Isolation and Structure Elucidation of Diterpenes from Euphorbia pannonica, E. esula and E. falcata

Sulyok, Edvárd

doi:10.14232/phd.1913

Cited by 1 publication

(2 citation statements)

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“…We found that urinary PGE excretion of healthy premature infants was very low during the first wk, and it was rapidly increasing until the third wk and remained practically unchanged during the next two wk of life (38). Brouhard et al (7), however, failed to observe any significant difference in PGE and prostaglandin A excretion between the neonates of different gestational and postnatal ages in the ranges of 3 1 to 35 wk and 1 to 28 days, respectively.…”

Section: Discussionmentioning

confidence: 53%

“…Evidences are accumulating to indicate that the newborn infants have significantly lower urinary PG excretion when compared with those of healthy children and adults (7,11,38). We found that urinary PGE excretion of healthy premature infants was very low during the first wk, and it was rapidly increasing until the third wk and remained practically unchanged during the next two wk of life (38).…”

Section: Discussionmentioning

confidence: 59%

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Furosemide-induced Alterations in the Electrolyte Status, the Function of Renin-Angiotensin-Aldosterone System, and the Urinary Excretion of Prostaglandins in Newborn Infants

et al. 1980

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SummaryTo assess the responsiveness of the renin-angiotensin-aldosterone system of the neonate to acute furosemide stimulation and the role of renal prostaglandins in mediating the response of the renin-angiotensin-aldosterone system, this study was carried out to determine simultaneously plasma renin activity, plasma aldoste---rone concentration, urinary aldosterone, E, and prostaglandin Fz, excretion along with determination of plasma electrolyte concentration and urinary electrolyte excretion.Measurements were made on 19 newborn infants with mean birth weight and gestational age of 3009 g (range, 2700 to 4150 g) and 38.7 wk (range, 36 to 41 wk) at the age of 4 to 7 days before and after IM administration of furosemide in a dose of 1 mg/kg.It was demonstrated that in response to furosemide, urine volume ( P < 0.001). urinary sodium ( P < 0.001). potassium ( P < OM), and chloride (P < 0.001) excretion increased significantly.Furosemide administration also resulted in a significant increase from 4.41 f 2.00 to 9.70 f 2.32 ng/ml/hr ( P < 0.02) in plasma renin activity, from 1.17 f 0.22 to 1.68 2 0.36 ng/ml ( P < 0.025) in plasma aldosterone, from 0.93 f 0.16 to 1.53 f 0.35 pg/12 hr ( P < 0.025) in urinary aldosterone, from 17.53 f 3.37 to 23.73 f 3.16 4 1 2 hr ( P < 0.025) in prostaglandin E, and from 16.48 2 4.12 to 26.27 2 4.12 ng/l2 hr ( P < 0.05) in prostaglandin Fz,.It is concluded that the renin-angiotensin-aldosterone system of the neonate responds to acute furosemide challenge in spite of its high baseline activity, and its response may be mediated by increased renal prostaglandin production. SpeculationThe demonstration of high basal activity of the renin-angiotensin-aldosterone system in "nonstimulated" healthy newborn infants prompted us to study whether this high baseline activity is or is not a rate-limiting determinant of the responsiveness of the renin-angiotensin-aldosterone system to furosemide stimulation. It is also to be clarified whether the increase in the activity of the renin-angiotensin-aldosterone system, if any, in response to furosemide administration could be ascribed to its direct effect on renal sodium transport and renal hemodynamics or whether it might be mediated by the furosemide-induced alterations in renal prostaglandin production.In a series of recent publications, it has been reported that the activity of renin-angiotensin-aldosterone system (RAAS) is greatly elevated in the neonatal period (3,5,6, 8,14,18,20,22,24,26,31).The pathogenesis of the increased activity is a matter of considerable interest and dispute. However, there is widespread agreement that several factors such as perinatal stress imposed by labor and delivery (6, 8,14,21,22), the low systemic blood pressure ( S ) , the low renal blood flow (34). and the renal tubular unresponsiveness to aldosterone during the neonatal period (15,33) might play an important role in producing hyperactivity of RAAS in the neonate.Furthermore, our most recent studies provided suggestive evidences that the increased endogenous pr...

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 59%