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J H Rankin

Publications and source records attributed to J H Rankin.

At least 37 records · Page 2Linked to original sources
PubMed1988

Forskolin dilates the maternal ovine placental vascular bed.

We have examined the placental vascular responses to forskolin in 8 near-term sheep. The drug was administered for 5 min at 1 ml/min of 10(-3) M forskolin via a retrograde uterine arterial catheter. Blood flows were measured with radioactive microspheres. Forskolin increased the nonplacental uterine blood flow from 0.318 +/- 0.031 (SEM) to 0.738 +/- 0.071 ml/min per g of tissue, P less than 0.001. The nonplacental uterine vascular resistance decreased from 308 +/- 26 to 132 +/- 12 mmHg/ml/min per g, P less than 0.001. Forskolin increased the placental blood flow from 1.8 +/- 0.18 to 2.08 +/- 0.16 ml/min per g of tissue, P less than 0.05. The placental vascular resistance decreased from 54.7 +/- 5.1 to 45.9 +/- 3.7 mmHg/ml/min per g, P less than 0.03. In the same animals we then infused angiotensin II at 5 micrograms/min via the jugular vein to induce placental vasoconstriction. In this series, the forskolin increased the nonplacental uterine blood flow from 0.141 +/- 0.016 to 0.485 +/- 0.079 ml/min per g of tissue, P less than 0.001, and the uterine vascular resistance decreased from 968 +/- 104 to 283 +/- 36 mmHg/ml/min per g, P less than 0.001. The placental blood flow increased from 2.08 +/- 0.012 to 2.69 +/- 0.17 ml/min per g of tissue, P less than 0.01 and placental vascular resistance decreased from 61.9 +/- 4.4 to 46.0 +/- 3.7 mmHg/ml/min per g, P less than 0.001.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1988

Prostaglandin I2 and the constricted maternal ovine placenta: effects of local infusion and placental age.

We have tested the hypotheses that systemic responses to the infusion of prostaglandin I2 may have masked the ability of this substance to dilate the maternal placenta and that the inability of prostaglandin I2 to dilate the maternal near-term placenta may be a function of placental age. Regional blood flows were measured with radioactive microspheres. In 8 near-term sheep the control flows were measured and angiotensin II (AII) infusion was begun at 5 micrograms/min and continued for the duration of the experiments. At t = 15 min, regional blood flows were again measured. Prostaglandin I2 was then infused via a retrograde uterine arterial catheter at 10 micrograms/min. At t = 30 min, the flows were again measured. At this time the infusion of prostaglandin I2 was stopped and at t = 45 min the blood flows were measured for the last time. AII increased the resistance of all tissues examined. The blood pressure increased with AII and did not change thereafter. The non-placental uterine tissue served by the retrograde catheter dilated with prostaglandin I2. The placental tissue had an initial resistance of 59 +/- 6 mmHg.ml-1.min.g which increased to 98 +/- 22 mmHg.ml-1.min.g with the infusion of AII (P less than 0.05). This resistance remained constant at 82 +/- 19 mmHg.ml-1.min.g with the administration of prostaglandin I2 and did not change after prostaglandin I2 was removed. The local application of prostaglandin I2 in the presence of AII induced vasoconstriction caused vasodilatation in the nonplacental vessels but could not change the AII induced constriction in the placental vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1988

Placental vascular response to prostaglandin I2 in the rabbit.

We have tested the hypothesis that the maternal placental refractoriness to prostaglandin I2 in the sheep is a species specific response by observing the response of the maternal placental vasculature of near-term rabbits to exogenous prostaglandin I2 infused at 10 micrograms/min for 5 min. Regional blood flows were measured with radioactive microspheres. Observations were made during the infusion of vehicle (control) and after 5 min of prostaglandin I2 infusion. The experiment was then repeated using microspheres of a different size. Fifteen and 25 mu spheres were used. If the same answer were obtained with both sphere sizes we would be confident that the result was not an artifact of shunted spheres. Seven rabbits were used in this study. The control (15 micron) blood pressure was 68 +/- 4 mmHg and prostaglandin I2 resulted in a depression of the pressure to 41 +/- 3 mmHg (P less than 0.001). The renal vascular resistance was 19.2 +/- 2.1 mmHg.ml-1.min. g in the control (15 micron) condition and 9.7 +/- 1.0 mmHg.ml-1.min.g after prostaglandin I2 (P less than 0.002). Prostaglandin I2 acted as a vasodilator in this organ as would be expected. The nonplacental uterine tissue had a control (15 micron) resistance of 624 +/- 125 and 612 +/- 184 mmHg.ml-1.min.g after prostaglandin I2 (NS). Using 25 mu spheres the results were 383 +/- 28 and 341 +/- 44 mmHg.ml-1.min.g respectively (NS). Shunting was observed in this organ but the direction of the responses to prostaglandin I2 was not affected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Ovine fetal electrocortical activity and regional cerebral blood flow.

