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PubMed1988

Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

Surgical removal of one or both atrial appendages was employed in rats to reduce the intrinsic stores of atriopeptin (AP). In conscious rats (with intact baroreceptor reflexes), bilateral or unilateral atrial appendectomy suppressed the diuresis and natriuresis produced by acute volume expansion. Surprisingly, volume expansion (with 4% bovine serum albumin in saline at 1.5 ml/kg per min for 15 min) did not result in an increase in plasma AP immunoreactivity (APir) in control or atrial-appendectomized conscious rats. Previous studies demonstrated that acute volume expansion in anesthetized animals caused increased plasma APir. Indeed, we found that volume expansion causes comparable diuresis-natriuresis in conscious and chloral hydrate-anesthetized rats, but only the latter group exhibits an increase in plasma APir. Brattleboro rats, which are deficient in vasopressin, exhibit the same response as Long-Evans controls in that acute volume expansion in conscious animals produces a pronounced diuresis and natriuresis but no APir release, but when these same animals are anesthetized, there is a simultaneous induction of diuresis-natriuresis and APir release by volume expansion. Plasma AP does not increase in conscious rats despite a large volume load, 30-40% of the total blood volume given in 15 min, and the natriuresis-diuresis appears to also be independent of vasopressin. On the other hand, the diuresis induced by acute volume expansion in anesthetized rats seems dependent on the elevated APir, since rats made autoimmune to AP (which are nonresponsive to exogenous AP infusions) exhibit a diuresis in conscious but not anesthetized rats. We therefore conclude that the participation of AP in volume homeostasis is more likely in pathophysiological states and that another mechanism or possibly another atrial factor mediates the diuresis-natriuresis induced by volume expansion in conscious rats.

Anesthesia↗
PubMed1995

Diuresis and voiding pattern in healthy schoolchildren.

OBJECTIVE: To analyse how differences in diuresis affect the normal pattern of micturition of healthy children. SUBJECTS AND METHODS: Two hundred and six healthy continent schoolchildren, aged 7-15 years, completed a frequency/volume chart for 24 h by recording the time and volume of each micturition. Several diuresis variables were calculated from these charts and compared with sex, age, oral fluid intake, functional bladder capacity, voiding intervals and volumes. RESULTS: The weight-corrected mean diuresis per 24 h varied 10-fold between individuals, independently of recorded fluid intake. In the majority, the diuresis decreased during the night, but the opposite diurnal pattern occurred in 12% of the children. The individual night-time diuresis was positively correlated with functional bladder capacity and the daytime diuresis was positively correlated with voiding frequency. CONCLUSIONS: The weight-corrected diuresis varies many-fold among healthy continent children. A substantial proportion has a reversed diurnal pattern with a larger diuresis during the night. The individual bladder size is adapted to accommodate their typical nightly urine production.

Adolescent↗
PubMed1971

Urine concentration during solute diuresis in potassium-depleted rabbits. Evidence for a defect in tubular sodium transport.

1. The relationship between osmolal clearance (C(osm)) and the reabsorption of solute-free water by the kidney (T(H2O) (c)) was examined during 10% mannitol and 2.3% saline diuresis in normal and potassium-depleted rabbits.2. In normal rabbits at osmolal clearances close to 3.0 ml./min, T(H2O) (c) during mannitol diuresis was 0.87 +/- 0.06 ml./min and during saline diuresis 1.19 +/- 0.07 ml./min. The mean difference in T(H2O) (c) of 0.32 +/- 0.05 ml./min was highly significant (P < 0.001).3. In one group of potassium-depleted rabbits with a reduction in maximal urinary concentration, T(H2O) (c) during both mannitol and saline diureses was reduced significantly below normal and the increment in T(H2O) (c) normally seen during saline diuresis was abolished.4. In a second group of potassium-depleted rabbits maximal urinary concentration (1253 +/- 88 m-osmole/kg H(2)O) was not significantly different from that in normal rabbits (1272 +/- 116 m-osmole/kg H(2)O). In these animals, T(H2O) (c) at osmolal clearances close to 3.0 ml./min was not significantly different during mannitol diuresis (0.83 +/- 0.07 ml./min) from that in normal animals, whereas it was reduced significantly during saline diuresis (0.89 +/- 0.07 ml./min, P < 0.001) and the difference in T(H2O) (c) normally seen between mannitol and saline diuresis was abolished.5. The inability to increase T(H2O) (c) during saline diuresis above that achieved during mannitol appears to be the earliest manifestation of the concentrating defect associated with potassium depletion. It probably results from an impairment of sodium transport by the ascending limb of the loop of Henle. This is supported by the fact that potassium-depleted rabbits excreted a greater percentage of the filtered load of sodium than did normal controls.

