Cardiac design and pressure-volume characteristics of the left ventricle in normotensive (WKY) and hypertensive (SHR) rats after various dietary sodium treatments

Normotensive (WKY) and hypertensive rats (SHR) from 5 to 13-14 weeks of age were given 'low' (LNa; 0.5 mmol Na 100 g-1 food), 'control' (CNa; 5 or 12 mmol), 'high' (HNa; 50 mmol) and in SHR also 'medium low' (mLNa; 2 mmol) and 'very high' (vHNa; 120 mmol) sodium diets, to explore how such 240-fold variations in Na intake affect cardiac design. This was assessed in isolated perfused, temporarily-arrested hearts by recordings of left ventricular (LV) diastolic pressure-volume relationships (P/V), LV and RV weights, and by calculations of the ratio between LV wall thickness and internal radius (w/ri), after in vivo recordings of awake mean arterial pressure (MAP) and heart rate (HR). In WKY, where MAP was the same in all diet groups, the HNa group showed an increased w/ri due to a 20% reduction of LV diastolic volume, with signs of reduced wall compliance compared with CNa. The LNa WKY showed less marked changes in the same direction. In the SHR LNa group, where MAP was lowered about 20 mmHg, LV diastolic volume was reduced nearly 20% at a modest w/ri increase, while HNa and Cna SHR had equal MAP, LV weights, P/V and w/ri relationships. However, in vHNa SHR, where MAP was elevated about 25 mmHg, the LV showed a mainly eccentric hypertrophy with 15% increase of diastolic volume at a slight increase of w/ri. These differentiated, and in WKY and SHR partially differing structural cardiac adaptations consequent to changes in Na intake, can hardly be ascribed only to the respective pre- and afterload alterations, suggesting that also altered neuro-hormonal profiles may have contributed with 'trophic' influences.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium appetite as well as 24-h variations of fluid balance, mean arterial pressure and heart rate in spontaneously hypertensive (SHR) and normotensive (WKY) rats, when on various sodium diets

Young SHR and WKY rats were compared, first, concerning sodium (Na) appetite during 'rest', mild social stress and ACTH injections, second, concerning the diurnal patterns of water intake, urine output, mean arterial pressure (MAP) and heart rate (HR) while on various Na diets: 0.5 mmol Na(LNa), 5 or 12-13 mmol Na (CNa), 50 (HNa) or 120 mmol Na (vHNa) per 100 g food. Sodium appetite and water intake were about 50% higher in SHR than in WKY (4-4.5 vs 2.5-3 mmol Na per 100 g body wt day-1). It was modestly increased by both social stress and ACTH, and more so in WKY, thereby approaching that in SHR. Concerning the various Na diets and their influences, daytime resting MAP was modestly lowered in LNaSHR and slightly increased in vHNaSHR compared with CNaSHR but largely equal in all WKY groups. Food-water consumption was concentrated to the active night period, but even high Na-water intakes caused no signs of sustained hypervolaemia, because each intake bout was in both SHR and WKY eliminated by urine within 30-40 min. However, particularly the vHNa diet in SHR also increased the frequency of drinking, and each bout caused transient, evidently neurogenic MAP and HR increases which occurred too rapidly to be consequences of blood volume expansion. As a result, the diurnal MAP-HR patterns in SHR varied markedly with the Na diets, in vHNa group resulting in considerably raised average diurnal MAP levels even though resting daytime MAP was here nearly the same as in CNaSHR. These findings illustrate how largely continuous diurnal recordings are needed to judge correctly the relationships between, for example, Na intake, volume equilibrium and MAP. Finally, the relevance of these results in rats for also judging the control of Na balance in man is discussed.     

Effects of high and low sodium diets on the resistance vessels and their adrenergic vasoconstrictor fibre control in normotensive (WKY) and hypertensive (SHR) rats