Fetuses of 12 near-term sheep were prepared for microsphere determination of cerebral blood flow. Experiments were performed 5 days postsurgery. The regional blood flows were measured in successive high (HV), low (LV) and high voltage electrocorticographic states. Comparisons were made between the observations made in the LV and averaged flanking HV cycles. Total cerebral blood flow was 95 +/- 8, 119 +/- 11 and 100 +/- 9 ml/min/100 g in HV, LV and HV, respectively. Low voltage electrocortical activity increased average cerebral blood flow by 22% (P less than 0.01). Significant changes were seen in all regions except the occipital cortex. The maximum change was observed in the thalamus in which the flows were 152 +/- 23, 243 +/- 35 and 138 +/- 20 ml/min/per 100 g tissue, respectively. The increase was 68% (P less than 0.001). The percent changes seen in the cerebrum are as follows: Frontal grey + 18%, frontal white + 22%, parietal white + 22%, temporal + 18%. A + 17% change was seen in the cord (P less than 0.03). It is concluded that in low voltage electrocortical activity all of the brain, except the occipital region, shows an increase in cerebral blood flow. This is probably secondary to a variance in cerebral activity. This preparation may be useful in localizing function in the fetal brain.

Animals↗
PubMed1986

Maternal ovine placental vascular responses to adenosine.

We have examined the effect of adenosine given via retrograde uterine artery catheter at 25 mg/min to nine chronically catheterized near-term sheep pretreated with angiotensin II, 5 micrograms/min, via the jugular vein. Blood flows were measured by the microsphere technique. Flows were measured at rest, after 10 minutes of angiotensin II infusion, and after 1.5 minute of adenosine infusion. Blood pressure increased with angiotensin II infusion from 101 +/- 2.63 to 130 +/- 4.33 mm Hg (p less than 0.05) and then remained unchanged with local adenosine infusion at 129 +/- 4.33 mm Hg (NS). Organ resistances were: Tissue Control Angiotensin II Adenosine Uterine resistance/gm 299 +/- 0.04 767 +/- 83 (p less than 0.05) 355 +/- 37.7 (p less than 0.05) Cotyledonary resistance/gm 37.9 +/- 4.83 48.1 +/- 4.93 (p less than 0.05) 50.10 +/- 5.27 (p less than 0.05) The experimental uterine tissue resistance increased with angiotensin II and showed vasodilation in response to adenosine. The cotyledonary resistance increased with angiotensin II infusion but showed no change in response to adenosine. The maternal-placental response was anomalous. Angiotensin II-induced maternal-placental vasoconstriction cannot be opposed by the exogenous administration of adenosine.

Adenosine↗
PubMed1986

Maternal insulin and placental 3-O-methyl glucose transport.

The effects of insulin in the maternal circulation on the placental clearance of 3-O-methyl glucose were investigated in 7 animals in the presence of a constant maternal glucose concentration. While maternal insulin concentration changed from 12 +/- 4 to 175 +/- 33 mu Units/ml, the placental clearance remained constant at 16.2 +/- 1.2 (control) and 15 +/- 1.3 ml/min per kg fetus under the influence of the insulin. To test the secondary hypothesis that in the control condition the hexose transport system was saturated, we performed a further series of experiments in 6 fasted animals. In these animals the control maternal plasma insulin concentration was 2 +/- 0.3 mu Units/ml and after the infusion of insulin it increased to 562 +/- 26 mu Units/ml. Under conditions of constant maternal and fetal plasma glucose concentrations, this massive elevation of plasma insulin did not change the placental clearance of 3MeG which was 15.2 +/- 1.6 in the control condition and 13.3 +/- ml/min per kg under the influence of high insulin. We conclude that maternal insulin ranging from 2 mu Units/ml to supraphysiologic doses does not effect a physiologically significant change in placental hexose transfer. Placental glucose transfer can probably therefore, be changed only be changing the concentration of glucose in the maternal and fetal plasma.