Animals↗
PubMed1977

Immersion diuresis in dogs.

The mechanism of diuresis during the 1st h of immersion was investigated using anesthetized dogs. Four different experiments were carried out. First, left atrial transmural pressure was measured before, during, and after immersion. The data suggest that, although the left atrium may or may not be stretched depending on the conditions of immersion, the amount of diuresis is independent of the amount of left atrial stretch, and therefore a causal relationship between diuresis and left atrial stretch could not be established. Second, bilateral cervical vagotomy was carried out. Immersion diuresis sometimes occurred despite this vagotomy, suggesting that the left atrial stretch reflex was not participating in those cases. Third, negative-pressure breathing was carried out to simulate the negative transthoracic pressure associated with uncompensated immersion. The average left atrial transmural pressure did not change. A slight hemodilution and a moderate diuresis occurred. There was no correlation between changes in left atrial transmural pressure and changes in urine ouput. Fourth, blood studies were done on splenectomized dogs subjected to immersion. Hemodilution occurred and was most marked in dogs which had had their kidneys removed. The hemodilution is sufficient to explain the early phase of the immersion diuresis. The data suggest that, in anesthetized dogs, hemodilution is the probable initiator of diuresis upon immersion and that, in dogs, left atrial stretch is unrelated to diuresis during immersion or negative-pressure breathing.

Animals↗
PubMed1976

Cross-circulation study of natriuretic factors in postobstructive diuresis.

To study the role of circulating natriuretic factors in the postobstructive diuresis that occurs after relief of bilateral, but not unilateral ureteral ligation, cross-circulation was carried out between normal recipient rats and donor rats have either 24-h bilateral (BUL) or unilateral (UUL) ureteral ligation. With BUL donors, there was a rapid marked increase in sodium and water excretion in the recipient rats, sustained for 80-140 min, with a peak approximately 10 times control values. With UUL donors, no significant natriuretic response occurred. Changes in glomerular filtration rate, renal plasma flow, blood pressure, hematocrit, or circulating levels of aldosterone or Pitressin did not explain the diuresis-natriuresis produced by cross-circulation with BUL donors. Differences in the intrinsic renal damage produced by bilateral as compared to unilateral ureteral obstruction did not appear to account for this response, since UUL donors given an acute urea load and urine reinfusion caused a similar diuresis-natriuresis. Moreover, normal donor rats given a urea load also caused a diuresis-natriuresis nearly equal to that produced by BUL rats, and the relationship between increased urea excretion and sodium excretion or urine flow in the recipients was not different in the two groups. Total urine reinfusion for 3 h in donor rats produced a significant, although less marked, diuresis-natriuresis in recipient animals, with only a slight elevation of the blood urea nitrogen level, much less increase in urea excretion rate, and no significant relationship between urea excretion and sodium excretion or urine flow. The results indicate that potent natriuretic factors, which act by decreasing the tubular reabsorption of sodium and water, are present in the blood of rats with bilateral, but not unilateral, ureteral ligation. High blood and urine urea levels appear to be the factors responsible for the marked natriuresis-diuresis occurring in normal rats during cross-circulation with BUL donors, although suggestive evidence of other natriuretic factors in urine reinfused intravenously was also obtained. The data suggest that urea osmotic diuresis is an important mechanism for determining the striking difference between the postobstructive diuresis observed after relief of bilateral as compared to unilateral ureteral ligation.

Adenosine Triphosphatases↗
PubMed1980

Renal function, plasma renin, and spontaneous diuresis in an advanced stage of hypertension in rats.