As part of our studies in normotensive (WKY) and hypertensive (SHR) rats concerning the cardiovascular effects of 240-fold variations in sodium (Na) intake, the present experiments explore how vascular design, smooth-muscle sensitivity to noradrenaline and adrenergic vasoconstrictor fibre function are affected. In vitro comparisons were performed on pair-perfused hindquarter vascular beds and on paired small mesenteric arteries (diameter 150-200 micron), using a two-vessel Mulvany-Halpern myograph. Preparations were taken from WKY and SHR which between 5 and 12-13 weeks of age were on 'low' (LNa, 0.5), 'control' (CNa, 5), 'high' (HNa, 50) or 'very high' (vHNa, 120 mmol Na 100 g-1 food) sodium diets. Structural vascular adaptation occurred only when arterial pressure was altered (only in LNa SHR). In both preparations smooth-muscle sensitivity and dose-response curves to noradrenaline remained unaffected by the Na diets. However, in both LNa groups the frequency-response curves to vasoconstrictor fibre stimulation in the small arteries were displaced to the right of the CNa one, with generally attenuated responses, while the curves of particularly the vHNa arteries were displaced to the left, with enhanced responses. Inhibition of NaKATPase by ouabain particularly enhanced the neurogenic responses, but to similar extents in all Na groups. Thus, low sodium intake apparently reduces the transmitter release/impulse in adrenergic neurons, while it increases the transmitter stores. High sodium intake has the opposite effects. These adaptations of adrenergic neuronal function may be one of the most important long-term consequences of altered sodium intake.     

Electrophysiological and mechanical characteristics of isolated hearts from spontaneously hypertensive (SHR) and normotensive (WKY) rats on very high- and low-sodium diets

Electrophysiological, mechanical, dimensional and coronary flow characteristics were studied on papillary strips and on isolated hearts, from spontaneously hypertensive (SHR) and normotensive (WKY) rats respectively, which from 5 to 15 weeks of age had been on either 'low' (LNa, 0.5 mmol 100 g-1 food), control (CNa, 5) 'high' (HNa, 50) or 'very high' (vHNa, 120) sodium diets. With respect to cardiac electrophysiological characteristics, contractility, and maximal stroke volume capacity only minor, if any, differences were observed between the various Na diet groups, both in WKY and SHR. This is in accordance with our earlier findings concerning vascular smooth muscle, where a largely unchanged sensitivity and responsiveness to, for example, noradrenaline was noted. Further, only to the extent that the various Na diets had also caused changes in average blood pressure levels, adaptations of cardiac and coronary resistance vessel design were observed, in general agreement with our earlier findings in other preparations and experimental designs. The largely unaffected functional characteristics of cardiac as well as vascular effector cells, despite 240-fold long-term variations in sodium intake, are in sharp contrast to the marked changes that have been shown to affect the adrenergic nerves, as here chronic low-Na intakes cause reductions of transmitter release/impulse, and vice versa at high Na intakes. This latter type of change seems to be by far the most important functional deviation affecting cardiovascular control during long-term alterations of sodium intake, as it can markedly affect both cardiac and vascular influences on haemodynamics, even though the respective effector functions seem to be surprisingly little influenced directly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood pressure and heart rate responses to mental stress in spontaneously hypertensive (SHB) and normotensive (WKY) rats on various sodium diets

Normotensive (WKY) and hypertensive rats (SHR) were, from 5 to 12 weeks of age, given 'low' (LNa), 'control' and 'high' (HNa) Na diets (0.5, 5 and 50 mmol X 100 g-1 food, respectively, during weekly recordings of body weight, conscious indirect systolic blood pressure (SBP) and heart rate (HR). During the last week, mean arterial pressure (MAP) and HR responses to standardized stress stimuli (air jet) were recorded before and after sequential cardiac nerve blockade. While resting, SBP was about equal in all WKY groups, but it was significantly reduced in SHR-LNa (152 mmHg versus 174 and 178 mmHg in SHR controls and HNa; P less than 0.05). In both LNa groups HR was elevated nearly 25% compared with controls, being in SHR 513 versus 419 bpm (P less than 0.01) and in WKY 489 versus 393 bpm (P less than 0.01). Cardiac nerve blockade indicated that this HR elevation was about equally due to elevations of sympathetic activity and 'intrinsic' pacemaker activity. SHR-LNa also showed attenuated MAP elevations to acute mental stress. There were, however, no significant differences between groups concerning haematocrit or plasma Na-K levels. The results suggest that SHR have a greater salt requirement than WKY, as Na restriction to one-tenth of normal led to a considerable MAP reduction in SHR despite compensatory sympathetic activation, and also to attenuated pressor responses to mental stress. Further, the cardiovascular effects in SHR were much more extensive when on a low-Na diet than when Na intake was increased tenfold above normal.     

