Prevention of contrast media-induced renal dysfunction with prostaglandin E1: a randomized, double-blind, placebo-controlled study.

Preexisting renal impairment is an all-encompassing risk factor for radiocontrast-associated nephrotoxicity. Renal impairment appears to be associated with the inadequate production of renal prostaglandins at the critical time of radiocontrast administration and for a variable time period afterward. We prospectively studied 130 patients with chronic renal insufficiency (serum creatinine > or =1.5 mg/dL) who were undergoing radiocontrast administration. Using a double-blind, randomized, prospective technique, patients were assigned to either placebo or one of three prostaglandin E1 (PGE1) treatment groups (10, 20, or 40 ng/kg/min). Infusion was started 60 +/- 30 minutes before the administration of radiocontrast and was continued for a total of 6 hours. In the placebo group, radiocontrast administration resulted in a mean increase (+/- SD) in serum creatinine of 0.72 +/- 1.15 mg/dL at 48 hours. This increase was less in each of the PGE1 treatment groups after 48 hours, with a significant difference between placebo and the 20 ng/kg/min PGE1 group (P = 0.01). Using baseline adjusted means, analysis of covariance with baseline serum creatinine as the covariable demonstrated significant differences between the placebo and 20 ng/kg/min PGE1 group (P = 0.03) and between the placebo and 10 ng/kg/min PGE1 group P = 0.047). In a subgroup analysis of the diabetic patients, the increase in serum creatinine was less pronounced in the three PGE1 groups versus the placebo group, and the 20 ng/kg/min PGE1 group had the most favorable outcome. The parenteral administration of PGE1 immediately before radiocontrast exposure and continued for a period of 5 to 5.5 hours significantly reduced the elevation of serum creatinine poststudy. The most effective of the three PGE1 dosing regimens was 20 ng/kg/min.

Effect of prostaglandin E1 on extravascular lung water in patients with severe heart failure.

Prostaglandin E ( 1 ) (PGE ( 1 ) ) is a naturally occurring paracrine hormone that is used pharmacologically for treatment of peripheral occlusive arterial disease and to maintain ductus-arteriosus patency in neonates with congenital heart disease until the primary condition is operable. PGE ( 1 ) treatment also has been associated with reduction in pulmonary arterial pressure and increase in cardiac output in patients with left ventricular failure. In contrast, in isolated cases, patients with heart failure reportedly have developed pulmonary edema while receiving PGE ( 1 ). Therefore, to better define the effect of PGE ( 1 ) in heart failure, this double-blind study investigated the effect of PGE ( 1 ) on extravascular lung water in intensive-care patients with severe heart failure (New York Heart Association [NYHA] classes III and IV) and slightly above-normal extravascular lung water. Intravenous infusion of 60 microg PGE ( 1 ) (Prostavasin; Schwarz Pharma, Monheim, Germany) over a period of 2 hours caused no significant change in lung water relative to the baseline values (9.8 +/- 4.3 mL/kg before the infusion, 9.3 +/- 3.2 mL/kg after 1 hour, and 9.4 +/- 3.5 mL/kg after 2 hours) or to values observed in placebo-treated patients (6.5 +/- 3.3 mL/kg before the infusion, 7.1 +/- 2.7 mL/kg after 1 hour, and 7.0 +/- 3.2 mL/kg after 2 hours). Thus, administration of PGE ( 1 ) is unlikely to cause or worsen pulmonary edema in patients with severe heart failure (NYHA classes III and IV).

[Effect of prostaglandin E1 on extravascular lung water in patients with severe heart failure]. / Wirkung von Prostaglandin E1 auf das extravaskuläre Lungenwasser bei Patienten mit schwerer Herzinsuffizienz.

Prostaglandin E1 (PGE1) is a physiologic vasodilator, which is broadly used in the therapy of peripheral arterial occlusive disease. In addition, the successful use of PGE1 in patients with severe heart failure has been described in several studies, where a decrease in pulmonary artery pressure and an increase in cardiac output were observed. In contrast to these positive effects, the development of lung edema was reported in individual cases after the infusion of PGE1 in patients with heart disease. We therefore conducted a double-blind study to evaluate the effect of PGE1 on extravascular lung water (EVLW) in patients with heart failure (NYHA III-IV) and borderline increased EVLW. Seven patients received an infusion of PGE1 (Prostavasin) at a dosage of 60 micrograms over 2 hours, while in 6 patients (control group) isotonic saline was given as placebo. EVLW was measured using a double indicator method at time points -15 h, -9 h before and at the start of the infusion, 1 h and 2 h during infusion, as well as +1 h, +4 h, +7 h, and +22 h after termination of the infusion. Infusion of PGE1 did not alter EVLW both in comparison to pre-study values (9.8 +/- 4.3 ml/kg bw preinfusion. 9.3 +/- 3.2 ml/kg bw after 1 hour and 9.4 +/- 3.5 ml/kg bw after 2 hours) or to the control group (6.5 +/- 3.3 ml/kg bw preinfusion, 7.1 +/- 2.7 ml/kg bw after 1 hour and 7.0 +/- 3.2 ml/kg bw after 2 hours). We conclude that there is no evidence that PGE1 might contribute to the development, or worsening of lung edema by inducing extravascular lung water accumulation and can, thus, be savely given to patients with even a severe degree of heart failure (NYHA III-IV).

High resolution analysis and differential condensation in RBA-banded human chromosomes.

Human prophase, premetaphase, and mid-metaphase chromosomes are prepared and analyzed using the thymidine cell synchronization technique and R-banding patterns (RBA). Haploid sets with 700-1000 bands can be demonstrated. Sequences of chromosomes of different degrees of condensation are helpful for a better understanding and classification of regions of extended chromosomes. A considerable variation in the condensation of parts of homologous chromosomes is reflected in the variability of the arm ratio. This differential condensation of chromosomes is entirely effected by variation of the degree of condensation in AT rich interbands and can be attributed to the degree of labeling by BrdU.