Relationship of renal function and plasma renin level to a spontaneous diuresis in an advanced stage of hypertension was examined in the stroke-prone spontaneously hypertensive rats (SHRSP). For a comparison, it was also investigated in 2 kidney 1 clip (1CR) and 2 kidney 2 clip (2CR) models of renovascular hypertensive rats. The spontaneous diuresis was usually associated with an elevation of plasma renin level and an impairment of renal function in SHRSP and 1CR. In SHRSP, renal plasma flow showed an inverse correlation to the plasma renin level. The diuresis, however, is not prerequisite to the increase in plasma renin or to the renal impairment, since the latter changes were not always accompanied by diuresis. No correlations were found between these factors in 2CR. Remittent diuresis was observed in many 2CRs and 2 SHRSPs with normal renal function, indicating that renal damage underlies the continuous progression of the diuresis observed in most cases of SHRSP and 1CR. Both sodium and potassium balances tended to be negative in 1CR and 2CR in the diuretic phase, whereas potassium alone showed this tendency in SHRSP. The negative balances, if any, were not due to an excessive loss of the electrolytes but attributed mainly to a decrease in intake. The critical level of blood pressure for the spontaneous diuresis was highest in SHRSP and lowest in 1CR. It is probable that an interaction and cooperation between high blood pressure, impaired renal function and high plasma renin participate in the mechanism of the spontaneous diuresis during the development of malignant phase of hypertension of the rat.

Aldosterone↗
PubMed1980

Clonidine-induced diuresis in the rat: evidence for a renal site of action.

Clonidine, an alpha adrenergic agonist which causes a diuresis in experimental animals, was studied in unanesthetized, conscious Brattleboro rats heterozygous or homozygous for hereditary hypothalamic diabetes insipidus to determine if the diuresis was due to alpha adrenergic inhibition of antidiuretic hormone (ADH) release or to another mechanism of action. Heterozygous rats given clonidine s.c. in doses of 50 to 300 mu/kg b.w. exhibited a prompt dose-related diuresis. The diuresis was transient and could not be maintained beyond 4 hr even when clonidine was administered continuously by s.c. osmotic minipump. In response to clonidine-induced diuresis, plasma osmolality increased acutely from 300 +/- 1 to 310 +/- 1 mOsM/kg by 60 min after injection. Base-line plasma ADH was 5.1 +/- 0.9 mu/ml, remained unchanged at 15 min after clonidine injection but increased to 21.6 +/- 7.2 muU/ml by 60 min and was accompanied by an increase in urinary ADH excretion from 19.6 +/- 3.7 to 48.6 +/- 5.3 muU/hr. In parallel with the drug-induced diuresis, there was an increase in urinary excretion of creatinine, sodium and total solute. The alpha blocking agent phenoxybenzamine did not prevent the diuresis after clonidine injection. Clonidine antagonized the antidiuresis after clonidine injection. Clonidine antagonized the antidiuretic action of ADH administered to rats homozygous for diabetes insipidus. Thus, clonidine-induced diuresis does not appear to be due to alpha adrenergic inhibition of ADH release but rather to direct renal effects.

Animals↗
PubMed1993

Relationship between plasma beta 2-microglobulin and residual diuresis in continuous ambulatory peritoneal dialysis and hemodialysis patients.

To evaluate whether the continuous ambulatory peritoneal dialysis (CAPD) technique is able per se to obtain lower beta 2-microglobulin (beta 2M) plasma levels than hemodialysis (HD) or whether other factors, such as residual diuresis, can make a significant contribution, we compared 69 CAPD and 38 cuprophan HD patients, matched for age and dialysis duration. Residual diuresis was 680.3 +/- 531.8 mL/day in CAPD and 285.5 +/- 381.8 mL/day in HD (p < 0.001) subjects. Daily diuresis was > 300 mL/day in 63.8% of CAPD and in 31.6% of HD patients. The beta 2M plasma levels were 26.3 +/- 9.9 mg/L and 34.9 +/- 13.3 mg/L (p < 0.001) in CAPD and HD, respectively. In both groups the difference was significant when we compared the patients with diuresis below versus above 300 mL/day (p < 0.001). Instead, the differences were not significant upon comparing the CAPD and HD patients with the same amount of daily diuresis. The comparison between beta 2M plasma levels and residual diuresis showed a significant inverse correlation in both groups (p < 0.001). We conclude that the dialysis technique itself does not affect beta 2M plasma levels. The diuresis volume may be a very important factor in lowering beta 2M levels in both CAPD and HD patients. CAPD's capacity to maintain a higher diuresis for longer than HD may account for the lower beta 2M plasma levels in CAPD patients.

Aged↗
PubMed1997

The polyuria of solute diuresis.