Differential haemodynamic effects of atrial natriuretic peptide (ANP) in normotensive and spontaneously hypertensive rats

Central haemodynamic parameters and cardiac performance were measured in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) control rats after a 10-min infusion of rat ANP (103-125), 1 micrograms kg-1 min-1. Mean Arterial blood pressure (MAP) decreased by approximately 10% in both groups of rats. Heart rate (HR) increased slightly in both strains during the infusion. In the normotensive group the fall in MAP was due to a reduction in cardiac output (CO) while in the SHR there was a decrease in CO as well as in total peripheral resistance (TPR). The ANP infusion also reduced central blood volume (CBV) and stroke volume (SV) in both groups of rats. The reduction in CBV and CO was significantly more pronounced in the WKY strain. Left ventricular end diastolic pressure (LVEDP) and cardiac contractility (dP/dt) did not change while central venous pressure (CVP) was slightly decreased in the WKY group as a result of the ANP infusion. We conclude that ANP reduces MAP in normotensive animals by a reduction in CO. In the SHR a reduction in TPR also contributes to the fall in MAP. Atrial natriuretic peptide did not exert any negative inotropic effects, but the reduction of CO was due to an increased venous compliance.     

Blood pressure and heart rate responses to mental stress in spontaneously hypertensive (SHR) and normotensive (WKY) rats on various sodium diets

Normotensive (WKY) and hypertensive rats (SHR) were, from 5 to 12 weeks of age, given ‘low’ (LNa), ‘control’ and ‘high’ (HNa) Na diets (0.5, 5 and 50 mmol-100 g^-1 food, respectively, during weekly recordings of body weight, conscious indirect systolic blood pressure (SBP) and heart rate (HR). During the last week, mean arterial pressure (MAP) and HR responses to standardized stress stimuli (air jet) were recorded before and after sequential cardiac nerve blockade. While resting, SBP was about equal in all WKY groups, but it was significantly reduced in SHR-LNa (152 mmHg versus 174 and 178 mmHg in SHR controls and HNa; P < 0.05). In both LNa groups HR was elevated nearly 25% compared with controls, being in SHR 513 versus 419 bpm (P < 0.01) and in WKY 489 versus 393 bpm (P < 0.01). Cardiac nerve blockade indicated that this HR elevation was about equally due to elevations of sympathetic activity and ‘intrinsic’ pacemaker activity. SHR-LNa also showed attenuated MAP elevations to acute mental stress. There were, however, no significant differences between groups concerning haematocrit or plasma Na-K levels. The results suggest that SHR have a greater salt requirement than WKY, as Na restriction to one-tenth of normal led to a considerable MAP reduction in SHR despite compensatory sympathetic activation, and also to attenuated pressor responses to mental stress. Further, the cardiovascular effects in SHR were much more extensive when on a low-Na diet than when Na intake was increased tenfold above normal.     

Central haemodynamics during morphine abstinence in anaesthetized rats

Central haemodynamics were studied in one group of morphine-dependent rats, and in a non-dependent control group. before and after administration of repeated bolus doses of naloxone. Dependence was induced by s.c. morphine pellet implantations. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO) and mean transit time (MTT) were measured in the conscious state, after induction of chloralose anaesthesia and after the administration of naloxone (0.005, 0.05, 0.5 and5 mg kg 1 i.v.). Total peripheral resistance (TPR), stroke volume (SV) and central blood volume (CBV) were subsequently calculated. The haemodynamic variables did not differ significantly in the conscious state, except for a lower SV, when compared with the non-dependent control group. However, in response to anaesthesia the dependent rats exhibited a greater fall in MAP, mainly due to a TPR decrease. Naloxone elicited a marked increase in MAP in the morphine-dependent group, which was mainly caused by an increase in TPR. Naloxone induced no significant change compared with the control group in CO and CBV, while SV increased concomitantly with a lowered HR after naloxone in the morphine-dependent group. These results suggest that the withdrawal hypertension during morphine abstinence was mainly explained by an increase in TPR, reflecting an augmented tone of the resistance vessels. The minor changes in CBV indicate that the tone of the venous capacitance vessels was largely unaffected by naloxone-induced morphine abstinence.     

