Search PubMed⌕ Search

Biomedical subjects

M A Heymann

Publications and source records attributed to M A Heymann.

At least 145 records · Page 8Linked to original sources
PubMed1978

Effects of pharmacologic agents on umbilical blood flow in fetal lambs in utero.

We studied the effects of pharmacologic agents on umbilical blood flow and umbilical-placental vascular resistance in 18 fetal lambs in utero. Three groups of drugs were identified: the first had no effect on umbilical blood flow or umbilical-placental vascular resistance; the second altered umbilical blood flow secondary to changes in heart rate and placental perfusion pressure, but did not change umbilical-placental vascular resistance; the third decreased umbilical blood flow and increased umbilical-placental vascular resistance. The studies suggest mechanisms by which umbilical blood flow is regulated in the fetal lamb.

Acetylcholine↗
PubMed1978

The developmental response of the ductus arteriosus to oxygen.

We studied the isometric contractile effects of increased PO2 on isolated rings of lamb ductus arteriosus (from three different gestational age groups). When rings were stretched to initial lengths that result in a maximal contractile response for rings in that age group, the oxygen-induced contraction was 5.91 +/- 0.72 g/mm2 (+/-SEM, n = 18) in animals older than 135 days, 5.55 +/- 1.23 g/mm2 (n = 18) in animals between 111 and 130 days, and 3.85 +/- 0.75 g/mm2 (n = 19) in animals between 87 and 110 days. Only in the most immature vessels could a decrease in the tissue's response to oxygen be observed.

Animals↗
PubMed1978

Models of congenital heart disease in fetal lambs.

Intracardiac flow patterns were chronically altered by partially obstructing left ventricular (LV) inflow or outflow in midgestational fetal lambs. Physiological measurements of the fetal circulation were made serially through indwelling catheters and the use of radioactive microspheres. With LV inflow obstruction, mean LV output (LVO) decreased to 30% of control (P less than 0.01). Within seven days, the LV/right ventricular (RV) weight ratio decreased to 70% of control (P less than 0.01), and the mean LV/RV chamber volume decreased to less than one-half of control (P less than 0.001), simulating an early form of the hypoplastic left heart syndrome. With LV outflow obstruction, mean LVO decreased to 64% of control (P less than 0.05). Mean LV/RV wall thickness doubled (P less than 0.0001) and mean LF/RV chamber volume decreased to less than one-half of control (P less than 0.0001). Within four to ten days after increasing LV afterload, a large increase in LV mass occurred, which was demonstrated by morphometric analysis to be due to hyperplasia of ventricular myocytes. LV chamber volume decreased somewhat, simulating moderately severe congenital aortic stenosis. Over the long term (30--36 days), the mean LV/RV weight ratio decreased and the LV chamber was nearly obliterated, simulating very severe congenital aortic stenosis. The results suggest that by varying preload and afterload in both ventricles of the fetus, various forms of congenital heart disease may be simulated.

Animals↗
PubMed1978

Developmental aspects of the pituitary-adrenal axis response to hemorrhagic stress in lamb fetuses in utero.

Plasma ACTH and corticosteroid concentrations were measured by radioimmunoassay in chronically catheterized fetuses of 32 pregnant sheep. Fetal plasma ACTH levels 38+/-5 pg/ml (means+/-SEM) were slightly (P < 0.05) lower than maternal 54+/-4 pg/ml levels. No general rise in fetal plasma ACTH concentration was noted before 140 days gestation; however, fetal plasma corticoid levels began to increase after about 125 days. This suggested that an increase in fetal adrenal responsiveness to endogenous ACTH occurred during gestation. Hemorrhage of 15% of estimated blood volume decreased mean arterial pressure from 54+/-3 to 36+/-3 torr and increased plasma ACTH from 30+/-5 to 130+/-30 pg/ml in fetuses older than 0.80 gestation. In fetuses younger than 0.67 gestation, 15% hemorrhage caused no change in plasma ACTH levels despite a significant fall in mean arterial pressure. This suggests that system(s) subserving the ACTH response to mild hemorrhage are either absent or nonfunctional in the younger fetuses. The hemorrhage-induced increase in plasma ACTH levels was associated with a small rise in plasma corticoids in fetuses younger than 0.94 gestation. In older fetuses, a similar increase in plasma ACTH was associated with a pronounced increase in plasma corticoid levels. This also suggests that an increase in adrenal responsiveness to endogenous ACTH occurs during gestation. No detectable changes in maternal plasma ACTH or corticoids were found in response to fetal hemorrhage, thus the fetal pituitary-adrenal axis can autonomously respond to stress.

Adrenal Cortex Hormones↗
PubMed1978

Hemodynamic effects of prostaglandin E1 on lambs in utero.

Fetal tissues and the uteroplacental circulation are known to be exquisitely sensitive to the prostaglandins. E-series prostaglandins cause generalized vasodilatation in mature animals. This phenomenon is observed in the fetus but its effects are markedly obscured by the decrease in umbilical-placental flow. Comparison to hemodynamic data in hypoxemic fetuses clearly demonstrates that these effects are both qualitatively and quantitatively different, and therefore are likely to be due either to the direct effect of the drug, or to reflexes elicited by the marked compromise of the umbilical-placental flow.

Animals↗
PubMed1978

Problem of patent ductus arteriosus in premature infants.

Postanatal closure of the ductus arteriosus depends on the level of O2 to which it is exposed. Certain vasoactive substances may also play a role in this constriction. The response to O2 is not as well developed in immature fetal animals and this probably explains the high incidence of patent ductus arteriosus (PDA) in premature human infants. The magnitude of shunting through a PDA depends on its size and the relationship between the pulmonary and systemic vascular resistances. Factors affecting the pulmonary vascular resistance (such as hypoxia) will therefore affect the shunt. The ability of the infant to handle the volume overload also depends on maturity of the infant since myocardial development may not be complete even at term. The clinical manifestations and management of PDA with and without pulmonary disease are described. Recent attempts at pharmacological closure of the PDA are presented.

