Systemic and Regional Hemodynamic Alterations in Toxemia

Assali, N.S.; Holm, L. W.; Parker, Harold R.

doi:10.1161/01.cir.30.2s2.ii-53

Cited by 25 publications

(19 citation statements)

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“…The few reports that deal with hemodynamics in hypertensive pregnant women yield conflicting results and no firm agreement exists regarding the level of car diac output in this condition [15][16][17][18], Some of these dis crepancies may be due to nonuniform selection of pa tients. Because most prior studies have used invasive methods that can elicit stimulation of the sympathetic nervous system, they may not have been performed under truly basal conditions.…”

Section: Discussionmentioning

confidence: 99%

Maternal Echocardiography in Hypertensive Pregnancies

Degani

Abinader²,

Lewinsky³

et al. 1989

Gynecol Obstet Invest

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Echocardiographic hemodynamic and left ventricular parameters were determined in 14 normotensive and 18 hypertensive women during the last trimester of pregnancy. The hypertensive patients had significantly higher mean values of total peripheral resistance (p < 0.001), maximum velocity of posterior wall motion (p < 0.05), mean velocity of circumferential fiber shortening (p < 0.01) and percent fiber shortening of left ventricular diameter (p < 0.05). The mean values for heart rate, stroke volume, cardiac output, cardiac index, left ventricular posterior wall thickness and septal thickness did not differ significantly in both groups. These results reflect increased cardiac contractility related to elevated peripheral vascular resistance in subjects with pregnancy-induced hypertension.

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Section: Discussionmentioning

confidence: 99%

Maternal Echocardiography in Hypertensive Pregnancies

Degani

Abinader²,

Lewinsky³

et al. 1989

Gynecol Obstet Invest

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“…The group consisted of 16 patients with a mean age of 28 years (range [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] and with a mean blood pressure of 153/ 103 mm Hg (range 173-142/117-90). All had proteinuria detected using a routine method, minimal 1.2 g/ day (range 0.2-5.5) and maximal 3.9 g/day (range 0.4-15.4).…”

Section: Patientsmentioning

confidence: 99%

“…Exclusion criteria were blood pressure elevation or proteinuria before, during or after delivery; symptoms of kidney, cardiovascular, liver, endocrine, or cerebrovascular disorders; or medical therapy. The group consisted of 18 patients with a mean age of 26 years (range [17][18][19][20][21][22][23][24][25][26][27][28][29][30], and a mean blood pressure of 108/64 mm Hg (range 125-93/80-50). Mean gestational age was 40 weeks (range 37-42) at delivery and 36 weeks at last examination in pregnancy.…”

Section: Patientsmentioning

confidence: 99%

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Preeclampsia -- a state of prostaglandin deficiency? Urinary prostaglandin excretion, the renin-aldosterone system, and circulating catecholamines in preeclampsia.

Pedersen¹,

Christensen²,

Christensen³

et al. 1983

Hypertension

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SUMMARY Urinary excretion of prostaglandin E 2 (PGE 2 ) and F^ (PGF^), plasma concentrations of renin, aldosterone, norepinephrine (NE) and epinephrine (E) were determined during pregnancy, 5 days, 3, and 6 months after delivery in preeciampsia, normotensive pregnant, and nonpregnant control subjects. The PGE 2 was higher in normotensive pregnant control subjects than in nonpregnant subjects. In preeciampsia, PGE, was reduced to nonpregnant level. PGF^ was the same in preeciampsia and in normotensive pregnancy, but elevated when compared to the normotensive nonpregnant control group. Plasma concentrations of renin and aldosterone were increased during pregnancy, but considerably less in preeciampsia than during normotensive pregnancy. NE and E were the same as in nonpregnant subjects during both hypertensive and normotensive pregnancy. All parameters were normal 3 months after delivery. There were no correlations between PGE 2 , PGF^, plasma concentrations of renin, aldosterone, NE, or E and blood pressure level in third trimester either in preeciampsia or in normotensive pregnancy. PGE, was positively correlated to plasma concentrations of renin. It is suggested that the lack of renal PGE 2 in preeciampsia might be responsible for the decrease in renal blood flow and sodium excretion. It is hypothesized that preeciampsia is a state of prostaglandin deficiency. The changes in the renin-aldosterone system may be secondary to changes in prostaglandin concentration both in preeciampsia and normotensive pregnancy. Received March 16, 1982, revision accepted August 12, 1982 with simultaneous evaluation of urinary prostaglandin excretion, the renin-aldosterone system, and sympathetic adrenergic activity in preeciampsia and normotensive pregnancy both before and after delivery.In the present study we measured urinary excretion of prostaglandin E 2 (PGE 2 ), prostaglandin F 2a (PGF 2 J, plasma renin concentration, plasma aldosterone concentration, plasma norepinephrine (NE) and plasma epinephrine (E) in patients with preeciampsia and in normotensive pregnant and nonpregnant control subjects. The pregnant groups were studied during pregnancy and 5 days, 3, and 6 months after delivery. To reveal possible pressor or depressor mechanisms in preeciampsia, it was our purpose to study changes in these parameters, correlations between these parameters and blood pressure, and relationships between urinary prostaglandins, the renin-aldosterone system, and the sympathetic nervous activity.

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“…It may be that the coagulation is mainly a phenomenon occurring within the placenta in which infarction occurs because of hyper tensive vascular changes [8]. The hypertension of toxaemia is not of renal origin [23] but is due primarily to an increased reactivity of the arterioles [3,14]. These studies were designed to shed some further light on the possible causes of intravascular coagulation and also on the cause of the prote inuria.…”

Section: Discussionmentioning

confidence: 99%

Studies of Animal Models of ‘Toxaemia’ with Respect to Fibrinogen and Platelet Survival and Selectivity of Proteinuria

Wardle¹

1973

J Vasc Res

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Selenomethionine labelling of platelets and fibrinogen has been used in normal pregnant rats, and in non-pregnant and pregnant rats subjected to vasoconstriction by the use of ergometrine, pitressin, and 5-hydroxytryptophan. Since the latter agent only produced a generalised defibrination syndrome in pregnant animals, it is deduced that intravascular coagulation in ‘toxaemia’ also is within the placental bed. Further observations on DOCA hypertension microangiopathy emphasise the similarity of this model to malignant hypertension but its dissimilarity to toxaemia. Evidence from glomerular protein selectivity studies in rabbits indicates those mechanisms that cause increasing unselectivity of proteinuria.

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Systemic and Regional Hemodynamic Alterations in Toxemia

Cited by 25 publications

References 0 publications

Maternal Echocardiography in Hypertensive Pregnancies

Maternal Echocardiography in Hypertensive Pregnancies

Preeclampsia -- a state of prostaglandin deficiency? Urinary prostaglandin excretion, the renin-aldosterone system, and circulating catecholamines in preeclampsia.

Studies of Animal Models of ‘Toxaemia’ with Respect to Fibrinogen and Platelet Survival and Selectivity of Proteinuria

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