PubMed Health⌕ Search

Biomedical subjects

A M Rudolph

Publications and source records attributed to A M Rudolph.

At least 109 records · Page 6Linked to original sources
PubMed1984

Effects of fetal-maternal exchange transfusion on fetal oxygenation and blood flow distribution.

The effect of reducing hemoglobin affinity for O2 on fetal oxygenation was assessed in seven fetal lambs in which fetal blood was almost completely replaced by maternal blood 2-3 days postoperatively. Measurements of fetal blood gases and organ blood flow (radionuclide-labeled microsphere technique) were obtained before and 1 h after the exchange transfusion. Umbilical venous blood PO2 increased from 29 +/- 5 to 35 +/- 6 (SD) Torr (P less than 0.001) but hemoglobin O2 saturation decreased from 78.2 +/- 10.3 to 39.8 +/- 8.8% (P less than 0.001), resulting in a 46% decrease in umbilical venous blood O2 content. Since umbilical-placental blood flow also decreased (P less than 0.002), O2 delivery to the fetus decreased by 64% (P less than 0.002). Although O2 extraction increased from 32.5 +/- 6.8 to 50.9 +/- 9.0% (P less than 0.002), fetal O2 consumption fell from 7.28 +/- 1.97 to 4.10 +/- 1.20 ml X min-1 X kg-1 (P less than 0.02), and metabolic acidemia developed. No significant change in fetal cardiac output was observed. Blood flow increased significantly to the myocardium and adrenals but fell in the placenta, carcass, and lungs and was maintained in other organs. This resulted in a significant decrease in the amount of O2 delivered to all fetal organs except to the myocardium in which it was maintained. In the sheep the higher affinity of fetal blood hemoglobin for O2 helps maintain normal oxygenation during fetal life by facilitating O2 uptake at the placenta and unloading O2 in the tissues.

Animals↗
PubMed1984

Carotid arterial control of vasopressin secretion in sheep.

The purpose of this study was to test the role of carotid arterial mechanoreceptors in the control of vasopressin secretion in conscious 6- to 7-wk-old lambs. Bilateral carotid occlusion decreased lingual arterial pressure and stimulated reflex increases in heart rate and femoral arterial blood pressure but did not significantly alter plasma concentrations of vasopressin. Acute vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, did not significantly alter heart rate or blood pressure but did stimulate a slow increase in plasma vasopressin concentration, suggesting that afferent vagal fibers tonically inhibit vasopressin secretion. Bilateral carotid occlusion after vagosympathetic blockade stimulated a brisk increase in plasma vasopressin that was larger than the response to vagosympathetic blockade alone. These results suggest that vasopressin secretion in lambs is partially controlled by arterial mechanoreceptors in the carotid sinus and by extracarotid receptors with vagosympathetic afferent fibers.

Analysis of Variance↗
PubMed1984

Fetal adaptations to spontaneous hypoxemia and responses to maternal oxygen breathing.

Circulatory adaptations to spontaneous hypoxemia were assessed with the microsphere method at 119-123 days gestation in ovine fetuses who were subsequently found to be growth retarded. Combined ventricular output tended to be increased and it was redistributed so that oxygen delivery to the heart was increased by over 50%, oxygen delivery to the lung and placenta were decreased, and that to other organs, including the brain, were maintained. Maternal oxygen breathing for 1 h not only reversed these adaptations, but also produced an augmented lung blood flow. Umbilical blood flow was not affected. These findings have clinical implications for the growth-retarded fetus about to undergo the stress of labor.

Animals↗
PubMed1984

Role of thyroid hormone in postnatal circulatory and metabolic adjustments.

