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PubMed1993

Inhibition of sodium influx and improved preservation of rat hearts during hypothermic ischemia by furosemide and bumetanide: a 23Na- and 31P-NMR study.

The importance of the Na+/K+/Cl- co-transport system of the rat myocardial sarcolemma was studied under hypothermic ischemia by investigating the effect of the co-transport blockers furosemide and bumetanide on the sodium influx into the myocardium. The intracellular Na+ accumulation during hypothermic ischemia was followed by 23Na-NMR. For this purpose the shift reagent [Dy(TTHA)3-] (SR) was added to the Krebs-Henseleit (KH) perfusion solution. The same solution was also present during the hypothermic preservation. A significant reduction in the intracellular Na+ accumulation after 12 h was found when 100 microM furosemide was present during the perfusion and preservation periods. The intracellular Na+ levels returned to the pre-ischemic values after 1 h of reperfusion with KH in both the treated and control groups. Dose-response studies have indicated that 1-100 microM furosemide or 0.1 microM bumetanide added to the KH-SR solution reduced the Na+ influx significantly over 4 h of hypothermic ischemia. No statistically significant effect was found with furosemide concentration of 0.1 microM or with bumetanide concentrations higher or lower than 0.1 microM. 31P-NMR measurements showed no effect of the 100 microM furosemide on the intracellular ATP, the sum of inorganic phosphate and phosphomonoester, or pH levels over 4 h or after 12 h of hypothermic ischemia. Hearts treated with KH containing 100 microM furosemide showed, significantly higher functional recovery after 12 h of hypothermic ischemia than hearts treated only with KH. This study strongly indicates the existence of the Na+/K+/Cl- co-transport system in the intact rat heart sarcolemma, and its major role in sodium influx during hypothermic ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Effect of ramipril and furosemide treatment on interstitial remodeling in post-infarction heart failure rat hearts.

Extracellular matrix (ECM) remodeling and increased matrix metalloproteinase (MMP) expression and activity have been observed to be relevant in the development of heart failure (HF). We examined the effects of ramipril alone or with furosemide on ECM in a heart failure model. HF was induced by occlusion of the left coronary artery in spontaneously hypertensive rats (SHR). Rats were assigned to placebo (n=9), ramipril 1 mg/kg/day (n=11), furosemide 2 x 2 mg/kg/day (n=7) or both (1 mg/kg/day + 2 x 2 mg/kg/day n=8). LV-function, collagen content, MMP/TIMP (tissue inhibitor of matrix metalloproteinases) protein- and mRNA-expression were examined in non-infarcted LV tissue. MMP-2/TIMP-4 ratio was increased in HF. Ramipril reduced MMP-2 expression (active form), collagen type I mRNA expression and content and increased TIMP-4 levels associated with decreased left ventricular end diastolic pressure (LVEDP), mortality rate and increased LV pressure (LVP). Combination therapy with furosemide is less efficient with regard to collagen content and MMP-2 (active form) reduction but did not worsen beneficial effects of ramipril on LV function and mortality rate. Furosemide alone had no effect on MMP-2 (active form) expression, collagen content, LV function and mortality rate. Prevention of LV dilatation by ramipril was associated with decreased gelatinolytic activity and increased MMP-inhibition in heart failure SHR. Furthermore, ramipril reduced fibrosis by enhanced interstitial collagenase expression. Furosemide did not show the beneficial effects of ramipril on ECM remodeling but did not worsen LV function. Positive effects of furosemide treatment alone on LV remodeling and function were not observed.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Cyclic AMP and furosemide stimulate the Na(+)-K(+) ATPase in isolated rat jejunal cells.

The effect of cAMP on the activity of Na(+)-K(+) ATPase in the rat jejunum was studied by measuring the ouabain-sensitive (86)Rb accumulation by isolated villus cells. The cyclic nucleotide increased significantly (86)Rb accumulation by the enterocytes. The involvement of the NaKCl(2) symporter, the H(+)-K(+) exchanger and the Na(+)-K(+) pump was tested by measuring, respectively the furosemide-sensitive, the omeprazole sensitive, and the ouabain-sensitive (86)Rb accumulation. Furosemide significantly increased the basal level of intracellular (86)Rb and exerted overlapping effects with cAMP. Inhibiting the Na(+)-H(+) exchanger with amiloride, decreased the basal level of intracellular (86)Rb, and in its presence the stimulatory effect of cAMP was still observed but not that of furosemide. cAMP and furosemide did not exert any significant effect on (86)Rb accumulation by the enterocytes in presence of ouabain or in the absence of sodium but their stimulatory effect still appeared in the absence of chloride or in the presence of omeprazole or K(+)-channel blockers. These data suggest that cAMP and furosemide stimulate the Na(+)-K(+) ATPase in rat jejunal cells, and that this effect is, in the case of furosemide, mediated by an activation of the Na(+)-H(+) exchanger.

