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Biomedical subjects

D F Anderson

Publications and source records attributed to D F Anderson.

67 records · Page 4Linked to original sources
PubMed1980

Prediction of fetal drug concentrations.

Equations are derived for the fetal concentrations of a drug [F(t)] during and after the slow release of the drug into the maternal circulation. To solve these equations it is necessary to know the placental drug clearance (Cp), the clearance of the drug from the fetal circulation by the fetal tissues (Cf), and the volume of distribution of the drug in the fetal compartment (V). With these values for acetylsalicylic acid (aspirin) it can be shown that the maximum fetal aspirin concentration will be much less than the maximum maternal concentration and that after the release of aspirin has stopped, some drug is trapped in the fetal circulation. Therefore, there will be a period of time when the fetal plasma aspirin concentration is greater than maternal plasma aspirin concentration.

Aspirin↗
PubMed1980

The placental transfer of acetylsalicylic acid in near-term ewes.

The placental transfer of acetylsalicylic acid was studied in five near-term ewes and fetuses. The total clearance (Ctot) of acetylsalicylic acid from the fetal compartment was determined by bolus injection of 14C-acetylsalicylic acid into the fetal compartment. Ctot = Cp + Cf where Cp is the placental clearance and Cf is the fetal tissue clearance. 14C-acetylsalicylic acid was then infused into the ewe. Fetal (F) and maternal (M) steady-state concentrations of acetylsalicylic acid were measured. During steady-state conditions, the influx of acetylsalicylic acid into the fetal compartment will equal the efflux, or Cp X (M - F) = Cf X F. Combining these two equations yields the following description of placental clearance: Cp = Ctot x F/M. Using this equation, we calculated Cp = 0.57 +/- 0.12 ml/min . kg and Cf = 1.93 +/- 0.22 ml/min . kg. Maternal and fetal placental flows were also measured using radioactively labeled microspheres. From these flows, a 99% degree of diffusion limitation was determined for the placental transfer of acetylsalicylic acid.

Animals↗
PubMed1980

Responses of fetal sheep to simulated no-decompression dives.

The effect of simulated standard no-decompression dives to 60 and 100 ft of seawater was tested in 12 near term sheep carrying 16 fetuses. In the immediate postdive period there were no significant changes in fetal blood pressure or fetal placental or renal blood flow, but the maternal blood pressure was elevated and the maternal placental blood flow was depressed. Six surgically prepared fetuses were dived to 100 ft. Five died within 20 min of ascent and the sixth suffered severe cardiac arrhythmia and hypotension. At autopsy all fetuses were observed to have massive bubbling in the arterial system and heart. Five fetuses were dived to 100 ft without surgery. Two were alive 3 h later and no bubbles were present at autopsy, and three were born alive at term. With the 60-ft dives, three fetuses were subjected to surgery and all suffered massive bubbling. Two fetuses were dived to 60 ft without surgery; one was alive after 3 h and the other was born alive at term. We conclude that surgery and monitoring result in the formation of postdive gas bubbles that would not otherwise appear.

Animals↗
PubMed1980

Vascular response of the fetal placenta to local occlusion of the maternal placental vasculature.

Local regulation of fetal placental blood flow was studied in 6 near-term sheep. Maternal blood flow was reduced or eliminated to 6-17% of the placenta by ligation or embolization with non-radioactive microspheres. Maternal and fetal placental blood flows were measured, using radioactively-labelled microspheres, before and after vascular occlusion. The change in fetal placental blood flow was significantly different in the occluded as compared to the non-occluded cotyledons. Occlusion of the maternal placental vasculature was associated with a 40% decline in the adjacent fetal placental flow after 24 h. These data support the concept of a local regulatory interaction between fetal and maternal placental circulations wherein fetal placental blood flow is dependent upon the adjacent maternal flow.

Animals↗
PubMed1980

The measurement of placental drug clearance in near-term sheep: indomethacin.

A technique has been developed to measure diffusion limited placental clearance. The technique is demonstrated with indomethacin as the test substance. [14C]Indomethacin was injected as a bolus into the fetal hindlimb vein of eight chronically catheterized, near-term ewes and fetuses. Simultaneously, [3H]indomethacin was infused into the ewes. Maternal and fetal blood samples were taken before the injection of radioactivity and at 60-min intervals for 300 min. The blood was assayed for radioactivity. At the end of the experiment, fetal and maternal placental blood flows were measured with the radioactively labeled microsphere technique. The following formula was used to calculate the placental clearance (Cp) of indomethacin: Cp = Ctot X F/M where Ctot is the total clearance of indomethacin from the fetal circulation as measured by the rate of loss of [14C]indomethacin from the fetal circulation and is the sum of the placental clearance and the fetal tissue clearance (Cf), F and M are the fetal and maternal steady-state concentrations of [3H]indomethacin. The placental clearance of indomethacin was 2.10 +/- 0.32 ml/min/kg. The fetal tissue clearance of indomethacin was 3.63 +/- 0.58 ml/min/kg. The degree of diffusion limitation for the placental transfer of indomethacin was 97%.

Animals↗
PubMed1979

Effect of prostaglandin I2 on ovine placental vasculature.