Central haemodynamics during morphine abstinence in anaesthetized rats

Central haemodynamics were studied in one group of morphine-dependent rats, and in a non-dependent control group, before and after administration of repeated bolus doses of naloxone. Dependence was induced by s.c. morphine pellet implantations. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO) and mean transit time (MTT) were measured in the conscious state, after induction of chloralose anaesthesia and after the administration of naloxone (0.005, 0.05, 0.5 and 5 mg kg-1 i.v.). Total peripheral resistance (TPR), stroke volume (SV) and central blood volume (CBV) were subsequently calculated. The haemodynamic variables did not differ significantly in the conscious state, except for a lower SV, when compared with the non-dependent control group. However, in response to anaesthesia the dependent rats exhibited a greater fall in MAP, mainly due to a TPR decrease. Naloxone elicited a marked increase in MAP in the morphine-dependent group, which was mainly caused by an increase in TPR. Naloxone induced no significant change compared with the control group in CO and CBV, while SV increased concomitantly with a lowered HR after naloxone in the morphine-dependent group. These results suggest that the withdrawal hypertension during morphine abstinence was mainly explained by an increase in TPR, reflecting an augmented tone of the resistance vessels. The minor changes in CBV indicate that the tone of the venous capacitance vessels was largely unaffected by naloxone-induced morphine abstinence.     

Left ventricular hypertrophy improves cardiac performance in spontaneously hypertensive rats

Cardiac function was studied in spontaneously breathing, adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). By rapid intravenous blood infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV) was determined while the cardiac nervous control was pharmacologically blocked. Since SV is greatly influenced by the level of afterload (mean arterial pressure, MAP), SV was also determined at increased MAP (constriction of abdominal aorta) and at decreased MAP (vasodilation by hydralazine). At low LVEDP levels, a righward shift of the Frank-Starling relationship was observed in SHR. This rightward shift seems mainly to depend on the increased MAP present in SHR since it was less prominent if MAP was lowered to normotensive levels in SHR. Maximal SV during volume infusion was similar in SHR and WKY, despite a much higher MAP in SHR. When peak SV was instead compared at similar MAP levels for both (either at ‘normotensive’ or ‘hypertensive’ levels) it was always significantly greater in SHR, and was increased largely in proportion to their increased left ventricular weight. This indicates that the left ventricular hypertrophy present in SHR is, at least at this stage, a physiological adaptation of the heart to increase its performance, in order to maintain a normal SV and hence cardiac output, despite an increased arterial pressure.     

Omega-3 fatty acid supplementation enhances stroke volume and cardiac output during dynamic exercise

Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have beneficial effects on cardiovascular function. We tested the hypotheses that dietary supplementation with DHA (2 g/day) + EPA (3 g/day) enhances increases in stroke volume (SV) and cardiac output (CO) and decreases in systemic vascular resistance (SVR) during dynamic exercise. Healthy subjects received DHA + EPA (eight men, four women) or safflower oil (six men, three women) for 6 weeks. Both groups performed 20 min of bicycle exercise (10 min each at a low and moderate work intensity) before and after DHA + EPA or safflower oil treatment. Mean arterial pressure (MAP), heart rate (HR), SV, CO, and SVR were assessed before exercise and during both workloads. HR was unaffected by DHA + EPA and MAP was reduced, but only at rest (88 +/- 5 vs. 83 +/- 4 mm Hg). DHA + EPA augmented increases in SV (14.1 +/- 6.3 vs. 32.3 +/- 8.7 ml) and CO (8.5 +/- 1.0 vs. 10.3 +/- 1.2 L/min) and tended to attenuate decreases in SVR (-7.0 +/- 0.6 vs. -10.1 +/- 1.6 mm Hg L(-1) min(-1)) during the moderate workload. Safflower oil treatment had no effects on MAP, HR, SV, CO or SVR at rest or during exercise. DHA + EPA-induced increases in SV and CO imply that dietary supplementation with these fatty acids can increase oxygen delivery during exercise, which may have beneficial clinical implications for individuals with cardiovascular disease and reduced exercise tolerance.     

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats.

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/ri of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.     

Cardiovascular ‘reactivity’ to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats

Cardiovascular ‘reactivity’ to graded splanchnic nerve stimulations was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/r₁ of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.     

Osmotic and hypovolemic thirst in spontaneously hypertensive rats

Osmotic- and hypovolemic-induced water intake as well as urinary excretion of sodium and other solutes were compared in spontaneously hypertensive (SHR) and normotensive Wistar (NWR) rats. No significant differences were found between SHR and NWR in water intake and urinary excretion under conditions of euhydration and in response to 24 hr water deprivation. Administration of osmotic load (0.5 ml.100 g-1 body weight of 10% NaCl IV) elicited: (1) higher intake of water (by 1.77 +/- 0.60 ml.100 g-1 body weight), (2) lower urinary excretion of sodium and other solutes, and (3) greater retention of fluid in SHR than in NWR. Reduction of blood volume by amount equivalent to 1.8% of body weight decreased arterial blood pressure by 31.9 +/- 3.5 and 10.8 +/- 1.7 mmHg in SHR and NWR, respectively. In spite of significantly greater hypotension, bleeding elicited in SHR smaller elevation of water intake than in NWR (1.39 +/- 0.25 vs. 2.14 +/- 0.49 ml.100 g-1 body weight). The data provide evidence for existence of significant differences in the control of body fluid balance between SHR and NWR. It is suggested that hyperdipsia elicited by administration of the hyperosmotic load in SHR does not result from primary hyperresponsiveness of the thirst system to osmotic/sodium stimulation but is rather secondary to osmotic load retention.     