Amiloride↗
PubMed1994

Renal clearance of lomefloxacin is decreased by furosemide.

The interaction between lomefloxacin, a new quinolone, and furosemide, a loop diuretic, has been examined. Oral lomefloxacin 200 mg and furosemide 40 mg were given together or separately to 8 healthy subjects, and blood and urine samples were obtained over the following 12 h. The plasma concentrations of lomefloxacin following coadministration with furosemide were higher than after lomefloxacin alone and its AUC was increased, and its total and renal clearances were decreased. No change in the pharmacokinetics of furosemide was found after coadministration of lomefloxacin. As quinolones and furosemide are reported to be excreted in urine by the renal tubular anion transport system, the present results suggest that the renal tubular secretion of lomefloxacin is diminished by furosemide. It is not clear whether this pharmacokinetic interaction might be clinically important.

Adult↗
PubMed1991

Diuretic effect and disposition of furosemide in cystic fibrosis.

The pharmacodynamics and kinetics of single oral and intravenous doses of furosemide were studied in 9 patients (mean age 18.5 y) with cystic fibrosis. The diuretic effect of furosemide lasted for 6 h after oral administration and 2 h following intravenous injection of the drug. The patients with cystic fibrosis had a more pronounced diuretic response both to the oral and intravenous treatments than that reported in normals. Furosemide caused a marked decrease in urine pH for 5 h following the oral dose and between the 2nd and 3rd h after i.v. injection. The baseline nocturnal urine flow rate in 7 of the 9 patients given furosemide orally was increased by 30.6% compared to that reported in healthy subjects. The bioavailability of furosemide, its mean absorption rate and the mean plasma and urinary elimination half-lives both of the oral and the intravenous drug were similar to those reported in normal subjects. The patients with cystic fibrosis showed, however, about double normal mean total clearance after both the oral and i.v. treatments, and its renal clearance was almost half the plasma clearance. Nonrenal clearance was markedly increased in the patients, which agreed with a considerable decrease in the renal excretion of the drug. The mean apparent volume of distribution was also markedly increased compared to data in the literature. Oral furosemide resulted in a moderate increase in haematocrit and haemoglobin levels in 7 of 9 patients with cystic fibrosis and marked hypokalemia developed in 6 of the 9 patients 6 h after dosing. Pulmonary function tests performed at that time were changed in an inconsistent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Metamizole-furosemide interaction study in healthy volunteers.

The pharmacokinetic and pharmacodynamic interactions between metamizole (dipyrone) and furosemide were investigated in 9 of 12 healthy female subjects able to complete the study. They received oral metamizole 3 x 1 g for 3 days or placebo (cross-over) and on the last day of both study periods furosemide 20 mg IV. On the last two days a balanced sodium diet (120 mEq) and on Day 3 an oral water load (600 ml) were given. Metamizole significantly inhibited basal urine flow, whereas the fractional excretion of sodium and chloride and the 12 h-GFR remained unchanged. Metamizole significantly reduced furosemide clearance (175 vs 141 ml.min-1), furosemide-stimulated plasma renin activity (1.42 vs 0.79 ng AI.ml-1.h-1) and the urinary excretion of prostacyclin metabolites and of prostaglandin F2 alpha (by 70-81%). The renal clearance and terminal half-life of furosemide, peak renal chloride and volume excretion were unchanged. Thus, metamizole did not interact with the renal excretion and the diuretic effect of furosemide, although prostaglandin synthesis was significantly reduced.

Adult↗
PubMed1990

Effect of furosemide on angiotensin II-mediated prostaglandin I2 production in hypertensive subjects.