Polyuria is an important symptom or sign because of its potential severity, diverse causes, and interesting pathophysiology. Whereas polyuria induced by water diuresis is reasonably well understood and easily recognized by clinicians, that produced by solute diuresis is more likely to cause confusion. In this article, we focus on solute diuresis as a cause of polyuria, review the classification and pathophysiology of polyuria, and describe the clinical and laboratory studies useful for the evaluation of the polyuric patient. A stepwise, logical approach is provided (1) to determine whether a patient has a water diuresis, a solute diuresis, or both (concurrently), and (2) if a solute diuresis is present, to determine if it is caused by electrolytes (eg, sodium chloride sodium bicarbonate), by nonelectrolytes (eg, glucose, urea), or by both. How to assess these possibilities and to determine the specific cause of the diuresis is discussed in detail. Three representative case examples are provided. Selected causes of a solute diuresis also are reviewed.

Adult↗
PubMed1995

Effects of diuresis on micturition.

Micturition can be characterized experimentally by monitoring both the frequency and volume of micturition. Previous studies demonstrated that the functional capacity of the rat and rabbit bladder, as determined by cystometry, is approximately equal to the maximal single micturition volume as recorded over a 24 hour period. Studies in many laboratories have demonstrated that chronic increases in diuresis induce increases in micturition frequency and capacity, and an increase in bladder mass. The current study compares the temporal relationship among these parameters in three models of diuresis: streptozotocin-induced diabetes in rats, sucrose-induced diuresis in rats, and furosemide-induced diuresis in rabbits. In both sucrose diuresis in rats and furosemide diuresis in rabbits there were immediate increases in both the frequency and volume of micturition. The magnitude of the increases in micturition frequency and micturition volume paralleled the increase in the total volume of urine excreted. Bladder mass increased progressively over the time course of the study. Streptozotocin-induced diabetes resulted in a more gradual (but parallel) increase in micturition frequency and volume, and again a more gradual increase in bladder mass. These studies demonstrate that functional bladder capacity is increased immediately upon the initiation of diuresis with sucrose or furosemide, as is the frequency of micturition. This indicates that functional bladder capacity is probably under neuronal regulation and the change in capacity is not a function of the increased bladder mass which occurs at a later time period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Mechanisms of post-obstructive diuresis in the solitary hydronephrotic kidney of the rat.

1. In order to clarify further the phenomenon of post-obstructive diuresis, clearance and micropuncture experiments were done before and after relief of partial ureteral obstruction in rats with a solitary hydronephrotic kidney. 2. Glomerular filtration rate, urine flow and sodium excretion increased markedly, whereas surface nephron glomerular filtration rate increased only slightly and intratubular pressure, proximal and distal tubular water reabsorption did not change significantly. Decreased tubular reabsorption in deeper nephrons and collecting ducts appeared to be of major importance in the post-obstructive diuresis after relief of chronic obstruction. 3. In order to examine further the distinctive functional characteristics of the chronically hydro-nephrotic kidney, the results were compared with control rats having a solitary normal kidney or a solitary remnant kidney with an intact renal medulla. Urine flow rate and sodium excretion were higher and urine osmolality was lower (P less than 0-01) in post-obstructive kidneys when compared with either control group. There were no differences in glomerular filtration rate or surface nephron function which could account for the greater diuresis and natriuresis from the hydronephrotic kidney, thus confirming the importance of an abnormality in deep nephron or medullary function in post-obstructive diuresis. 4. There was a greater diuresis in post-obstructive rats with a marked increase in blood urea concentration. Water reabsorption in the distal nephron was decreased in such animals, as well as in urea-loaded rats with a remnant kidney, indicating the probable mechanism by which urea diuresis potentiates the phenomenon of post-obstructive diuresis.

Animals↗
PubMed1989

Studies on the adrenomedullary dependence of kappa-opioid agonist-induced diuresis in conscious rats.