Haemodynamics and plasma ANP (atrial natriuretic peptide) after acute blood volume expansion in normotensive and spontaneously hypertensive rats

Atrial natriuretic peptide (ANP) was measured in plasma during acute volume load in conscious, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. During basal conditions immunoreactive ANP were similar in the SHR (630 +/- 56 pmoles l-1) and the WKY (657 +/- 114 pmoles l-1) groups. An acute 10% and 20% whole blood volume expansion resulted in a linear increase in immunoreactive plasma ANP in the WKY. In the SHR the increase in plasma ANP was attenuated during the 20% volume load. During the 10% and 20% volume load central venous pressure (CVP), central blood volume (CBV) and cardiac output increased relatively more in the SHR compared with the WKY group. In contrast, the increase in peripheral blood volume (PBV) and decrease in heart rate (HR) was attenuated in the SH rats. In the SHR group there was a shift of the ANP vs. CVP and ANP vs. CBV curves to the right compared with the WKY. We conclude that acute volume loading is a potent stimulus for ANP release in WKY as well as SHR. However, in the SHR, ANP release was blunted in spite of the increased centralization of the volume load in this rat strain. Thus, the decreased responsiveness of the ANP hormonal system may contribute to the development and maintenance of hypertension in this genetic form of hypertension.     

Central,peripheral, and other blood volume changes during hemodialysis

Volume overload is a factor in development of hypertension in hemodialysis patients. Fluid removal by hemodialysis (HD), however, may cause intradialytic hypotension and associated symptoms. A better understanding of the relationships between blood pressure volume status and the pathophysiology of fluid removal during HD are, therefore, necessary to control blood pressure and to eliminate intradialytic hypotension. The objectives of the study were to determine the amount and direction of change of body fluid compartments after ultrafiltration (UF) and to determine whether any correlations exist between mean arterial pressure (MAP), change in circulating blood volume (deltaBV), total body water (TBW), central blood volume (which constitutes the volume of blood in the lungs, heart, and great vessels [CBV]), and intracellular and extracellular fluid volumes (ICF, ECF). The study population included 20 patients on regular HD. Each individual had their CBV, cardiac output, and peripheral vascular resistance (PVR) measured by means of saline dilution technique and deltaBV monitored by an online hematocrit sensor (Crit Line). MAP was calculated from measured blood pressure and ICF and ECF were measured using bioelectric impedance analysis techniques. Measurements were obtained before and after maximum UF measured by deltaBV (reduction of 6-10% by Crit Line). Ten healthy controls also had ECF and ICF values measured by bioelectric impedance analysis. Before HD, MAP correlated with TBW (r = 0.473, p = 0.035) and CBV (r = 0.419, p = 0.066), suggesting that hypertension here may be due to volume overload. Patients were ECF expanded before HD with an ECF:ICF ratio of 0.96, which was significantly higher than the control ratio of 0.74 (p < 0.0001). During UF, fluid was removed from both ECF and ICF, but more from the ECF volume ratio 0.92 post UF, a significant reduction (p < 0.0001). After UF, MAP no longer correlated with TBW or CBV but correlated with peripheral vascular resistance (r = 0.4575, p = 0.043). After UF, deltaBV correlated inversely with PVR (r = -0.50, p = 0.024). Despite the fall in deltaBV (7.11+/-2.49%) with UF, CBV was maintained. CBV were 0.899 L and 0.967 L pre and post UF, respectively. These data suggest that in hemodialysis patients, predialysis volume status influences predialysis blood pressure. UF causes BV to fall, but CBV is preferentially conserved by increasing PVR, which also maintains blood pressure. Failure of a PVR response likely leads to intradialytic hypotension.     