The role of angiotensin II (AII) in Prostaglandin I2 (PGI2) production following furosemide has been examined in a placebo-controlled, cross-over study. Furosemide 20 mg was injected intravenously in eight hypertensive subjects already treated with oral captopril 25 mg or a matching placebo. Urinary excretion of 6-keto-PGF1 alpha (a metabolite of PGI2) and PGE2, PRA and AII was increased following furosemide without captopril pretreatment. The rises in urinary 6-keto-PGF1 alpha and PGE2, and plasma AII after furosemide were prevented by the captopril pretreatment. Urinary volume, sodium and furosemide were not affected by captopril. The data indicate that the effect of furosemide on PGI2 production, as reflected by the urinary excretion of 6-keto-PGF1 alpha, was mediated by an action of AII.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Changes in renal clearance of furosemide due to changes in renal blood flow and plasma albumin concentration.

We have shown that, within therapeutic plasma concentrations, the unbound fraction of furosemide changes in direct proportion to the reciprocal of the plasma albumin concentration (correlation coefficient 0.99). Changes in the albumin concentration were produced by ultrafiltration of human plasma using a haemofiltration filter. Thus, we propose that, when studying changes in the pharmacokinetics of a highly protein bound drug, calculated changes in the unbound fraction offer an alternative to actual measurement of the unbound concentration, which is often difficult. Nine healthy volunteers receiving a continuous furosemide infusion were studied in normovolaemia and after dehydration (-1.4 kg), with and without pretreatment with an angiotensin converting enzyme inhibitor (captopril) or an a1-adrenoceptor blocking agent (prazosin). Significantly larger changes in the renal clearance of furosemide were found that could be explained by changes in the unbound fraction. Following dehydration, the unbound fraction of furosemide was decreased by about 5%, while its renal clearance fell by 27%, 33% and 13% after pretreatment with placebo, captopril and prazosin, respectively. The secretory clearance of the unbound furosemide changed substantially and in parallel with changes in the renal blood flow. It is suggested that changes in the renal clearance and excretion of furosemide and its t1/2 are much more dependent on changes in renal blood flow than on changes in its unbound fraction.

Adult↗
PubMed1993

Furosemide stimulates renin expression in the kidneys of salt-supplemented rats.

This study was conducted to obtain information about a possible influence of salt transport by the thick ascending limb of Henle (TALH) and the macula densa on the expression of renin in the kidney. To this end, adult male rats were subcutaneously infused with furosemide (12 mg/24 h), an established inhibitor of TALH and macula densa salt transport, or with vehicle for 6 days. The animals had free access to chow, water and salt water (0.8% NaCl, 0.1% KCl) to maintain salt and water balance. Chronic furosemide treatment led to a 20-fold increase in urine flow rates and 50% increase in kidney weights, while urine osmolality decreased by 60% and body weight gain decreased by 40% in the furosemide-treated animals. Plasma renin activities increased from 2.9 +/- 0.5 ng angiotensin I h-1 ml-1 in controls to 10.6 +/- 2.2 ng angiotensin I h-1 ml-1 in furosemide-treated rats. In parallel, kidney areas immunoreactive for renin increased by 80% and the renal content of renin mRNA increased by 120% in the animals receiving furosemide. Under the assumption that the effects seen on renal renin expression were primarily due to the inhibition of TALH and macula densa function by furosemide, our findings suggest that salt transport across the TALH and macula densa exerts a negative control function not only on the secretion but also on the expression of renin in the kidney.

Animals↗
PubMed1986

An experimental study using sodium salicylate to reduce cochlear changes induced by furosemide.

Furosemide is a loop diuretic which has been found to be ototoxic in humans and experimental animals. The ototoxic effects seem to be directed primarily towards the stria vascularis, since its shrinkage and extracellular edema have been observed in correlation with electrophysiologic changes. The present study was designed to examine the interaction of sodium salicylate and furosemide on the cochlear microstructures. Chinchillas weighing 400-600 g were used in all tests performed. The endocochlear potential (EP) was monitored continuously through a microelectrode inserted through the basilar membrane. A control group of animals was injected with 0.5 ml saline intravenously (IV) 30 min before 25 mg/kg furosemide was given. The experimental group of animals was injected with 50 mg/kg sodium salicylate IV 30 min before 25 mg/kg furosemide. The control animals were found to have a mean decrease in EP of 61.1 +/- 7.0 mV. In contrast, the experimental group had very little alteration of the EP following furosemide injection (18.7 +/- 3.9 mV). These findings suggest that sodium salicylate markedly reduces the ototoxic effect of furosemide. This effect may be mediated by an alteration of local or systemic prostaglandin metabolism, or may be due to inhibition of organic acid uptake in the cochlea.

