Predicting preeclampsia.

W F O'Brien

Home/Archive/PubMed

PubMed · 2137575

Predicting preeclampsia.

W F O'Brien

View original source ↗Export metadata ↓

Abstract

Recent studies suggest that drugs affecting prostacyclin and thromboxane production may be able to affect the development of preeclampsia. In order to use these agents effectively, we must be able to select properly women at high risk. This review evaluates a number of historic and physical factors and laboratory tests that may aid in the prediction of preeclampsia. Family history, parity, and the roll-over test are currently the most efficient methods that are widely available. Two relatively new laboratory tests, plasma fibronectin concentration and urinary calcium/creatinine ratio, hold the greatest promise for the near future.

Explore related subjects

Angiotensin II Antithrombin III Atrial Natriuretic Factor Blood Pressure Blood Proteins Calcium Cardenolides Digoxin Female Humans Iron Pre-Eclampsia Pregnancy Saponins Serum Albumin Uric Acid beta-Thromboglobulin Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

W F O'Brien. 1990. Predicting preeclampsia.. https://pubmed.ncbi.nlm.nih.gov/2137575/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

Sympathetic overactivity in patients with chronic renal failure.

BACKGROUND: Hypertension is a frequent complication of chronic renal failure, but its causes are not fully understood. There is indirect evidence that increased activity of the sympathetic nervous system might contribute to hypertension in patients with end-stage renal disease, but sympathetic-nerve discharge has not been measured directly in patients or animals with chronic renal failure. METHODS: We recorded the rate of postganglionic sympathetic-nerve discharge to the blood vessels in skeletal muscle by means of microelectrodes inserted into the peroneal nerve in 18 patients with native kidneys who were undergoing long-term treatment with hemodialysis (of whom 14 had hypertension), 5 patients receiving hemodialysis who had undergone bilateral nephrectomy (of whom 1 had hypertension), and 11 normal subjects. RESULTS. The mean (+/- SE) rate of sympathetic-nerve discharge was 2.5 times higher in the patients receiving hemodialysis who had not undergone nephrectomy than in the normal subjects (58 +/- 3 vs. 23 +/- 3 bursts per minute, P < 0.01). In contrast, the rate of sympathetic-nerve discharge was similar in the patients receiving hemodialysis who had undergone bilateral nephrectomy (21 +/- 6 bursts per minute) and the normal subjects. The rate of sympathetic-nerve discharge in the patients receiving hemodialysis who had not undergone nephrectomy was also significantly higher (P < 0.01) than that in the patients with bilateral nephrectomy, and it was accompanied in the former group by higher values for vascular resistance in the calf (45 +/- 4 vs. 22 +/- 4 units, P < 0.05) and mean arterial pressure (106 +/- 4 vs. 76 +/- 14 mm Hg, P < 0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. CONCLUSIONS: Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.

Angiotensin II↗

PubMed1992

Angiotensin II actions in paraventricular nucleus: functional evidence for neurotransmitter role in efferents originating in subfornical organ.

Angiotensin II (ANG) has been suggested to be the neurotransmitter utilised by subfornical organ (SFO) efferents projecting to the paraventricular nucleus (PVN). The PVN has been shown to be involved in mediating the cardiovascular response elicited by electrical stimulation of SFO. The possible role of ANG as a neurotransmitter in these pathways has been examined in the present study. The cardiovascular effects of ANG microinjection into the PVN were examined in urethane anaesthetized, male Sprague-Dawley rats. Microinjection of 20 ng or 50 ng ANG into PVN resulted in mean increases in blood pressure of 12.8 +/- 0.6 mmHg (P < 0.0005), and 16.2 +/- 1.4 mmHg (P < 0.0001) respectively, without effect on heart rate. These responses were significantly attenuated following systemic administration of losartan, an ANG type 1 receptor (AT1) antagonist (Control, +12.8 +/- 0.6 mmHg; post-losartan, +5.6 +/- 1.7 mmHg), but were unaffected by the AT2 receptor antagonist, PD123319 (Control, +10.8 +/- 1.6 mmHg; post-PD123319, +11.6 +/- 2.4 mmHg). Initial and later components of the biphasic pressor response elicited by electrical stimulation of SFO (200 microA, 10 Hz, 1 ms pulse width, 10 s) were also significantly attenuated by losartan, but unaffected by PD123319. The short latency increase in mean arterial pressure was 16.6 +/- 2.3 mmHg in comparison to a post-losartan increase of 9.3 +/- 1.6 mmHg (P < 0.001). Similarly, the secondary response consisted of a control increase of 9.6 +/- 1.3 mmHg and a post-losartan increase of 3.4 +/- 0.9 mmHg (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1992

Noninvasive detection of left ventricular diastolic dysfunction using M-mode echocardiography to assess left ventricular posterior wall kinetics in hypertrophic cardiomyopathy.

In patients with hypertrophic cardiomyopathy (HC), it is difficult to determine the severity of left ventricular (LV) diastolic dysfunction. Three different patterns of LV posterior wall motion were found by M-mode echocardiography in patients with HC, and the use of these patterns is proposed as a new noninvasive index of the severity of LV diastolic dysfunction. M-mode echocardiograms were recorded prospectively from 35 patients with HC, and the posterior wall motion pattern in late systole and early diastole was classified into the following 3 types: (1) normal motion (n = 9); (2) flat motion--flat motion from late systole to early diastole, followed by rapid backward movement (n = 13); and (3) downward motion--slow backward movement from late systole (n = 13). There were no differences in the severity or type of hypertrophy, LV systolic function and pulsed Doppler indexes of LV filling among these 3 groups. However, LV end-diastolic pressure was increased in the groups with flat (15 +/- 6 mm Hg) and downward (16 +/- 9 mm Hg) motion. Furthermore, the maximal rate of decrease in LV pressure (normal 1,450 +/- 300, flat 1,250 +/- 300 and downward 860 +/- 80 mm Hg/s) and the time constant of LV pressure reduction (normal 60 +/- 15, flat 70 +/- 25 and downward 101 +/- 34 ms) showed a stepwise deterioration from the normal to the flat and then to the downward motion groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