To assess the role of the early postnatal surge in plasma thyroid hormone concentrations on cardiovascular and metabolic adaptations, we measured cardiac output, total oxygen consumption, and plasma triiodothyronine (T3) concentrations in three groups of lambs in the first 6 h after delivery. 15 fetal lambs were prepared at gestational ages of 128-129 d by placing catheters in the brachiocephalic artery, descending aorta, distal inferior vena cava, left atrium, and pulmonary artery so that measurements could be made soon after delivery. They were divided into three groups: Group I comprised five control animals; Group II consisted of five fetuses in which thyroidectomy was performed at surgery at 129 d gestation; and Group III consisted of five animals in which thyroidectomy was performed at term gestation during delivery by caesarian section, prior to severing the umbilical cord. The lambs in Group I exhibited a rapid postnatal rise in T3 concentrations, similar to that described previously, reaching a peak value of about 5 ng/ml. Although the postnatal surge in T3 concentration was arrested in Group II and III animals, Group II had no detectable plasma T3, while the Group III animals had T3 concentrations of about 0.8 ng/ml, which were within the range previously reported for term lamb fetuses. The lambs in group II showed 40-50% lower left ventricular outputs (190 vs. 297 ml/kg per min), systemic blood flows (155 vs. 286 ml/kg per min), and oxygen consumptions (9.8 vs. 20.2 ml/kg per min) as compared with Group I animals over the entire 6-h period. The lambs in Group II also had significantly lower heart rates (131 vs. 192 beats/min) and mean systemic arterial pressures (56 vs. 72 torr). However, there were no significant differences for any of these measurements between the Group III and Group I lambs. The reduction in cardiac output in the Group II animals were reflected in a significantly lower blood flow to the peripheral circulation, but there were no significant differences in blood flow to other organs in the three groups. These studies indicate that plasma thyroid concentrations in the 2-3 wk prior to delivery and not the increase in thyroid hormone concentrations which occur after birth are important for postnatal cardiovascular and metabolic adjustments. We speculate that lack of circulating triiodothyronine in late gestation may affect postnatal cardiovascular adaptation by modifying normal beta adrenergic receptor development.

Animals↗
PubMed1984

Effects of nitroprusside on cardiac function, blood flow distribution, and oxygen consumption in the conscious young lamb.

Resting cardiac output is high relative to body weight during the neonatal period and there is a limited reserve for further increasing cardiac output. We assessed the effect on the circulation of reducing peripheral vascular resistance by infusing high doses of sodium nitroprusside in 1- and 3-week-old lambs. In a dose of 5 micrograms X kg-1 X min-1 over 1 h, nitroprusside caused a decrease in aortic and left atrial pressure, an increase in heart rate, and no significant changes in cardiac output or oxygen consumption. Infusing 10 micrograms X kg-1 X min-1 for 2 h resulted in an initial marked decrease in aortic pressure, cardiac output, and also heart rate. Within 50 min aortic pressure gradually increased, but was still well below control levels, while cardiac output returned to control level and heart rate slowly increased. Distribution of cardiac output and organ blood flows was measured by the radionuclide microsphere method. Blood flows to the kidneys and to the skin fell markedly, but flows to other organs did not change significantly.

Aging↗
PubMed1984

Can maternal stress alter fetal adrenocorticotropin secretion?

The purpose of this study was to assess the role of increases in maternal plasma cortisol, within the range observed after stress, in the control of fetal ACTH responses to subsequent fetal stress. We infused cortisol or vehicle into the inferior venae cavae of pregnant ewes which, with their fetuses (120-130 days gestation), had been chronically catheterized. Five-hour maternal cortisol infusions produced increases in maternal plasma cortisol smaller in magnitude than those induced by hypoxia stress and resulted in physiological increases in fetal plasma cortisol. One hour after the end of the maternal cortisol infusion, fetal ACTH secretion was stimulated by infusion of sodium nitroprusside into the fetal inferior vena cava. After maternal cortisol infusion, the fetal ACTH and cortisol responses to fetal hypotension were inhibited. We conclude that increases in maternal cortisol alters the fetal ACTH response to stress.

Adrenocorticotropic Hormone↗
PubMed1984

Physiological inhibition of ovine fetal plasma renin activity by cortisol.