1. The dependence of kappa-opioid agonist-induced diuresis, upon an intact and functional adrenal medulla in conscious rats, was investigated in order to test the hypothesis that the diuresis is mediated by a blood-borne 'diuretic factor', of adrenomedullary origin, released by kappa-opioid receptor stimulation. 2. Confirming previous observations, adrenal demedullation significantly attenuated diuretic responses to the kappa-opioid agonists U50488H, ethylketocyclazocine (EKC) and tifluadom, but did not affect basal urine output, furosemide-induced diuresis or the antidiuretic response to the mu-opioid agonist, buprenorphine. Naloxone abolished U50488H-induced diuresis, confirming an involvement of opioid receptors. 3. Transfusion studies established that blood, from intact rats treated with U50488H, induced diuresis in intact and demedullated recipient rats, whether or not the recipients had been pretreated with naloxone. However, blood from demedullated rats treated with U50448H was unable to induce diuresis when administered to intact or demedullated recipients. 4. It is concluded that kappa-opioid agonist-induced diuresis is dependent upon an intact and functional adrenal medulla and appears to be mediated by a blood-borne 'diuretic factor' of adrenomedullary origin.

Adrenal Medulla↗
PubMed1988

Diuresis from atrial receptors after hypophysectomy and local ablation with no changes in plasma vasopressin.

Stimulation of the left atrial receptors in dogs anaesthetized with chloralose results in a reflex diuresis and natriuresis. The efferent limb of this reflex is though to have at least three components: nervous, haemodynamic and humoral. The present study was designed to investigate the humoral component in dogs anaesthetized with chloralose; to determine whether a humoral agent, other than vasopressin, might be causative in this reflex diuresis. The nervous and haemodynamic components were prevented by pharmacological denervation. Any possible contribution to the diuresis by a decrease in the plasma concentration of vasopressin was prevented by the removal of the pituitary gland. In animals in which a spontaneous diuresis followed hypophysectomy, an infusion of arginine vasopressin sufficient to maintain urine flow in the normal range for these dogs anaesthetized with chloralose was given. Distension of small balloons at the pulmonary vein-atrial junctions and in the left atrial appendage discretely to stimulate the atrial receptors in eleven dogs anaesthetized with chloralose resulted in a significant diuresis. It was concluded that a blood-borne agent other than vasopressin was responsible for the observed diuresis. At the moment it is not known whether vasopressin or the diuretic agent, or both, are involved in the diuresis accompanying the stimulation of atrial receptors.

Animals↗
PubMed1993

Desmopressin in elderly subjects with increased nocturnal diuresis. A two-month treatment study.

This study describes changes in diuresis during a two-month treatment with 40 micrograms desmopressin (Minirin) in a group of elderly persons with increased nocturnal diuresis and decreased ADH secretion. The average age of the men (n = 7) was 72 +/- 4 years and of the women (n = 14) 73 +/- 6 years. Nocturnal diuresis decreased after one and two months by 21% and 20% in the men and by 36% and 34% in the women, respectively. Half of the change persisted among the women but not among the men one month after the treatment. The decrease in nocturnal diuresis was greatest among those who, before the treatment, had a large part of their diuresis during the night. Diuresis during the day changed only insignificantly. Body weight did not change during treatment, nor did blood pressure, osmolality, sodium or potassium in serum. Sleep improved during treatment. In one case, side-effects were observed, with a feeling of swelling in the body and decreased diuresis in the morning.

Administration, Intranasal↗
PubMed1979

[Studies of the effect of synthetic oxytocin and neurohypophyseal extract on diuresis of water-laden cattle].

The action of synthetic oxytocin and Glanduphen, a neurohypophyseal extract preparation, on the diuresis of six heads of cattle in lactation was studied, following intraruminal application of water. Intravenous injection of something between 10 and 30 I.U. of oxytocin reduced diuresis by 54 per cent on average, within 30 minutes from treatment. Urine-borne Cl- -concentrations went up by 315 per cent on average and quantitative Cl- -secretion by 87 per cent. The values recorded in response to the administration of doses between 10 and 40 I.U. of Glanduphen were 44, 785, and 344 per cent. Additional application of Glanduphen within 30 minutes from oxytocin injection caused less pronounced inhibition of diuresis or even some activation of diuresis. Literature on renal effects of vasopressin and of oxytocin was analysed, in that context, and the conclusion was drawn that antidiuretic effects were recordable neither from man nor from animals unless they were exposed to excessive application of water. The same hormone preparations, however, caused increase of diuresis in thirty animals with low rates of diuresis and higher osmotic urine pressure. Rise in saluresis was a most common result of vasopressin or oxytocin administration and did in no way depend on the diuresis level.

Animals↗
PubMed1993

[Diagnosis of urine transport disorders. Diuresis renography].