The response of the placental circulations to prostaglandin I2 (maternal dose 20 microgram/kg, fetal dose 180 microgram/kg) was observed in 10 near-term sheep with chronically implanted vascular catheters. The blood flows before and 90 s after the injection of prostaglandin I2 were measured using radioactive microspheres. The injection of prostaglandin I2 to the mother decreased th blood pressure from 109 +/- 4 to 69 +/- 5 mmHg (P < 0.001) and increased the vascular resistance of the maternal cotyledons from 0.166 +/- 0.018 to 0.209 +/- 0.02 mmHg/(ml/min) (P < 0.001). The vascular bed of the non-cotyledonary uterus vasodilated as the resistance fell from 0.705 +/- 0.02 to 0.266 +/- 0.02 mmHg/(ml/min). (P < 0.001). Prostaglandin I2 caused the fetal arteriovenous pressure to fall from 37.6 +/- 1.35 to 26.0 +/- 1.6 mmHg. There was no significant change in the vascular resistance of the fetal cotyledons. We observed vasodilation in the fetal membranes as vascular resistance fell from 1.06 +/- 0.14 to 0.75 +/- 0.10 mmHg/(ml/min) (P < 0.001). The infusion of prostaglandin I2 significantly depressed the response of the placenta and uterus to norepinephrine. We have not proved that prostaglandin I2 plays a direct role in maintaining placental vascular homeostasis but it may modulate the response of this organ to exogenous vasoactive agents.

Animals↗
PubMed1979

Placental transfer of dexamethasone in near-term sheep.

The placental transfer of 3H-dexamethasone was studied in six near-term sheep. The placental clearance of 3H-dexamethasone was 18.8 +/- 3.5 ml/min per kg of fetal weight. The clearance of dexamethasone by the fetal tissues was 9.3 +/- w.5 ml/min per kg. The maximum placental clearance was 285 +/- 24 ml/min and the degree of diffusion limitation to the placental transfer of dexamethasone was 78 +/- 4%. The placental transfer of dexamethasone is therefore limited primarily by the nature of the placental barrier.

Animals↗
PubMed1967

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Canada↗
PubMedDate not supplied

Current topic: water volume of the ovine conceptus; point of view.

The sheep is the only species for which there is sufficient information to justify an overview of maternofetal water transfer. Current information points to the following conclusions: (1) the site of water exchange between mother and conceptus is mainly the placenta; (2) the pressure that initiates transfer to the fetus is the osmotic pressure of solutes that are present in higher concentrations in fetal plasma than in maternal plasma, such as urea, fructose, amino acids, bicarbonate and lactate; (3) maternal ultrafiltrate thus attracted into the conceptus arrives there mostly denuded of electrolytes and is strongly hypotonic; thus it is the transfer of electrolyte that restrains the transfer of water; (4) maternofetal transfer of water is strongly facilitated by angiotensin I in the fetal circulation by a sequence of events that has not yet been elucidated; (5) the net combined osmotic and hydrostatic pressure that drives water across the placenta is of the order of only 20 to 80 mm Hg; (6) it is necessary to make a sharp distinction between transfer from mother to conceptus and transfer from one compartment to another compartment within the conceptus. Finally, the review lists certain precautions to be taken in the further study of water exchange between mother and conceptus.

Animals↗
PubMedDate not supplied

A beam intensity monitor for the Loma Linda cancer therapy proton accelerator.

A beam intensity monitor was tested in a 230-MeV proton beam at the Loma Linda Proton Therapy Accelerator during its commissioning at Fermi National Accelerator Laboratory. The intensity monitor was designed to regulate the beam intensity extracted from the proton synchrotron. The proton beam is tunable between 70 and 250 MeV with an adjustable intensity between 10(10) and 10(11) protons per spill. A beam spill is typically 1 s long with a 2-s repetition period. The intensity monitor must be radiation hard, expose minimum mass to the beam, and measure intensity to 1% in 1-ms time intervals. To this end, a 5-cm-thick xenon gas scintillator optically coupled to a photomultiplier tube (PMT) was tested to measure its response to the proton beam. The gas cell was operated at 1.2 atm of pressure and has 12.7-microns-thick titanium entrance and exit foils. The total mass exposed to the beam is 0.14 g/cm2 and is dominated by the titanium windows. This mass corresponds to a range attenuation equal to 1.4 mm of water. The energy lost to the xenon gas is about 70 keV per proton. Each passing proton will produce approximately 2000 photons. With a detection efficiency on the order of 0.05% for this UV light, one would anticipate over 10(10) photoelectrons per second. In a 1-ms time bin there will be approximately 10(7) photoelectrons. This yields a resolution limited by systematics. For unregulated 0.4-s proton spills, we observe a response bandwidth in excess of 10(4) Hz. While signal-to-noise and linearity were not easily measured, we estimate as few as 10(3) protons can be observed suggesting a dynamic range in excess of 10(5) is available.

Humans↗
PubMedDate not supplied

Fetal heart rate and umbilical blood flow.

It has been suggested previously that norepinephrine does not change fetal placental vascular resistance but does change placental blood flow by changing fetal heart rate. We have tested the hypothesis that fetal heart rate is a determinant of fetal placental blood flow by observing changes in placental vascular resistance in 10 chronically catheterized near-term sheep fetuses. Pressures and flow were observed in the control condition and 150 s after the initiation of infusion of norepinephrine at 50 micrograms/min. The fetuses were then given 1.5 mg of atropine and control observations were again made. The norepinephrine infusion was repeated and pressures and blood flows were measured after 150 s. Atropine increased the fetal heart rate from 168 +/- 6 to 205 +/- 12 beats/min. Placental vascular resistance did not change. Norepinephrine resulted in bradycardia, hypertension and an increased placental vascular resistance. After pretreatment with atropine, norepinephrine resulted in tachycardia, hypertension and an increased placental vascular resistance. We conclude that fetal heart rate is not a major determinant of blood flow and that high doses of norepinephrine cause vasoconstriction of the placental vascular bed of the near-term sheep fetus.

Animals↗