***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Fifteen preterm infants with patent ductus arteriosus and respiratory distress syndrome were given indomethacin ( 0.2 mg/kg ) at 12 h intervals up to three times , either orally or intravenously , in an uncontrolled , non-r and omized study . Serum indomethacin concentrations were determined in blood sample s taken 12 h after dosing . There was considerable variability in the serum indomethacin concentrations , especially after oral administration , although the mean concentrations after each of the three doses were similar after both oral and intravenous administration . The frequency of closures and transient closures of the ductus arteriosus was also similar for both routes of administration . There was , however , no relation between concentration and effect in individual patients . The sustained exposure to indomethacin which appears to be necessary for ductal closure can sometimes be attained by oral administration To determine if dopamine would prevent the renal side effects of  indomethacin , fifteen preterm infants were r and omized into two groups : seven received indomethacin alone , and eight received indomethacin together with low dose dopamine infusion . Infants who received indomethacin together with dopamine had significantly higher UV ( p less than 0.005 ) , CNa ( p less than 0.005 ) , Cosm ( p less than 0.005 ) and FENA ( p less than 0.005 ) than those of infants who received indomethacin alone . There was , however , no significant difference in Ccr and FNa between the groups . These data indicate that dopamine overcomes indomethacins renal side effects of tubular origin , but it can not prevent the renal vasoconstrictive action of vasoconstrictor hormones following the inhibition of prostagl and in synthesis by indomethacin . Considering that RBF and GFR turn to normal approximately 12 hours after the last dose of indomethacin , and that with the use of dopamine  systemic blood pressure and peripheral circulation can also be normalized and to some extent myocardiac contractility improved , low doses of dopamine can be used instead of furosemide in the sick preterm infant with PDA when indomethacin therapy is indicated Furosemide stimulates the renal synthesis of prostagl and in E2 , a potent dilator of the ductus arteriosus . We administered this drug to 33 premature infants with the respiratory-distress syndrome , to determine whether it increased the incidence of patent ductus arteriosus .  Chlorothiazide , a diuretic that does not stimulate prostagl and in E synthesis , was used as the control drug in 33 other infants . During the study , the incidence of patent ductus arteriosus was significantly higher ( P less than 0.02 ) in the furosemide group ( 18 of 33 infants ) than in the chlorothiazide group ( 8 of 33 ) . Eleven infants in the furosemide group and seven in the chlorothiazide group required ductal ligation ( P greater than 0.2 ) . An additional six infants ( all from the furosemide group ) who did not have evidence of a patent ductus during the study were later found to have one . Overall survival was 76 and 61 per cent in the furosemide and chlorothiazide groups , respectively ( P greater than 0.2 ) . Small ( less than twofold ) increases in the urinary excretion of prostagl and in E were seen after the initial dose of both drugs . When the analysis was repeated after the fifth day of life , prostagl and in E excretion tripled after furosemide administration , whereas no increase occurred with chlorothiazide . We conclude that furosemide increases the incidence of patent ductus arteriosus in premature infants with the respiratory-distress syndrome , probably through a prostagl and in-mediated process The relative potency of four non-steroidal anti-inflammatory drugs ( NSAIDs ) - indomethacin , flurbiprofen , sulindac and piroxicam - in inhibiting  frusemide-stimulated natriuresis and creatinine clearance was investigated in a placebo controlled cross-over study using healthy volunteers . All four drugs tested significantly inhibited the action of frusemide  and they were equipotent in their effects . If it is accepted that sulindac is renal sparing with respect to inhibition of prostagl and in synthesis , our observations raise two possibilities concerning the underlying mechanism of antagonism : a ) that inhibition of renal prostagl and in synthesis is not important ; b ) that sulindac interacts with frusemide in a manner different from other NSAIDs To determine if furosemide would prevent the renal side effects of indomethacin therapy in premature infants with patent ductus arteriosus , 19 premature infants were r and omized into two groups : nine received indomethacin alone , and ten received indomethacin followed immediately by furosemide . There was no significant difference between the groups in birth weight , gestational age , postnatal age , and in cardiopulmonary or renal status at the time of study . Infants who received indomethacin and furosemide had significantly higher urine output ( P less than 0.05 ) , higher FENa and FECl ( P less than 0.01 ) , and higher glomerular filtration rate ( P less than 0.05 ) than those of infants who received indomethacin alone . Seven infants in each group responded to indomethacin therapy with disappearance of PDA murmur and improvement of cardiovascular status . The results of this study suggest that furosemide may prevent the renal side effects of indomethacin therapy and yet not affect the efficacy of indomethacin in the closure of a PDA Renal function and changes in the activity of selected vasoactive hormones during prolonged indomethacin therapy ( 1 week ) were studied in 11 very-low-birth-weight infants with symptomatic patent ductus arteriosus . The initiation of indomethacin therapy was associated with a reduction in diuresis , a transient decrease in creatinine clearance , and an increase in body weight ( P less than 0.01 ) . Furthermore , there was a transient trend toward hyponatremia and hyperkalemia . This acute renal dysfunction was compatible with a complex picture of renal hypoperfusion associated with a fall of plasma renin activity from high levels prior to indomethacin treatment , with a transient rise in the plasma level of arginine vasopressin and with suppressed renal and systemic prostagl and in synthesis . During treatment , an effective circulatory volume was restored by closing the ductus . In parallel , PRA and AVP plasma concentrations returned to nearly normal values . Subsequently , kidney function was not further impaired despite continued indomethacin therapy . These observations suggest that prolonged indomethacin therapy for prevention of sPDA relapse probably constitutes no further risk to kidney function after successful pharmacologically induced ductal constriction To determine whether furosemide could prevent renal side effects of indomethacin ( INN , indometacin ) used for the pharmacologic closure of the patent ductus arteriosus ( PDA ) in preterm infants Nonsteroidal anti-inflammatory drugs ( NSAID ) suppress prostagl and in-dependent renal blood flow and furosemide-induced diuresis in patients with cirrhosis and ascites . Since sulindac may selectively spare inhibition of renal prostagl and ins , we evaluated the interactions of acute administration of sulindac or indomethacin with furosemide in 15 patients with cirrhosis and ascites . Prior to furosemide , indomethacin reduced creatinine clearance ( by 55 % ) , urinary volume ( by 82 % ) , sodium ( by 93 % ) , and prostagl and in E2 ( by 87 % ) ( all P less than 0.05 ) , whereas sulindac had no effect . However , both drugs reduced furosemide-induced diuresis .  Indomethacin appeared slightly more potent in reducing the diuresis ( 55 % v 38 % ) , natriuresis ( 67 % v 52 % ) , and prostagl and in E2 ( PGE2 ) release ( 81 % v 74 % ) . In a similar protocol in healthy subjects , furosemide-induced diuresis and natriuresis were also blunted by both drugs . Thus , under conditions of enhanced prostagl and in activity from furosemide , sulindac does affect renal function . These data suggest that renal function should be monitored in patients with cirrhosis and ascites who receive sulindac as well as other NSAID 
    Output:
    
After the first dose of indomethacin , patients receiving furosemide had higher urine output , fractional excretion of sodium , and osmolar clearance than controls .
Thus , dehydration appears to be a contraindication for furosemide administration in premature infants treated with indomethacin for symptomatic PDA .