasma values. The total protein concentration increased or remained the same during the initial 90 min of heat exposure; it then stabilized in the younger men and decreased in the older men. DISCUSSION Compared with the younger men, the older men in this study showed an impaired ability to maintain their core temperature and plasma volume during a passive heat challenge. By carefully examining the time course of the changes in body fluids during the 180-min heat exposure, we may be able to identify potential causes for these age-related differences. The most striking difference in the plasma responses of the two groups was the lack of hemodilution during the first 30 min of heat exposure in the older men. Since hemodilution is thought to be due to a transient imbalance of venous and arteriolar tone (Harrison, 1986), this finding suggests that with increasing age, the veins become less responsive to environmental changes. Changes in the structure of cutaneous veins might increase wall stiffness or increased sympathetic tone might prevent venous relaxation in response to body heating as part of an overall change in the autonomic nervous function. Differences in the fitness levels of the two groups may have contributed to the heat response differences. The maximum oxygen consumption of the older men was significantly lower than that of the younger men, as would be expected in an older population with a similar life-style (Astrand, 1960). Although we did not specifically assess daily energy requirements, neither group participated in regular exercise or had jobs that required hard physical labor. If a significant training effect had been present, then a more sensitive sweating response would have maintained lower temperatures in the trained group. The absolute rectal temperatures were not significantly different after the first 30 min of heat exposure, and the total body weight loss of the two groups was similar. Therefore it is unlikely that the differences in body fluids in this study were due to a training difference. Our finding of elevated plasma osmolality in healthy older subjects under resting conditions agrees with the findings of Crowe et al. (1987). However, it is unclear whether the higher osmolalities indicate that the older men were dehydrated or whether they resulted from an age-related
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FLUID REPLACEMENT AND HEAT STRESS difference in sodium regulation. Baseline dehydration could explain the failure of the older men to hemodilute during acute heat exposure (Sawka et al., 1984). However, if the older men were dehydrated, then they should have had higher resting hematocrits and plasma protein concentrations. The similar rate of loss of plasma volume during the final 2 h of heat exposure suggests that the mechanisms responsible for fluid shifts during these stages of heat exposure were not altered by age. The total body sweat loss was similar for the two groups and, therefore, probably contributed equally to the hemoconcentration response. However, the greater loss of plasma proteins in the older men during the final hour of heat exposure suggests that older men may have greater difficulty restricting splanchnic blood flow during prolonged heat exposure (Horowitz, 1984). If the heat exposure had been extended in this study, greater differences in plasma volume might have occurred. We conclude that a difference exists in the ability of young and older healthy men to maintain plasma volume during passive heat exposure. This difference may contribute to the greater rate of rise in core temperature in the older group and, therefore, might affect heat tolerance. Our findings suggest that future studies should focus on age-related changes in vascular responsiveness to uncover mechanisms of greater heat strain in the elderly. REFERENCES Abboud, F.M., D.L. Eckberg, U.J. Johannsen, and A.L. Mark. 1979 Carotid and cardiopulmonary baroreceptor control of splanchnic and forearm vascular resistance during venous pooling in man. J. Physiol. 286:173-184. Astrand, I. 1960 Aerobic work capacity in men and women with special reference to age. Acta Physiol. Scand. 49 Suppl. 169:92. Barcroft, J., J.C. Meahins, H.W. Davis, J. Scott, and W.J. Fetter. 1922 The relation of the external temperature to blood volume. Phi Trans. R. Soc. London, Ser. B 211:455-464. Bass, D.E., and A. Henschel. 1956 Responses of body fluid compartments to heat and cold. Physiol. Rev. 3:128-144. Bass, D.E., C.R. Kleeman, M. Quinn, A. Henschel, and A.H. Hegnauer. 1955 Mechanisms of acclimatization to heat in man. Medicine 34:323-380. Bevilacqua, M., G. Norbiato, E. Chebat, U. Raggi, P. Cavaiani, R. Guzzetti, and P. Bertora. 1987 Osmotic and nonosmotic control of vasopressin release in the elderly: effect of metoclopramide. J. Clin. Endocrinol. Metab. 65:1243-1247. Crowe, M.J., M.L. Forsling, B.J. Rolls, P.A. Phillips, J.G.G. Ledingham, and R.F. Smith. 1987 Altered water excretion in healthy elderly men. Age and Aging 16:285-293. Epstein, M., and N.K. Hollenberg. 1976 Age as a determinant of renal sodium conservation in normal man. J. Lab. Clin. Med. 87:411-417.
