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Biomedical subjects

D E Van Orden

Publications and source records attributed to D E Van Orden.

11 recordsLinked to original sources
PubMed1979

Dysmenorrhea: treatment with an antiprostaglandin.

Painful menses, one of the most frequent gynecologic complaints, is incapacitating for many women. It has recently been proposed that increased endometrial prostaglandin production and prostaglandin-induced myometrial contractility may be responsible for dysmenorrhea. In this prospective, double-blind, 3-way, crossover study, relief of pain by an antiprostaglanding drug, ibuprofen (400 mg), was compared with propoxyphene (64 mg) and placebo in 22 women with severe primary dysmenorrhea. Ibuprofen was significantly more effective in 18 patients when compared to the other 2 treatment regimens (P less than 0.001), while propoxyphene was superior to placebo in 13 patients (P less than 0.05). Prostaglandin E and F synthesis rates in endometrial biopsy specimens taken on the second day of treatment in 2 patients during each treatment cycle were lowest during ibuprofen in one case but showed no definite pattern in the second.

Adolescent↗
PubMed1978

Effects of indomethacin on the vascular abnormalities of Bartter's syndrome.

We examined the hypothesis that the vascular abnormalities of Bartter's syndrome are due to excess production of prostaglandin. Balance studies and vascular reactivity studies were performed before and after indomethacin (200 mg/day) in a patient with well-documented Bartter's syndrome. During indomethacin, potassium balance became positive, serum potassium rose from 2.1--3 mEq/1 in the absence of potassium supplementation, plasma renin activity decreased from 55--3.2 ng/day and peripheral plasma PGA-like activity fell from 1460 +/- 220 to 456 +/- 71 pg/ml. Before indomethacin, forearm vasoconstrictor responses to brachial arterial infusions of angiotensin II, norepinephrine and to neurogenic reflex stimulation elicited by lower body suction were greatly depressed compared to those of normal subjects. During indomethacin these responses were restored to normal. The dose of intravenous angiotensin II required to increase diastolic blood pressure 20 mm Hg decreased from 160--30 ng/kg/min. These data support the hypothesis that the vascular insensitivity to exogenous angiotensin II, norepinephrine and to neurogenic reflex stimulation observed in this patient with Bartter's syndrome is due to excess prostaglandin. Moreover, stimulation of the renin-angiotensin-aldosterone system in this syndrome appears to be a compensatory adaptation to excess prostaglandin production.

Adult↗
PubMed1978

Phenylbutazone-induced decrease in renal blood flow.

Phenylbutazone (Butazolidin), and anti-inflammatory agent, has been reported to decrease renal excretion of sodium and water. Whether or not an alteration in renal hemodynamics could be involved in producing these effects was tested in anesthetized dogs. Renal blood flow (RBF) was monitored with electromagnetic flow probes. After i.v. administration of phenylbutazone, 2 mg/kg, RBF fell by 20%. Glomerular filtration rate, sodium and water excretion were also decreased and blood pressure increased slightly. The reduction of RBF and glomerular filtration rate by phenylbutazone indicates that a hemodynamic mechanism could be involved in the retention of sodium and water induced by this agent. The decreased blood flow was correlated with a depressed renal secretion of prostaglandin E. Also, in animals pretreated with indomethacin, another inhibitor of prostaglandin synthesis, administration of phenylbutazone did not result in any additional changes in renal hemodynamics or excretion of sodium and water. In addition, phenylbutazone antagonized the ability of furosemide to increase RBF, an inhibition which has previously been shown to occur with indomethacin. Thus, phenylbutazone appears to alter renal mechanisms in a manner similar to indomethacin.

Animals↗
PubMed1978

Plasma prostaglandins in pregnancy.