Voluntary drinking and hydration in trained, heat-acclimatized girls exercising in a hot and humid climate

This study examined the effects of beverage composition on the voluntary drinking pattern, body fluid balance and body temperature responses of heat-acclimatized trained girls exercising intermittently in outdoor conditions (WBGT = 30.9 ± 0.2°C). Twelve trained, heat-acclimatized girls (age = 10.6 ± 0.2 years) performed three 3-h sessions, each consisting of four 20-min cycling bouts at 60% VO₂max, alternating with 25-min rest. One of three beverages was assigned: unflavored water (W), flavored water (FW) or flavored water plus 6% carbohydrate and 18 mmol/l NaCl (CNa). Drinking was ad libitum. Total intake was similar among conditions (W = 953.3 ± 107.8 ; FW = 1026.5 ± 138.1; CNa = 906.4 ± 107.5 g). A mild hypohydration occurred during the three conditions (W = −1.12%; FW = −0.95%; CNa = −0.74% BW, P > 0.05). Sweat loss, higher than previously reported for sedentary girls, was not different among conditions (W = 1,051.5 ± 90.8; FW = 979.9 ± 72.8; CNa = 1,052.7 ± 52.6 g). The average amount of urine produced (W = 269.8 ± 85.9; FW = 320.8 ± 87.2; CNa = 85.6 ± 9.3 g) was 73 and 68% higher during FW and W, respectively, compared to CNa (CNa vs. FW, P < 0.05). The increase in rectal temperature, heart rate and all perceptual variables did not differ among conditions. In conclusion, flavoring of the water and addition of 6% carbohydrate plus 18 mmol/l NaCl do not prevent mild hypohydration in trained, heat-acclimatized girls with high sweating rates. However, there is a tendency towards a greater fluid retention with the CNa beverage. An erratum to this article can be found at     

应用二氧化碳重复呼吸法测定正常人心排血量的初步观察

二氧化碳重复呼吸法测定心排血量是无创测定心脏功能的一种方法，它既可以用于静态测定，更适合于运动状态下的监测。我们应用此方法初步观察了４１个正常人在静态及运动状态下的心排血量，结果表明，大多数受试者的态心排血量和每搏血量均正常，随着负荷的增加，ＣＯ、ＳＶ和ＨＲ也相应增加，但当负荷达一定水平时，ＣＯ的增加则主要靠心率的增加来完成。     

Effects of ageing on cardiac performance and coronary flow in spontaneously hypertensive and normotensive rats

The aim of the present study was to assess the influence of ageing on cardiac function and coronary flow in Wistar Kyoto normotensive rats (WKY, 16 and 78 weeks of age) and spontaneously hypertensive rats (SHR) of the same age. Cardiac function was determined on isolated hearts by means of an antegrade heart perfusion technique. Left atrial pressure and peak aortic pressure could be altered independently of each other. Recordings of cardiac output and coronary flow were then obtained at both normotensive and hypertensive levels of peak aortic pressures. Peak stroke volume (SV) was reduced with age in both WKY and SHR. Peak SV determined at normotensive pressure loads became diminished with age in WKY, while it at hypertensive pressure loads showed a small decline with age, since peak SV was low as early as 16 weeks of age. The age-dependent fall in cardiac performance was greater in SHR than in WKY, due to the enhanced peak SV in 16-week-old SHR at hypertensive pressure loads. Peak SV was markedly decreased at normotensive pressure levels in both 16- and 78-week-old SHR v. age-matched WKY. Coronary flow per unit tissue declined with age both in WKY and SHR. Coronary flow was also lower in SHR compared to age-matched WKY. With ageing this elevated performance was reduced down to the same level as in 78-week-old WKY. The age-related coronary flow reduction and the consistently reduced flow in SHR indicate a structural narrowing of the coronary vascular bed, particularly in SHR.     

Ventricular morphology and pumping ability of exercised spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) and two strains of normotensive Wistar rats were subjected to a 5 day/wk swimming program to determine whether the heart of the SHR could respond to an additional stimulus to cardiac growth. Swimming was tolerated well by all rats. Although body weight of the exercised groups was not significantly reduced, both the right and left ventricular weights of all exercised groups were increased. Left ventricular circumference and chamber volume were increased without a change in free wall thickness in all exercised groups. Ventricular performance was assessed by peak cardiac output and stroke volume attained during rapid intravenous volume loading, both before and after autonomic inhibition. After combined cholinergic and beta-adrenergic inhibition, all exercised rats had slower heart rates and higher peak stroke volume than respectively sedentary controls. Thus, exercised SHR had the same alterations in cardiac mass and performance as exercised normotensive rats. Despite the initial presence of left ventricular hypertrophy, the SHR responded appropriately to an additional stimulus for adaptive cardiac growth.