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Biomedical subjects

M Wohlert

Publications and source records attributed to M Wohlert.

30 records · Page 2Linked to original sources
PubMed1984

Circulating immune complexes and hypertension in pregnancy.

Eighteen patients with pre-eclampsia, 10 patients with essential and 9 with transient hypertension during pregnancy, were investigated regarding circulating immune complexes by a Clq-binding assay and a PEG precipitation assay. The women were studied during pregnancy, 2 and 5 days after childbirth, and also 3 and 6 months afterwards. The frequency of circulating immune complexes was not significantly increased in any of the groups when compared with that in 18 normotensive pregnant control subjects and 19 non-pregnant controls. Thus Clq-binding and PEG-precipitable immune complexes are a feature neither of normal pregnancy, nor of pregnancy complicated by hypertension or pre-eclampsia.

Antigen-Antibody Complex↗
PubMed1983

Prostaglandins, renin, aldosterone, and catecholamines in preeclampsia.

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin (PRC), aldosterone (PAC), noradrenaline (PNA) and adrenaline (PA) were determined in the third trimester of pregnancy, 5 days and 3 months after delivery in preeclampsia and normotensive pregnant and non-pregnant control subjects. PGE2 was higher in pregnant control subjects than in non-pregnant subjects, but reduced to non-pregnant level in preeclampsia. PGF2 alpha was the same in preeclampsia and normotensive pregnancy but higher than in the non-pregnant group. PRC and PAC were increased during pregnancy, but considerably lesser in preeclampsia than during normotensive pregnancy. PNA and PA were the same in all three groups. All parameters were normal 3 months after delivery. There were no correlations between any of the hormones and blood pressure in any of the groups. PGE2 was positively correlated to PRC. The lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion, and the changes in PRC and PAC are supposed to be secondary to changes in PGE2. It is hypothesised that preeclampsia is a state of prostaglandin deficiency.

Aldosterone↗
PubMed1983

The influence of normotensive pregnancy and pre-eclampsia on angiotensin-converting enzyme.

Serum angiotensin-converting enzyme (SACE) levels were determined in normotensive pregnant subjects and patients with pre-eclampsia in the third trimester of pregnancy and 5 days, 3 and 6 months after parturition, and also in the first and second trimester in the normotensive group. SACE levels were reduced during pregnancy and 5 days after delivery in the normotensive subjects compared with the levels 3 and 6 months after delivery and to the non-pregnant control subjects. After correction for plasma volume expansion, SACE was reduced in first and second trimester only. In pre-eclampsia both SACE and corrected SACE were significantly lower in third trimester and 5 days after parturition than 3 and 6 months after delivery and in non-pregnant control subjects. The reason for the reduced level of SACE in first and second trimester during normal pregnancy is not known. The low SACE levels in pre-eclampsia may be a secondary phenomenon due to a decreased placental synthesis without primary importance for the blood pressure regulation.

Adolescent↗
PubMed1982

Incidence of chromosome abnormalities in newborn children. Comparison between incidences in 1969-1974 and 1980-1982 in the same area.

As part of an ongoing study of the influence of environmental factors on pregnancy, childbirth, and fetuses, comparisons have been made between incidences in 1969-1974 and in 1980-1982 of chromosome aberrations in liveborn children in the same area of Denmark. The incidence of chromosome aberrations in the first period was 2.6 per 1000, compared with 41. per 1000 during the latter period. However, the difference was mainly due to an increase in inversions, and this in turn was due to a difference in chromosome staining methods between the two periods. It is concluded that the Danish study and similar studies in the United States, Canada, and Scotland indicate that early detection of chromosome aberrations by chromosome examination at birth is indicated in order to be able to inform and counsel parents of children with chromosome aberrations. Chromosome examination at birth is also of importance in the diagnosis of structural inheritable chromosome aberrations and consequent family investigation and genetic counseling.

Chromosome Aberrations↗
PubMed1982

Plasma noradrenaline and adrenaline in pre-eclampsia, essential hypertension in pregnancy and normotensive pregnant control subjects.

Noradrenaline and adrenaline in plasma were determined in 15 patients with pre-eclampsia, 10 pregnant patients with essential hypertension, 2 patients with transient hypertension in pregnancy, 11 normotensive pregnant control subjects, and 16 non-pregnant normotensive control subjects. Measurements were performed in the second and third trimester, 5 days, and 3 months after delivery. Comparison within groups showed no significant differences in plasma noradrenaline or adrenaline between levels in pregnancy, 5 days after delivery, and 3 months after delivery in neither pre-eclampsia, essential hypertension nor normotensive pregnant control subjects. Comparison between groups showed no significant differences between the levels in pre-eclampsia, essential hypertension and normotensive pregnant control subjects, neither in pregnancy nor after delivery. Plasma noradrenaline and adrenaline in pregnancy were the same as in normotensive non-pregnant control subjects. Plasma noradrenaline and blood pressure were not correlated in any of the groups. It is concluded that the sympathetic adrenergic activity evaluated by plasma catecholamines is normal in patients with pre-eclampsia and pregnant patients with essential hypertension.

Adolescent↗
PubMed1982

Prostaglandins, catecholamines, renin and aldosterone during hypertensive and normotensive pregnancy.

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin (PRC), aldosterone (PAC), noradrenaline (PNA) and adrenaline (PA) were determined in the third trimester of pregnancy, 5 days and 3 months after delivery in preeclampsia and normotensive pregnant and non-pregnant control subjects. PGE2 was higher in pregnant control subjects than in non-pregnant subjects, but reduced to non-pregnant level in preeclampsia. PGF2 alpha was the same in preeclampsia and normotensive pregnancy but higher than in the non-pregnant group. PRC and PAC were increased during pregnancy, but considerably lesser in preeclampsia than during normotensive pregnancy. PNA and PA were the same in all three groups. All parameters were normal 3 months after delivery. There were no correlations between any of the hormones and blood pressure in any of the groups. PGE2 was positively correlated to PRC. The lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion, and the changes in PRC and PAC are supposed to be secondary to changes in PGE2. It is hypothesised that preeclampsia is a state of prostaglandin deficiency.

Aldosterone↗
PubMedDate not supplied

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

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin, aldosterone, norepinephrine (NE) and epinephrine (E) were determined during pregnancy, 5 days, 3, and 6 months after delivery in preeclampsia, normotensive pregnant, and nonpregnant control subjects. The PGE2 was higher in normotensive pregnant control subjects than in nonpregnant subjects. In preeclampsia, PGE2 was reduced to nonpregnant level. PGF2 alpha was the same in preeclampsia 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 preeclampsia 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 PGE2, PGF2 alpha, plasma concentrations of renin, aldosterone, NE, or E and blood pressure level in third trimester either in preeclampsia or in normotensive pregnancy. PGE2 was positively correlated to plasma concentrations of renin. It is suggested that the lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion. It is hypothesized that preeclampsia is a state of prostaglandin deficiency. The changes in the renin-aldosterone system may be secondary to changes in prostaglandin concentration both in preeclampsia and normotensive pregnancy.

Aldosterone↗