Plasma prostaglandins were determined by radioimmunoassay in 92 pregnant and 14 nonpregnant women. There was significant elevation of PGA-like material in the first trimester of pregnancy (1744 pg/ml) over that seen in nonpregnant women (576 pg/ml) with continuation of that elevation in the second and third trimesters. No significant difference existed among PGE levels of the nonpregnant group (251 pg/ml) and the first two trimesters of pregnancy (384 pg/ml and 294 pg/ml); the PGE level of the third trimester group (443 pg/ml) was significantly elevated over that of the nonpregnant group. PGF levels remained constant during all trimesters (135 pg/ml, 144 pg/ml, and 130 pg/ml) but exhibited plasma concentrations significantly higher than the nonpregnant group (78 pg/ml). Potential role (s) of prostaglandins as mediators of cardiovascular and renal changes of pregnancy are discussed.

Cardiovascular Physiological Phenomena↗
PubMed1977

Role of endogenous prostaglandins in regulation of uterine blood flow and adrenergic neurotransmission.

Earlier studies from these laboratories have demonstrated that prostaglandins (PG's) of the A and E series are potent uterine vasodilators whereas PGF's do not significantly alter uterine vascular resistance. In addition, PGE's and PGF's are also able to modify adrenergic vasoconstrictor responses in the canine uterus. In the present study the role of endogenous prostaglandins in regulating uterine vascular resistance and adrenergic neurotransmission was evaluated. Intra-arterial infusion of the prostaglandin synthesis inhibitor meclofenamate resulted in a significant reduction in PGE levels in uterine venous plasma and increased vascular resistance. Uterine vasoconstrictor responses produced by sympathetic nerve stimulation and norepinephrine were enhanced when endogenous PG synthesis was inhibited. During sympathetic nerve stimulation, uterine venous plasma levels of radioimmunoassayable prostaglandins of the E of F series did not change, suggesting that the adrenergic activation of PG synthesis is not detectable in uterine venous efferent. These data suggest that endogenous prostaglandins of the E series appear to play an important role in regulating uterine blood flow (I) by relaxing uterine vascular smooth muscle and (2) by depressing adrenergic vasoconstrictor responses.

Animals↗
PubMed1977

Radioimmunoassay of PGE and an approach to the specific measurement of PGE1.

A specific radioimmunoassay for prostaglandins of the E series is presented. Several refinements of the conventional procedures used for unknown sample preparation prior to assay are described. Validation of the method through recovery of labeled and unlabeled prostaglandin E from plasma indicates: 74% extraction efficiency, 80% chromatographic separation efficiency, and a 67% overall recovery figure for the complete assay. The development of an "absorbed system" approach for measuring one E prostaglandin (PGE1) without interference from the other E prostaglandin (PGE2) is also described. A preliminary study of rat tissue and male plasma samples measured by these assay systems is included. Alternate approaches to the development of a specific PGE1 assay, although less feasible in these authors' hands, are discussed.

Animals↗
PubMed1977

A technique for the immunohistochemical localization of prostaglandin E.

Prostaglandin E (PGE) has been localized via the unlabeled antibody technique in freeze-dried and ethanol-fixed cryostat sections. Discrete perivascular and stromal localization was present in the uterus prepared by the method presented, but not in classically fixed specimens. Absorption of the anti-PGE by addition of free PGE was ineffective; whereas, removal of PGE-reactive antibodies from the anti-serum was effectively accomplished with an Affigel-101-PGE immunoadsorbant column.

Animals↗
PubMed1976

Ethacrynic acid induced release of prostaglandin E to increase renal blood flow.

Ethacrynic acid administered to anesthetized dogs was found to increase the level of prostaglandin E as determined by radioimmunoassay in renal venous blood at the time when renal blood flow was increased by this agent. No change was found in the renal venous level of prostaglandin F. When ethacrynic acid was administered after treatment with indomethacin, which blocks the increase in renal blood flow induced by the natriuretic agent, no increase in the renal venous level of prostaglandin E was seen. Thus, the dilation of the renal vasculature would appear to be caused by a stimulation of synthesis and release of prostaglandin E by ethacrynic acid.

Animals↗