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Biomedical subjects

G Aisenbrey

Publications and source records attributed to G Aisenbrey.

7 recordsLinked to original sources
PubMed1992

Prenatal diagnosis of transient myeloproliferative disorder via percutaneous umbilical blood sampling. Report of two cases in fetuses affected by Down's syndrome.

Since its initial description in 1982, percutaneous umbilical blood sampling has become useful in diagnosing, monitoring, and even treating a variety of fetal disorders. Recently two percutaneous umbilical blood samples were evaluated in which the white blood cell count was markedly elevated with many circulating blasts. Both samples exhibited the morphologic features of a transient myeloproliferative disorder, characteristically seen in neonates and infants with Down's syndrome. In both cases, antenatal clinical and ultrasound abnormalities also were suggestive of Down's syndrome, which was confirmed by cytogenetic studies. Although the peripheral blood abnormalities persisted at birth, both patients experienced spontaneous remission of the transient myeloproliferative disorder by 5 weeks of age. To our knowledge, these two cases of Down's syndrome represent the first reported examples of the intrauterine diagnosis of transient myeloproliferative disorders.

Adult↗
PubMed1991

How do perinatologists manage preeclampsia?

The members of the Society of Perinatal Obstetricians were surveyed regarding management of preeclampsia, with focus on drug therapy, use of invasive monitors, and both general policies and treatment of hypothetical cases of preterm severe preeclampsia. There was agreement that magnesium sulfate should be given to all patients with preeclampsia during labor and postpartum and that blood pressure should be held to about 160/105 mmHg. The drugs of choice for control of blood pressure were hydralazine, alpha-methyldopamine, and cardioselective beta-blockers. Most perinatologists use invasive monitors only for specific indications, but a substantial minority use either arterial lines or central venous pressure monitors routinely in severe preeclampsia. There was no consensus with respect to management of preterm, severe preeclampsia, but even among the 49% of respondents who volunteered an unequivocal policy of "deliver regardless of gestational age," over three fourths would hospitalize and observe in selected cases meeting American College of Obstetrics and Gynecology criteria for severe preeclampsia.

Adrenergic beta-Antagonists↗
PubMed1986

Aggressive angiomyxoma of the vulva.

An unusual myxoid and vascular appearing neoplasm of the vulva, termed an aggressive angiomyxoma, is described in a 36-year-old Hispanic woman. The clinical presentation and recurrence pattern were typical for previously described neoplasms of the same cellular pattern. The histopathology, difficulties in determining the surgical margins, and the treatment of this tumor are discussed.

Adult↗
PubMed1985

Atrial myxoma as a complication of tocolytic therapy. A case report.

A 27-year-old woman who presented with premature labor was given ritodrine for tocolysis. During the administration of the beta-sympathomimetics she developed cardiac changes, including subendocardial ischemia on EKG and an intermittent early diastolic sound. Echocardiography revealed a large left atrial myxoma. It was removed during pregnancy, and the patient tolerated the procedure well. The mechanism of the ischemia was believed to result from the space-occupying mass of the myxoma, preventing adequate atrial filling and subsequent congestive failure. It is recommended that patients who develop cardiac symptoms during tocolysis with beta-sympathomimetics undergo further investigation to rule out under-lying pathology.

Adult↗
PubMed1978

Prostaglandin-mediated hyperemia and renin-mediated hypertension during acute ureteral obstruction.

Acute elevation of ureteral pressure to 100 mm Hg in anesthetized dogs (n=7) resulted in an increase (P less than 0.005) in systemic blood pressure form 151 +/- 7 to 163 +/- 7 mm Hg, a transient (approximately 15 min) increase (P less than 0.05) in renal blood flow from 413 +/- 27 to 465 +/- 27 ml/min and a rise (P less than 0.05) in plasma renin activity from 6.0 +/- 1.6 to 10.3 +/- 2.1 ng/ml/hr. Pretreatment with a competitive inhibitor of angiotensin II, i.e. sar1gly8AII, abolished the hypertensive response to acute ureteral obstruction, and pretreatment with 2 mg/kg of either indomethacin (n=6) or meclofenamate (n=3), 15 min before obstruction, prevented the hyperemic response. These results suggest that acute ureteral obstruction leads to hypertension via activation of the renin-angiotensin system and hyperemia via a prostaglandin-initiated mechanism.

Acute Disease↗
PubMed1975

Effect of angiotensin II and an angiotensin II inhibitor on renin secretion in the dog.

This study examined the effect of angiotensin II (AII) and (Sar-1Gly-8) AII, a competitive inhibitor of AII, on renin release in anesthetized dogs. An intravenous infusion of AII (25 ng/kg per min) raised BP 24 mmHg and lowered plasma renin activity (PRA) from 18.8 plus or minus 2.8 to 6.2 plus or minus 1. 3 ng/ml per h (P smaller than .001). When the intravenous infusion of AII inhibitor (1.0 mug/kg per min) was superimposed on the AII infusion, PRA rose from 6.5 plus or minus 22 to 12.3 plus or minus 3.6 ng/ml per h (P smaller than .02). Renal hemodynamics, BP, and urinary sodium excretion (UNaV) reverted toward pre-AII control values. A small dose of AII inhibitor (0.1 mu/kg per min) was then infused into one renal artery in animals receiving the constant intravenous infusion of AII. Renin secretion rate (RSR) increased significantly, not only in the infused kidney, but also in the contralateral kidney. In the latter there were no changes in renal hemodynamics or UNaV, and RSR was unimpaired by denervation of that kidney. The results suggest that the AII inhibitor blocks both the vascular and the renin-suppressing actions of AII and that the latter effect is more susceptible to inhibition.

Aminohippuric Acids↗