Animals↗
PubMed1978

Effects of hypothermia and rewarming on the neonatal circulation.

Thirteen unanesthetized lambs, aged 1-3 days, were cooled from 40 degrees to 30 degrees C and then rewarmed. During cooling, heart rate dropped from 196 +/- 47 to 140 +/- 42 beats per minute, a 29% change; cardiac output, femoral arterial and pulse pressures did not change significantly; but inferior vena cava pressure (IVC) increased from 5 to 9 mm of mercury, and left ventricular end diastolic pressure (LVEDP) increased from 8 to 25 mm/Hg. Mean pulmonary arterial pressure increased from 29 to 40 mm/Hg. Metabolic acidosis and hypoxia developed during the cooling. There were marked changes in the distribution of cardiac output; the proportion of cardiac output increased by 450% to brown fat, 66% to the skeletal muscles, and 30% to the right ventricular myocardium and atria. No significant change in the distribution to the left ventricule and septum was observed. Distribution to the other organs decreased markedly. After rewarming, all the previous parameters returned to normal except CVP and LVEDP, which remained elevated.

Acidosis↗
PubMed1977

Ductus arteriosus responses to prostaglandin E1 at high and low oxygen concentrations.

It previously has been suggested that prostaglandin E1 (PGE1) relaxes the ductus arteriosus in a low but not in an elevated oxygen environment. However, in the experiments reported here PGE1 relaxed rings on fetal lamb ductus arteriosus in vitro at both low (14 to 20 torr) and high (680 to 720 torr) oxygen tensions. The threshold concentration for PGE1 was 10(-10) M in either PO2 and the ED50's of PGE1 relaxation in high and low oxygen were 8.5 +/- 3.4 x 10(-10) M and 5.5 +/- 0.7 x 10(-10) M respectively. The magnitude of the relaxation was greater for the oxygen contracted ductus arteriosus than for that exposed to low oxygen. It is suggested that earlier reports of the lack of response of the ductus arteriosus to PGE1 in a high oxygen environment following relaxation in a low oxygen environment may be related to loss of response of the ductus arteriosus to repeated doses of PGE1 rather than to differences in PO2. Prostaglandin E1 therefore may play a significant role in the regulation of ductus arteriosus tone in the elevated oxygen environment of the newborn as well as the low oxygen environment of the fetus.

Animals↗
PubMed1977

Medical treatment of the ductus arteriosus.

Prostaglandin administered by aortic infusion prevents ductus closure when this is desirable--as in term infants with pulmonary atresia or critical pulmonic stenosis--raising arterial oxygen tension to levels compatible with life. On the other hand, in prematures with persistent patency of the ductus, administering indomethacin inhibits prostaglandin sysnthesis, inducing closure, and can obviate surgery.

Animals↗
PubMed1977

Differential effects of digoxin at comparable concentrations in tissues of fetal and adult sheep.

Electrocardiogram (ECG) electrodes and carotid arterial and superior vena caval (SVC) catheters were placed in eight nonpregnant ewes and 11 fetuses (109-129 days gestation) to measure heart rate, arterial presssure, P-R interval, left ventricular pre-ejection period (PEP), and left ventricular ejection time (LVET), before and after digoxin infusion into the SVC. After the ewes were killed, the steady state concentration of digoxin in plasma was related to the concentration in midbrain and left ventricular free wall. Although concentrations of digoxin in tissue differed between fetuses and ewes, tissue-plasma ratios were similar; the myocardial-plasma ratio was 87 for fetuses and 90 for ewes and the midbrain-plasma ratios were 6.4 and 5.3, respectively. In spite of these similarities, physiological and toxic effects differed at comparable plasma concentrations. Reduction in PEP/LVET ratio was greater in ewes than fetuses, and P-R interval prolongation was linearly related to digoxin concentration in fetuses but uncommon at plasma concentrations below 2 ng/ml in ewes. Arrhythmias occurred in six ewes, but in only one fetus, even though the mean steady state concentration of digoxin in plasma was 4.5 ng/ml in the fetuses and 2.3 ng/ml in the ewes. Atropine had little effect on digoxin-induced P-R interrval prolongation, and isoproterenol produced no tachyarrhythmias in the fetuses. Age-related differences in inotropic and arrhythmogenic effects of digoxin exist exist and are related to differences in drug response rather than drug kinetics; this provides experimental support for the different dosage responses.

Animals↗
PubMed1977

Ductus arteriosus dilatation by prostaglandin E1 in infants with pulmonary atresia.

Infants with pulmonary atresia depend on patency of the ductus arteriosus for survival in the immediate postnatal period. Despite continuing hypoxemia after birth the ductus arteriosus usually constricts, thus reducing pulmonary blood flow. This often occurs while awaiting surgical palliation or correction, leading either to marked deterioration in the infant's condition, or death. In ten infants with pulmonary atresia, we infused prostaglandin E1 (PGE1) at a rate of 0.1 mug/kg/min in six and 0.05 mug/kg/min in four into the descending aorta at the orifice of the ductus arteriosus. The ductus arteriosus was effectively dilated; at the narrowest point the diameter, measured in eight infants, almost doubled. In all ten infants arterial blood PO2 increased, averaging 24.6 mm Hg before and 43.7 mm Hg after the infusion was started. Infusion of PGE1 directly into the aorta adjacent to the ductus arteriosus avoided the complications of pyrexia, muscular twitching, and excitability which may be related to the effects of prostaglandins on the central nervous system.

Cardiac Catheterization↗