Animals↗
PubMed1986

A comparison of the pharmacokinetics and diuretic effects of two loop diuretics, torasemide and furosemide, in normal volunteers.

The diuretic effects of torasemide and furosemide at three different steady-state plasma and urinary drug levels were compared in a randomized cross-over study in 6 healthy volunteers. Each trial with either torasemide or furosemide consisted of four consecutive periods of 90 min, the first being a control period, and during the three other periods, increasing doses of drug were administered. Each 90-min period was itself divided into three 30 min blood sampling and urinary collection periods. The urinary losses of water and electrolytes were compensated within each 30-min period by intravenous infusion of saline (NaCl) and 5% glucose solutions, to which KCl was added. A constant dose of calcium gluconate was given to compensate, at least in part, any calcium loss. Data from each 30 min control and the 3 drug dose periods, corresponding to full steady-state conditions, were used for clearance determinations and measurement of plasma and urinary drug concentrations. Urine volume, osmolar clearance, absolute and fractional urinary excretion of sodium, potassium, chloride, calcium and magnesium and creatinine clearance increased similarly after torasemide and furosemide according to the logarithm of the dose of the drug. Free water clearance stabilized at a constant level with torasemide and increased continuously after each dose of furosemide. During each of the three drug administration periods, the plasma levels of torasemide were not significantly different from those of furosemide, whereas the urinary concentrations and absolute excretion rates of torasemide were more than 5-times lower than those of furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

The effect of furosemide on luminal sodium, chloride and potassium transport in the early distal tubule of Amphiuma kidney. Effects of potassium adaptation.

Previous experiments in the early distal tubule of the doubly perfused kidney of Amphiuma demonstrated net reabsorption of potassium (K) which is reversed to net K secretion after K adaptation. Furthermore, it is known that this particular segment exhibits extensive chloride (Cl) net reabsorption which depends on the presence of sodium (Na) and which is inhibited by furosemide. In order to test for a possible interrelationship between NaCl and K transport, K activity in lumen and cell, transepithelial electrical potential difference, peritubular cell membrane potentials and volume reabsorption were measured in control animals and after K adaptation, in presence and absence of furosemide. In control animals the direction of net K transport is reversed from reabsorption to secretion upon addition of furosemide or following the removal of Cl from the tubular lumen. Volume reabsorption is inhibited by some 80%. In K adapted animals a similar inhibition of volume reabsorption is observed, however K secretion is not further enhanced. In control as well as in K-adapted animals intracellular K activities are still above electrochemical equilibrium after furosemide. The data suggest that a common transport system for Na, Cl and K is present in the luminal cell membrane which is inhibited by furosemide. K secretion observed in controls after furosemide and in K-adapted animals is driven by the cell to lumen electrochemical gradient for K across the K permeable luminal cell membrane. The shift of the luminal pump-leak system towards K secretion following K adaptation may be explained by an increase of the luminal K conductance and/or by a reduction of the activity of the luminal cotransport system. However, other mechanisms may also contribute to the observed phenomenon of K adaptation and cannot be ruled out at present.

Adaptation, Physiological↗
PubMed1983

Bioavailability of two preparations of furosemide and their pharmacological activity in normal volunteers.

The relative bioavailability and diuretic effect of 2 commercially available tablet preparations of furosemide 40 mg was examined in 10 healthy male volunteers. A close linear relationship between the urinary excretion rate of furosemide and the rate of sodium ion excretion in urine and/or flow rate of urine was demonstrated. There were no significant differences in the urinary excretion of furosemide, sodium and potassium ions or urinary volume following the oral doses. The difference in drug content affected the urinary recovery of furosemide over 24 h but had no effect on the pharmacological response. The analytical power of ANOVA using the various parameters of the responses to furosemide was no lower than when the parameters of urinary excretion of furosemide were used.

Adult↗
PubMed1976

[Cyclic AMP and plasma renin activity in renal vein blood after amitryptiline, theophylline, furosemide and beta adrenergic blocking substances (author's transl)].