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FLUID REPLACEMENT AND HEAT STRESS Fortney, S.M., C.B. Wenger, J.R. Bove, and E.R. Nadel. 1984 Effect of hyperosmolality on control of blood flow and sweating. J. Appl. Physiol. 57:1688-1695. Glickman, N., F.K. Hick, R.W. Keeton, and M.M. Montgomery. 1941 Blood volume change in men exposed to hot environmental conditions for a few hours. Am. J. Physiol. 134:165-176. Harrison, M.H. 1986 Heat and exercise. Effects on blood volume. Sports Med. 3:214-223. Helderman, J.H., R.E. Vestal, J.W. Rowe, J.D. Tobin, R. Andres, and G.L. Robertson. 1978 The response of arginine vasopressin to intravenous ethanol and hypertonic saline in man: the impact of aging. J. Gerontol. 33:39-47. Horowitz, M. 1984 Thermal dehydration and plasma volume regulation: mechanisms and control. Pp. 389-394 in Thermal Physiology, J.R.S. Hales, ed. Raven, New York. Jackson, R.A. 1795 A Treatise on the Fevers of Jamaica. Robert Campbell, Philadelphia. 19 pp. Khokhar, A.M., J.D. Slater, M.L. Forsling, and N.N. Payne. 1976 Effect of vasopressin on plasma volume and renin release in man. Clin. Sci. Mol. Med. 50:415-424. Kramer, J.H. 1988 Atrial natriuretic hormones. Gen. Pharmacol. 19:747-753. Laragh, J.H., and S.A. Atlas. 1988 Atrial natriuretic hormone: a regulator of blood pressure and volume homeostasis. Kidney Int. Suppl. 25:S64-S71. Leaf, A. 1984 Dehydration in elderly (editorial). N. Engl. J. Med. 311:791-792. Ledingham, J.G., M.J. Crowe, M.L. Forsling, P.A. Phillips, and B.J. Rolls. 1987 Effects of aging on vasopressin secretion, water excretion, and thirst in man. Kidney Int. Suppl. 21:S90-S92. Lindeman, R.K., H.C. Van Buren, and L.G. Raisz. 1960 Osmolar renal concentrating ability in healthy young men and hospitalized patients without renal disease. N. Engl. J. Med. 262:1306-1314. Miescher, E., and S.M. Fortney. 1989 Responses to dehydration and rehydration during heat exposure in young and older men. Am. J. Physiol. 257:R1050-R1057. Miller, M. 1987 Fluid and electrolyte balance in the elderly. Geriatrics 42:65-76. Moore, W.W. 1971 Antidiuretic hormone levels in normal subjects. Fed. Proc. Fed. Am. Soc. Exp. Biol. 30:1387-1394. Nadel, E.R. 1985 Recent advances in temperature regulation during exercise in humans Fed. Proc. Fed. Am. Soc. Exp. Biol. 44:2286-2292. Phillips, P.A., B.J. Rolls, J.G. Ledingham, M.L. Forsling, J.J. Morton, M.J. Crowe and L.Wollner. 1984 Reduced thirst after water deprivation in healthy elderly men. N. Engl. J. Med. 311:753-759. Piscopo, J. 1985 Fitness and Aging. John Wiley & Sons, New York. 462 pp. Rocker, L., K. Kirsch, J. Wicke, and H. Stoboy. 1976 Role of proteins in the regulation of plasma volume during heat stress and exercise. Isr. J. Med. Sci. 12:840-843.
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FLUID REPLACEMENT AND HEAT STRESS Rowe, J.W., N.W. Shock, and R.A. DeFronzo. 1976 The influence of age on the renal response to water deprivation in man. Nephron 17:270-278. Sawka, M.N., R.P. Francesconi, N.A. Pimental, and K.B. Pandolf. 1984 Hydration and vascular fluid shifts during exercise in the heat. J. Appl. Physiol. 56:91-96. Segar, W.E., and W.W. Moore. 1968 The regulation of antidiuretic hormone release in man. 1. Effects of change in position and ambient temperature on blood ADH levels J. Clin. Invest. 47:2143-2151. Senay, L.C., Jr. 1970 Movement of water, protein and crystalloids between vascular and extravascular compartments in heat-exposed men during dehydration and following limited relief of dehydration. J. Physiol. 210:617-635. Spangler, P.F., T.R. Risley, and D.D. Bilyew. 1984 The management of dehydration and incontinence in nonambulatory geriatric patients. J. Appl. Behav. Anal. 17:397-401. Wambach, G., and W. Kaufmann. 1988 Standardization of plasma determination of atrial natriuretic peptide (ANP). Z. Kardiol. 77 Suppl. 2:31-35. Wasserman, K., and H.S. Mayerson. 1952 Mechanism of plasma protein changes following saline infusions. Am. J. Physiol. 170:1-10. Wyndham, C.H., A.J. Benade, C.G. Williams, N.B. Strydom, A. Goldin, and A.J. Heyns. 1968 Changes in central circulation and body fluid spaces during acclimatization to heat. J. Appl. Physiol. 25:586-593. Yamasaki, Y., T. Nishiuchi, A. Kojima, H. Saito, and S. Saito. 1988 Effects of an oral water load and intravenous administration of isotonic glucose, hypertonic saline, mannitol and furosemide on the release of atrial natriuretic peptide in men. Acta Endocrinol. 119:269-276.
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