The purpose of this study was to test the hypothesis that physiological increases in the fetal plasma cortisol concentration after basal and stimulated levels of PRA and vasopressin. Seven fetal sheep, between 121 and 131 days gestation, were infused with cortisol (4 micrograms/min) or vehicle for 5 h. One hour after the end of cortisol or vehicle infusion, sodium nitroprusside was infused into the fetus (100 micrograms/min, iv) to stimulate fetal hormone secretion. Cortisol, but not vehicle, infusion increased the fetal plasma cortisol concentration and decreased fetal PRA, but did not alter the fetal plasma vasopressin concentration. Cortisol-infused fetuses responded to nitroprusside with slightly smaller PRA responses but with equal vasopressin responses compared to those of vehicle-infused controls. Fetal blood pressure was not affected by either cortisol or vehicle infusion. Nitroprusside caused a slightly greater reduction in pressure in fetuses receiving cortisol infusion compared to those receiving the vehicle. We conclude that physiological increases in fetal plasma cortisol decrease fetal PRA without altering the fetal plasma vasopressin concentration. The results suggest that repeated fetal stress might produce progressive reduction of fetal PRA activity and might, therefore, alter cardiovascular homeostasis.

Animals↗
PubMed1983

Heart rate and blood pressure responses to umbilical cord compression in fetal lambs with special reference to the mechanism of variable deceleration.

We examined heart rate and blood pressure responses to umbilical cord compression in fetal lambs. Fetal heart rate (FHR) responses resembling variable deceleration occurred only after umbilical blood flow was reduced by at least 50%. These changes during partial cord occlusion varied directly with the reduced umbilical blood flow and were abolished by atropine; no significant changes in arterial pressure were observed. Complete cord occlusion caused severe bradycardia, a progressive increase in arterial pressure, and delayed recovery of FHR. With partial cord occlusion, the bradycardia was of chemoreceptor origin and was vagally mediated; with complete occlusion the bradycardia may have resulted from both chemoreceptor and baroreceptor stimulation. During prolonged partial cord occlusion, FHR decreased initially, then recovered to above control value; this occurred in the face of a significant acidosis. Thus, FHR responses to cord compression are dependent on the actual percentage of reduction in umbilical blood flow and on its duration.

Animals↗
PubMed1983

The effect of reducing umbilical blood flow on fetal oxygenation.

To assess the effect of various degrees of umbilical cord compression on fetal oxygenation, we instrumented fetal lambs at 120 to 128 days' gestation. An electromagnetic flow transducer was placed around the common umbilical artery to record umbilical blood flow flow continuously. Catheters were passed into an umbilical vein and a hind limb artery and vein, and a balloon occluder was placed around the umbilical cord. After recovery from operation, umbilical blood flow was reduced to 75%, 50%, and 25% of control values by controlled cord occlusion. Umbilical venous oxygen content did not change during cord compression; thus, oxygen delivery was linearly related to umbilical blood flow. Oxygen consumption of the fetus was maintained with reduction of umbilical blood flow to about 50% of control values; further reductions were associated with a progressive fall in fetal oxygen consumption. With reduced umbilical flow, there was a progressive increase in oxygen extraction from a control of 33.6% +/- 4.8% to 67.7% +/- 11.3% during 75% reduction of flow.

Animals↗
PubMed1983

Phasic blood flow patterns in the superior and inferior venae cavae and umbilical vein of fetal sheep.

Measurements of phasic blood flow in the inferior and superior venae cavae and umbilical vein of fetal sheep (gestational age, 121 to 140 days) were made with chronically implanted electromagnetic flow transducers. In the venae cavae blood flow was inversely related to phasic changes in venous and/or intrathoracic pressure. During fetal apnea a forward surge of flow occurred during ventricular systole (systolic surge) and ventricular diastole (diastolic surge). Slower fetal heart rates were associated with a more prominent diastolic surge. Reductions in afterload caused by acetylcholine administration augmented the peak diastolic venous flow. In contrast, increased afterload caused by hypoxia and norepinephrine administration was associated with increased peak systolic flow. During regular fetal breathing movements the phasic flow pattern was determined largely by the respiratory cycle with the effect of the cardiac cycle superimposed. There was minimal venous pulsation in the intra-abdominal umbilical vein, compared with that of the intrathoracic venae cavae of the apneic fetus. Our findings demonstrate that fetal systemic vascular resistance profoundly influences right atrioventricular filling patterns.

