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Biomedical subjects

J H Rankin

Publications and source records attributed to J H Rankin.

At least 55 records · Page 3Linked to original sources
PubMed1981

Blood flow in the hypertrophied right ventricular myocardium of unanesthetized ponies.

To examine the effects of right ventricular (RV) hypertrophy on regional myocardial blood flow and coronary vascular reserve, hemodynamics and myocardial blood flow (15-micrometers radio-nuclide-labeled microspheres) were studied in 12 unanesthetized adult ponies before and during intravenous isoproterenol HCl infusion (1 microgram.kg-1.min-1). Six ponies served as controls, whereas in each of the others the main pulmonary artery (PA) had been banded 35-90 days prior to the study. Marked RV hypertrophy was present in PA-banded animals. In these ponies, there was a significant increase in RV systolic pressure (147%), heart rate (88%), RV tension-time index (279%), and RV myocardial blood flow (137%), while their RV coronary vascular resistance was only 40% of that for control ponies. Blood flow in right side of the interventricular septum was also significantly higher in the PA-banded ponies. Endo/epi perfusion ratio exceeded 1.00 for both ventricular freewalls in all animals. With isoproterenol infusion, there was a marked increase in myocardial blood flow in both groups. However, in PA-banded ponies the endo/epi flow ratio decreased precipitously below 1.00 in both ventricular freewalls. In control ponies this did not happen in the RV freewall, and RV coronary vascular resistance decreased to 19% of its control value. In PA-banded ponies, the magnitude of decline in RV coronary vascular resistance was much smaller, only 32% of that for control ponies. It is concluded that, unlike in LV hypertrophy, transmural myocardial blood flow per unit mass is much higher in the hypertrophied RV myocardium of adult resting ponies, and this higher RV perfusion occurs at the expense of curtailed RV coronary vascular reserve.

Animals↗
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 effect of pregnancy on the angiotensin II pressor response in the rabbit.

The pressor response to angiotensin II was measured in unanesthetized, chronically catheterized pregnant and nonpregnant rabbits. Angiotensin II was infused intravenously for 10 minutes at a dose of 50 and 124 ng/kg/min. No difference in control mean arterial blood pressure was observed between pregnant and nonpregnant rabbits. The pressure change in response to angiotensin II was significantly greater in nonpregnant rabbits than in pregnant rabbits (P less than 0.002). Plasma samples were analyzed for angiotensin II concentration by radioimmunoassay. The results showed that there was no difference in plasma angiotensin II concentration between pregnant and nonpregnant rabbits following angiotensin II infusions. In a separate series we observed the effect of 5 mg of phenoxybenzamine on the pressor response to angiotensin II. After phenoxybenzamine treatment the control mean arterial blood pressure was significantly greater in nonpregnant rabbits than in pregnant rabbits, but the change in pressure in response to angiotensin II in nonpregnant rabbits was not significantly different from that of pregnant rabbits. These results show (1) that pregnant rabbits have a decreased sensitivity to angiotensin II, (2) that this decreased sensitivity is not due to differences in plasma concentration of angiotensin II, and (3) that this differential sensitivity to angiotensin II can be prevented by alpha-receptor blockade.

Angiotensin II↗
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

Cerebral blood flow during normocapnic hyperoxia in the unanesthetized pony.

The effect of hyperoxia on cerebral blood flow (CBF) was examined in 12 unanesthetized ponies. CBF was determined using radioactive microspheres, 15 micrometer in diam, durijng inspriation of the following gases: 1) room air (control); 2) 40% I2 in N2; and 3) approximately 100% O2 with 2.2-4.5% CO2 added to maintain isocapnia. CBF did not change from control values during either level of hyperoxia. However, cerebrospinal fluid (CSF) carbon dioxide tension (PCO2) increased during 40% O2 (delta 1.0 Torr) and approximately 100% O2 (delta 2.9 Torr). This rise in CSF PCO2, not due to a change in CBF, may have resulted from a decrease in the CO2 carrying capacity of cerebral venous blood during hyperoxia (Haldane effect). Although respiration did not change during 40% O2, expired minute volume increased 25% during approximately 100% O2 due to an increase in tidal volume. This rise in respiration was not associated with changes in any of the conventional stimuli to breathing (arterial pH, O2 tension, or PCO2 or CSF pH). One possible explanation was that cerebral extracellular fluid pH, in the vicinity of the central chemoreceptors, or cerebral intracellular fluid pH changed in a direction unlike CSF pH. An alternate explanation was that the CO2 in the inspired gas activated CO2-sensitive receptors in the lungs.

Acid-Base Equilibrium↗
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

A quantitative examination of the use of fluorescein in predicting viability of skin flaps.

The use of fluorescein as a predictor of skin viability in the rat flap model of avascular skin necrosis is well known in the field of plastic surgery. Inherent in this model are several faults that must be corrected if it is to become a valid standard. Fluorescence readings are one of the main variables in flap models. By carefully shaving rat backs with a double-edged razor, taking fluorescence readings in a uniformly darkened space, carefully tattooing the exact extent of both the bright and the mottled areas of fluorescence on the flap, and placing a plastic barrier between the flap and the body to prevent any part of the flap from acting as a graft, we were able to quantitatively predict which portions of a flap would survive and which would die after fourteen days. The bright fluorescent area (mean = 11.99 cm2, SEM +/- 0.53 cm2) is equal to the amount of tissue that will survive (mean = 11.91 cm2, SEM +/- 0.50 cm2; NS), while the sum of the nonfluorescent area and the mottled fluorescent area (mean = 27.69(2), SEM +/- 0.52 cm2) is equal to the amount of tissue that will die (mean = 27.99 cm2, SEM +/- 0.52 cm2; NS).

Animals↗
PubMed1979

Ovine placental vascular responses to indomethacin.

The administration of 10 mg/kg indomethacin to chronically catheterized near-term sheep resulted in a change in cotyledonary vascular resistance from 0.133 +/- 0.016 to 0.180 +/- 0.022 (mmHg . min)/ml (P less than 0.001). The noncotyledonary uterine vascular resistance increased to 191% of the original value (P less than 0.001) and the renal vascular resistance increased to 147% of the control value (P less than 0.001). The maternal blood pressure increased from 96 +/- 3.4 to 108 +/- 3.4 mmHg (P less than 0.001). Indomethacin (12 mg/kg) was given to nine fetuses, and observations were made in the control condition and at 15, 120, and 240 min. Cotyledonary vascular resistances were 144%, 152%, and 213% of the control values at those times. All changes were significant (P less than 0.03). The umbilical vascular resistance rose slowly throughout the study even though the concentration of indomethacin was falling during that time. These data suggest that this response may be an indirect effect. In the maternal circulation the rapid increase in the cotyledonary vascular resistance seen after indomethacin was probably due to a decreased level of endogenous prostaglandin synthesis.

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↗