Congenital urinary tract malformations are frequently the cause of urinary transport disturbances. However, not all the malformations or obstructions presenting sonographically as hydronephrosis have to be treated surgically. The Whitaker test, an invasive diagnostic procedure to establish the urodynamic relevance of an obstruction, does not provide a reliable estimate of prognosis; spontaneous cures in cases of obstruction have been reported. Diuresis renography offers several advantages as compared with the Whitaker test, for example a more physiological basis, less observer dependency, better reproducibility and--last but not least--non-invasiveness. However, diuresis renography has to be carried out according to a strictly standardized protocol. Sufficient hydration (20 mg/kg body weight) and bladder catheterization (to rule our reflectory transport disturbances) are mandatory. Today, 123I-OIH or 99mTc-MAG3 are the radiopharmaceuticals of choice; the activity for children has to be reduced in relation to body surface. To stimulate diuresis, furosemide (0.5-1 mg/kg of body weight) has to be given. For the evaluation of diuresis renography, sequential scintigrams as well as functional curves have to be used. It is strongly recommended that diuresis renography be combined with clearance determinations separately for the two kidneys. The interpretation of diuresis renography should not rely only on quantitative curve parameters but--above all--on visual analysis of the functional curves. However, in cases of proven obstruction, diuresis renography--like the Whitaker test--cannot accurately predict the prognosis in any individual case. If renal function is normal and there is no difference between the left and the right kidney, a wait-and-see attitude seems to be justified.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1998

[Renal urodilatin secretion is associated with diuresis and natriuresis after spontaneous, supraventricular tachycardia].

Patients with paroxysmal supraventricular tachycardia (SVT) may have a polyuria after termination of tachycardia. There is increasing evidence that the renal peptide urodilatin (ANP (95-126))--and not plasma ANP (ANP (99-126))--is the member of the natriuretic peptide family mediating natriuresis and diuresis in man. In patients with SVT we, therefore, analyzed the relationship between diuresis, natriuresis, plasma ANP, urinary urodilatin excretion and renal excretion of cyclic GMP, the second messenger in the ANP system. During and after clinical presentation with spontaneously occurring SVT, two patients with AV-nodal and one patient with atrioventricular reentry tachycardia (heart rate 160 to 200 bpm) were studied. Urinary urodilatin excretion was correlated to diuresis (r = 0.73) and natriuresis (r = 0.93); similarly urinary cyclic GMP excretion was related to diuresis (r = 0.80) and natriuresis (r = 0.87; p < 0.001, respectively). In contrast, there was no significant correlation between plasma ANP concentrations and diuresis (r = 0.28, n.s.) or natriuresis (r = 0.11, n.s.). As an explorative analysis, stepwise multiple linear regression identified urinary urodilatin as the most important contributor to diuresis and natriuresis after SVT. These data on polyuria after spontaneous SVT further support the view that in man urodilatin is the member of the natriuretic peptide family participating in kidney physiology.

Adult↗
PubMed1981

Effect of diuresis on the performance of the failing left ventricle in man.

To determine the effect of diuresis on the performance of the failing left ventricle, we measured cardiac output, pulmonary wedge pressure and M-mode echo left ventricular diastolic dimension before and after diuresis in 13 patients with heart failure. Diuresis increased stroke volume (43 +/- 23 ml to 50 +/- 18 ml (p less than 0.05)) and decreased pulmonary wedge pressure (28 +/- 3 mm Hg to 19 +/- 5 mm Hg (p less than 0.01)), mean blood pressure (100 +/- 14 mm Hg to 88 +/- 10 mm Hg (p less than 0.01)) and systemic vascular resistance (2,059 +/- 622 dynes-sec-cm-5 to 1,783 +/- 556 dynes-sec-cm-5 (p less than 0.05)). Echo left ventricular diastolic dimension was not changed by diuresis (6.0 +/- 0.8 cm to 6.0 +/- 0.8 cm). Percent change in stroke volume correlated with systemic vascular resistance (r = 0.60, p less than 0.05) and with left ventricular diastolic dimension (r = 0.62, p less than 0.05) but not with pulmonary wedge pressure (r = 0.12) or right atrial pressure (r = 0.04). Thus, diuresis improved the performance of the failing ventricle and reduced afterload, but it did not alter left ventricular diastolic dimension, an index of preload. These data suggest that diuresis improves ventricular function by decreasing afterload.

Aged↗