Acetylcholine↗
PubMed1983

Carotid vascular control of ACTH secretion in lambs.

To test the hypothesis that changes in carotid vascular pressure influence ovine ACTH and corticosteroid secretion, we subjected 6- to 7-wk-old conscious lambs to bilateral carotid occlusion with or without prior vagosympathetic blockade. Reversible vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, inhibited the reflex changes in heart rate after intravenous injection of phenylephrine or during carotid occlusion. Vagosympathetic blockade by itself did not alter arterial pressure or heart rate but did increase circulating levels of ACTH and corticosteroids. This suggests that afferent fibers in the vagosympathetic trunks tonically inhibit the secretion of ACTH. Bilateral carotid occlusion did not change plasma ACTH or corticosteroid concentrations. Bilateral carotid occlusion plus prior vagosympathetic blockade stimulated increases in plasma ACTH and corticosteroid concentrations that were larger than responses to vagosympathetic blockade alone. The results demonstrate that changes in carotid vascular pressure influence ovine ACTH and corticosteroid secretion only during vagosympathetic blockade and therefore suggest that carotid vascular mechanoreceptors interact with other mechanoreceptors having vagosympathetic afferent fibers.

Adrenal Cortex Hormones↗
PubMed1983

Chronic renal venous catheterization in fetal sheep.

To measure certain aspects of renal function it is necessary to monitor both renal arterial and venous blood. We describe a technique for chronically implanting a catheter in the renal vein of fetal lambs. Catheters have been inserted into the left renal vein in 11 fetuses at 120-125 days gestation and maintained for periods of 6-11 days (mean 8.7 +/- 2.2). We have determined that the catheter does not influence renal blood flow or alter renal morphology. We have also ascertained that the blood sampled from the renal venous catheter is not contaminated with blood from the inferior vena cava. This technique can be used to examine many aspects of renal physiology in the chronically instrumented fetal animal.

Animals↗
PubMed1983

Developmental changes in oxygenation and circulatory responses to hypoxemia in lambs.

We studied moderate [fractional inspired O2 (FIO2) 0.09] and severe (FIO2 0.06) hypoxemia in 21 lambs (group 1, 1 wk old; group 2, 3-4 wk old; group 3, 5-7 wk). With moderate hypoxemia, all groups increased heart rate, cardiac output, and pulmonary arterial pressure and decreased systemic and pulmonary vascular resistance; cardiac output and pulmonary arterial pressure increases were less in group 1, because of higher resting values. With severe hypoxemia, heart rate increased similarly, cardiac output was unchanged, and aortic pressure fell associated with severe metabolic acidosis or arrhythmias. Regional blood flow changed similarly in all groups; heart and brain flow increased, carcass flow was unchanged, and skin, GI tract, and kidney flow fell. O2 consumption (VO2) and mixed venous PO2 decreased, though O2 saturation was higher in group 1 due to the lower O2 half-saturation pressure of hemoglobin. With a given decreased VO2 there was more metabolic acidosis in older lambs and an increased VO2 after termination of hypoxemia, suggesting greater O2 debt. As in the fetus, young lambs are better able to tolerate a decreased VO2 than older lambs.

Aging↗
PubMed1983

Circulatory and humoral responses of sympathectomized fetal sheep to hypoxemia.

In fetal sheep, hypoxemia causes arterial hypertension, bradycardia, a redistribution of blood flow, and an increase in plasma vasopressin and catecholamine concentrations. To assess the role of the sympathetic nervous system in mediating these responses, we administered 6-hydroxydopamine to 11 chronically catheterized fetal sheep. Some of the responses to acute hypoxemia, achieved by administration of a low-O2 gas mixture to the ewe, were similar to those in intact fetal sheep. Fetal arterial O2 tension decreased from 22 +/- 3 to 12 +/- 3 (SD) Torr; fetal heart rate decreased transiently; combined ventricular output and umbilical-placental blood flow, as measured by the radionuclide-labeled microsphere technique, were maintained; cerebral, myocardial, and adrenal blood flow increased, and pulmonary blood flow decreased. However, there was no significant change in arterial pressure or blood flow to the peripheral, renal, and splanchnic circulations in the chemically sympathectomized fetuses in response to hypoxemia. The sympathetic nervous system is important in certain fetal vascular responses to hypoxemia but is not necessary for vascular responses in certain critical organs and thus is not crucial for fetal survival during hypoxia.