The influence of amitryptiline, theophylline and furosemide on the concentration of cyclic-AMP and plasma renin activity (PRA) was investigated in renal vein plasma. Additionally, the stimulating effect of furosemide on the PRA after application of the beta-adrenergic receptor antagonists propranolol and practolol and the cyclic AMP concentration in the plasma were measured. All drugs were given intravenously. After amitryptiline cyclic-AMP concentration increased about 1.5-fold compared with the basal value,PRA was not altered. After theophylline cyclic-AMP concentration increased about 1.2-fold, PRA 2.0-fold compared with the basal value, PRA was not altered. After theophylline cyclic-AMP concentration increased about 1.2-fold, PRA 2.0-fold coa increased within 7 min and no further increase was observed till the 15th min. After practolol cyclic-AMP concentration and PRA decreased about 20% compared with the basal value within 10 min. The stimulating effect of subsequently applied furosemide on PRA was not altered, but the cyclic-AMP concentration was not changed in this time by furosemide. After propranolol cyclic-AMP concentration and PRA decreased about 20% compared with the basal value. The cyclic-AMP concentration was not influenced by the following furosemide application, in agreement with the findings after practolol, however, PRA could be stimulated only in 36% of these patients under beta-receptor blockade. Our results show that changes of the concentrations of cyclic-AMP and of PRA are independent of each other. An elevated intracellular cyclic-AMP level due to the inhibition of phosphodiesterase is as a single factor unable to stimulate renin release. Our results give no evidence of a direct involvement of the adenylcyclase-system in the mechanism of renin release. The effect of propranolol and practolol on the basal value of PRA and cyclic-AMP is equal. The different influence of 10 mg propranolol and 20 mg practolol on the stimulating effect of 40 mg furosemide on the PRA can be interpreted as a dosage problem.

Adrenergic beta-Antagonists↗
PubMed1997

Intermittent administration of furosemide versus continuous infusion in the postoperative management of children following open heart surgery.

OBJECTIVE: To compare the amount of furosemide needed to fulfil defined criteria for renal output if given intermittently or as a continuous infusion and to compare the effect of these two regimens on hemodynamic variables and urine electrolyte concentrations. DESIGN: Prospective randomized study of postoperative hemodynamically stable pediatric cardiac patients. The patients were given furosemide according to the urine output, either as an intermittent bolus injection or as a continuous infusion. SETTING: Pediatric intensive care unit in a university hospital. PATIENTS: The patients were randomly assigned before admission to either the intermittent i.v. or the continuous furosemide i.v. infusion group. MEASUREMENTS AND RESULTS: Demographic and hemodynamic data were recorded for a maximum of 72 h, as were furosemide dose, urine output, and fluid and inotropic drug requirements. Forty-six patients completed the study. Maximal hourly urine output was significantly higher in the intermittent group. A significantly lower dose of furosemide in the intermittent group produced the same 24-h urine volume as in the continuous infusion group. CONCLUSIONS: Intermittent furosemide administration may be recommended in hemodynamically stable postoperative pediatric cardiac patients because of less drug requirement. However, the high maximal urine output may cause hemodynamic problems in patients who depend on high inotropic support.

Child, Preschool↗
PubMed2003

Effects of chronic furosemide treatment and age on cell division in the adult gerbil inner ear.

