Six-hour Infusion Research Articles

Induction of premature parturition in goats by prostaglandin F 2α administered into the uterine vein

Premature parturition was induced in goats by brief infusions of prostaglandin F 2α into uterine veins ipsilateral to the ovary containing the corpus luteum. Six-hour infusions at rates of 15, 7.5, 3.75 and 1.88 μg/min were luteolytic and consequently initiated labour. The lowest dose used (0.94 μg/min for 6 hours or 1.88 μg/min for 3 hours) caused no permanent change in circulating concentrations of progesterone and failed to initiate labour. Concentrations of Prostaglandin F in the utero-ovarian venous plasma resulting from infusions at rates of 1.88 and 7.5 μg/min were within the range of levels found previously in goats at the time of luteal regression preceding spontaneous delivery at term. All instances of luteolysis were followed by the delivery of live foetuses but all except one born 11 days prematurely died from respiratory failure. Lactation was established in 1 of the 5 does.

Prostatic tumor acid phosphatase production: Influence of antineoplastic agents

The administration of mithramycin and dactinomycin to several patients with widespread prostatic carcinoma consistently induced a substantial but brief reduction of serum acid phosphatase, indicating an inhibition on the synthesis of the enzyme produced by the tumor. The lowering of the elevated serum enzyme value is more pronounced and prolonged when Thiotepa (triethyleneiophosphoramide) is given concurrently with a daily four- to six-hour infusion of mithramycin for one week.

DEHYDROEPIANDROSTERONE IN BLOOD

We have reported on the liberation of dehydroepiandrosterone (DHEA) from human blood plasma following hydrolysis with commercial acid and alkaline phosphatases (Oertel & Eik-Nes, 1958). This communication deals with isolation of complexes containing DHEA and phosphate from human blood plasma after infusion of corticotrophin (ACTH). Blood was collected from the arm vein after a six-hour infusion of 25 I. U. of ACTH in four normal male subjects. The plasma was submitted to the following procedure: Extraction of free steroids: Four hundred ml. plasma were extracted three times with 400 ml. methylene chloride each time. The combined extracts were evaporated to dryness in vacuo at +40° C. Defatting of extract: The residue of the EtOH extract was suspended in 100 ml. 70% methanol (MeOH) and the sample kept at −15° C. for 15 hours, whereby most fatty material was precipitated. Following centrifugation at 2000 rpm, the supernatant was carefully decanted

Changes in plasma level of 17-hydroxy-corticosteroids induced by ACTH. III. Effects of various vehicles and modes of administration.

Based on their ascorbic-acid depleting potency, various preparations of ACTH did not differ in their ability to increase the plasma level of 17-hydroxycorticosteroids (17-OHCS) when a dose of 25 I.U. of ACTH was given intravenously as a six-hour infusion. When ACTH is injected intramuscularly it is apparently absorbed or destroyed faster than when given intravenously. When ACTH is injected intramuscularly it is apparently absorbed or destroyed faster than when given intravenously. Reduction in these rates of absorption or destruction can be achieved by giving ACTH intramuscularly either in gelatin or as a zinc protamine complex.

Changes in plasma levels of 17-hydroxycorticosteroids during the intravenous administration of ACTH. II. Response under various clinical conditions.

IN a previous paper from our laboratory (1), a test was described for the evaluation of adrenocortical capacity, based on changes in the circulating levels of 17-hydroxycorticosteroids in blood plasma during the intravenous infusion of 25 i.u of adrenocorticotropic hormone (ACTH) over six hours. No significant difference was found between plasma 17-hydroxycorticosteroid levels following the administration of 25 i.u of ACTH over six hours as compared with 50 i.u of ACTH during the same period. Furthermore, we were able to show that the administration of ACTH over six hours caused maximal stimulation of the adrenal cortex in the resting human. Continuous intravenous administration of optimal doses of ACTH— 25 i.u every six hours—did not raise significantly the levels of 17-hydroxycorticosteroids above those achieved after the six-hour infusion. It was pointed out that, for the test to be quantitatively significant, a stable adrenocortical steroid environment is required. This can be found under physiologic ...