Animals↗
PubMed1983

Baroreflex control of the circulation in chronically instrumented fetal lambs.

The role of the arterial baroreceptors in regulating the fetal circulation was studied in 18 chronically instrumented fetal lambs, 120-136 days gestation. The results were compared to those obtained in three sinoaortic denervated adult sheep. Nine fetuses underwent sinoaortic denervation and nine fetuses served as sham-operated controls. Two to 3 days after surgery, heart rate and blood pressure were recorded continuously and analyzed over 1-hour periods. In the denervated fetuses, marked fluctuations of the arterial pressure and heart rate were observed. Frequency distribution curves for mean arterial pressure and heart rate showed broader and flatter curves in the denervated fetuses. The average mean arterial pressure and heart rate were not significantly different between the two groups. However, the standard deviation as an index of variability of the mean arterial pressure increased from 2.7 +/- 0.9 (mean +/- standard deviation) in the control group to 6.5 +/- 2.4 in the denervated fetuses, and the standard deviation of the heart rate increased from 10.6 +/- 2.1 to 21.5 +/- 5.7. In the adult sheep, mean arterial pressure and heart rate increased on the 1st day after denervation and returned to near control values on the 3rd day. The variability of the mean arterial pressure increased, but that of the heart rate did not change. Fetal cardiac output and its distribution were measured by the radionuclide-labeled microsphere technique. Combined ventricular output was not statistically different between the groups, but the blood flow to the fetal body was 27% higher in the denervated fetuses. The calculated fetal body vascular resistance was 31% lower in the denervated lambs. This study indicates that the arterial baroreceptors are important in regulating variability of the arterial pressure and heart rate in fetal life, and also may have a significant role in maintaining the normal peripheral vascular resistance.

Animals↗
PubMed1983

Hepatic oxygen and glucose metabolism in the fetal lamb. Response to hypoxia.

Although the fetal liver is an active metabolic organ, its oxygen and glucose requirements have not previously been described. We measured hepatic blood flows and the oxygen and glucose differences across the liver in 12 late gestation fetal lambs in utero. Four animals were studied at least 1 wk postsurgically and again 2-5 d later to assess daily variations in hepatic blood flow and metabolism (group I). A second group of eight animals was studied 3-5 d postsurgically during a control period and during acute fetal hypoxia (group II). Under control conditions total hepatic blood flow averaged 400 ml/min per 100 g in both groups, and 75-80% was of umbilical origin. Liver blood flow and oxygen consumption were usually similar during repeated measurements, but in one animal varied considerably. During periods of normoxia, oxygen consumption for both the right and left lobes of liver was 4 ml/min per 100 g. Oxygen consumption of the whole liver accounted for 20% of total fetal oxygen consumption. This was achieved with oxygen extraction of 10-15%, so that hepatic venous blood was well oxygenated and provided an important source of oxygen for other fetal tissues. Under control conditions we could demonstrate no net hepatic uptake or release of glucose suggesting that the liver ultimately utilizes another carbon source to support its oxidative metabolism. During acute hypoxia total liver blood flow and its umbilical venous contribution both fell by 20%. Blood flow to the right lobe of the liver fell twice as much as that to the left lobe. Hepatic oxygen consumption was linearly related to oxygen delivery during the control and hypoxic periods. Consequently, right hepatic oxygen uptake fell by 45% whereas left hepatic oxygen uptake was unchanged, suggesting a functional difference between the lobes. During hypoxia glucose was released from both liver lobes; 6 mg/min per 100 g for the right lobe and 9 mg/min per 100 g for the left lobe. Total hepatic release of glucose was estimated to nearly equal umbilical uptake, so that 45% of the glucose available to fetal tissues was of hepatic origin. We conclude that the fetal liver responds to acute hypoxia by reducing its own oxygen consumption and releasing glucose to facilitate anaerobic metabolism.

Animals↗