Atrophy of the stria vascularis and spiral ligament and an associated decrease in the endocochlear potential (EP) are significant factors in age-related hearing loss (presbyacusis). To model this EP decrease, furosemide was delivered into the round-window niche of young adult gerbils by osmotic pump for seven days, chronically reducing the EP by 30-40 mV. Compound action potential (CAP) thresholds were correspondingly reduced by 30-40 dB SPL at high frequencies. Two weeks after withdrawal of furosemide, the treated ears showed an EP recovery of up to 20-30 mV along with a similar recovery of CAP thresholds. The influence of cell division on furosemide-induced and age-related decline of the EP was examined using a mitotic tracer, bromodeoxyuridine (BrdU). Cell proliferation was examined in three groups: young control, furosemide-treated, and aged cochleas. Sections immunostained for BrdU were bleached with H2O2 to eliminate ambiguities with melanin pigment in the inner ear. Cell types positively labeled for BrdU in all three groups included Schwann cells in Rosenthal's canal; glial cells in the osseous spiral lamina; fibrocytes in the limbus, sacculus, and spiral ligament (SL); epithelial cells in Reissner's and round-window membranes; intermediate cells in the stria vascularis; and vascular endothelial cells. Quantitative analysis showed that the mean number of BrdU-positive (BrdU+) intermediate cells in the stria did not differ significantly among the three groups. In contrast, there was a significant increase of BrdU + fibrocytes in the SL of furosemide-treated animals as compared to the young control group. Moreover, there was a significant decrease in labeled fibrocytes in the aged versus the young ears, particularly among the type II and type IV subtypes. The results suggest that the increased fibrocyte turnover in the SL after furosemide treatment may be related to the recovery of EP and CAP thresholds, supporting the hypothesis that fibrocyte proliferation may be essential for maintaining the EP and cochlear function in normal and damaged cochleas. Moreover, the decreased turnover of SL fibrocytes with age may be a contributing factor underlying the lateral wall pathology and consequent EP loss that often accompanies presbyacusis.

Action Potentials↗
PubMed1979

Effect of furosemide on hemodynamics and lung water in acute pulmonary edema secondary to myocardial infarction.

Hemodynamic studies were carried out in 19 patients with left ventricular failure complicating acute myocardial infarction. Fourteen patients were studied before and after the intravenous administration of 0.5 mg/kg of furosemide, and five patients served as a control group. Serial measurements included intracardiac pressures, cardiac output and lung water by a double isotope technique. A significant reduction was noted in right atrial (P less than 0.005), pulmonary arterial (P less than 0.0005) and pulmonary wedge pressures (P less than 0.0005) after administration of furosemide. Only the change in right atrial pressure was significantly different from that in the control group (P less than 0.05). Lung water was not changed in 4 patients studied 2 hours after administration of furosemide but was significantly changed in the remaining 10 patients studied 4 to 24 hours after furosemide (P = 0.0001). This change was also significantly different from values in the control group (P less than 0.05). The patients with no reduction in excess lung water also had a smaller reduction in pulmonary wedge pressure and a lower pretreatment stroke work index than the other patients. The mobilization of excess lung water in patients with acute myocardial infarction complicated by left ventricular failure has several features. Despite a prompt diuresis, the reduction in lung water is delayed for at least several hours after the administration of furosemide and may be related to the degree of left ventricular dysfunction. Venodilation may be a major result of treatment with furosemide.

Adult↗
PubMed1983

Hemodynamic comparison of primary venous or arteriolar dilatation and the subsequent effect of furosemide in left ventricular failure after acute myocardial infarction.

The hemodynamic effect of venous dilatation (intravenous isosorbide dinitrate [ISDN]) and arteriolar dilatation (intravenous hydralazine), both as firstline treatment and then combined with intravenous furosemide, were evaluated in a randomized, between-group comparison in 20 men with severe acute left-sided cardiac failure after myocardial infarction (MI). Both ISDN (50 to 200 micrograms/kg/hour) (Group 1) and hydralazine (0.15 mg/kg) (Group 2) reduced systemic arterial pressure (p less than 0.05) and vascular resistance (p less than 0.05). Pulmonary artery occluded pressure was reduced (p less than 0.01) only by ISDN, whereas heart rate (p less than 0.01), cardiac output (p less than 0.01) and stroke volume (p less than 0.05) were increased only after hydralazine. After ISDN, furosemide (1 mg/kg) decreased left-sided cardiac filling pressure by 1 mm Hg (p greater than 0.05), whereas after hydralazine, furosemide in a similar dose reduced pulmonary artery occluded pressure by 5 mm Hg (p less than 0.01). In both groups of patients, furosemide transiently increased systemic arterial pressure (p less than 0.05). Cardiac output was reduced (p less than 0.05) and systemic vascular resistance increased (p less than 0.05) in Group 1 patients after furosemide. Similar changes in both variables in Group 2 patients did not attain statistical significance. In conclusion, ISDN-induced venous dilatation is preferable to primary arteriolar dilatation by hydralazine as first-line treatment in acute left-sided cardiac failure. However, hydralazine and furosemide in combination were equally effective in reducing pulmonary artery occluded pressure and increasing cardiac output. The influences of each regimen on prognosis await further investigation.

Adult↗