3-O-Methylglucose↗
PubMed1985

The effect of prostacyclin on angiotensin II-induced placental vasoconstriction.

Significant alterations in vascular responsiveness to angiotensin II have been documented during pregnancy. We have observed that prostacyclin, a potent vasodilating prostaglandin, does not dilate the ovine placental vasculature. However, we thought it might modulate the placental vasoconstriction produced by angiotensin II. Regional blood flows and resistances were measured by the radioactive microsphere technique in six near-term sheep. Blood flows were measured in the control condition and 15 minutes after beginning an infusion of angiotensin II at 5 micrograms/min (T1). Additional measurements were made 15 minutes after the addition of 50 micrograms/min of prostacyclin to the angiotensin II infusate (T2) and 15 minutes after withdrawing prostacyclin from the angiotensin II infusion (T3). Mean arterial pressure rose in response to angiotensin II and decreased significantly with prostacyclin administration. The renal and uterine nonplacental vascular beds showed the expected vasoconstriction in response to angiotensin II, which was then reversed to control levels by prostacyclin infusion. Unexpectedly, prostacyclin did not reverse the angiotensin II vasoconstriction in the placenta but further increased resistance (p less than 0.03). Placental resistance changed from 0.33 +/- 0.04 peripheral resistance units in the control condition to 0.42 +/- 0.06 peripheral resistance units for T1 (p less than 0.03), and prostacyclin infusion further increased placental resistance to 0.63 +/- 0.10 peripheral resistance units for T2 (p less than 0.03). We conclude that the placental vascular response to prostacyclin is different from that of other organs and that prostacyclin does not dilate, but further constricts the placenta in the near-term sheep with angiotensin II-induced systemic vasoconstriction.

Angiotensin II↗
PubMed1985

Ovine placental vascular response to the local application of prostacyclin.

Rankin et al. have shown that prostacyclin does not dilate the ovine placenta, yet Clark et al. have shown that retrograde infusion of prostacyclin dilates the uterine vasculature. To determine the effects of prostacyclin on the sheep placenta, the two groups have collaborated. In five chronically catheterized near-term sheep, blood flows were measured by the radioactive microsphere technique. Control blood flows were measured and prostacyclin infused into the retrograde uterine artery catheter at 10 micrograms/min. The blood flows were again measured, and the area served by the catheter was then delineated by the injection of a green dye at the time of maternal euthanasia. The placenta and cotyledons were separated and the kidneys were obtained for assay. The systemic effects of prostacyclin were minimal and have been observed previously. The resistance of the myometrium fell from 566 +/- 99.9 to 322 +/- 63.9 mm Hg X ml-1 X min X gm (p less than 0.002). The placental tissue showed no change in resistance. When the tissues were combined, we observed a decrease in resistance from 0.38 +/- 0.18 to 0.32 +/- 0.14 mm Hg X ml-1 X min (p less than 0.004), thereby confirming the observation that there was indeed vasodilation downstream. However, the vasodilation was not in the placenta but in the myometrium, and we reconfirm our previous conclusion that prostacyclin does not dilate the sheep placenta.

Animals↗
PubMed1985

Placental vascular responses to leukotriene receptor antagonist FPL 55712.

We have previously shown that FPL 55712, a specific leukotriene receptor antagonist, potentiates estrogen induced uterine hyperemia in nonpregnant rabbits. We therefore chose to investigate the vascular responses of pregnant rabbits to leukotriene blockade. Nine unanesthetized animals carrying 46 viable fetuses were used in this study. Regional blood flows were measured by the radioactive microsphere technique. In 5 rabbits control blood flows were measured after vehicle administration and FPL 55712, 1 mg/kg bolus, followed by infusion of 100 micrograms/kg/min was given via the jugular vein. Regional blood flows were measured again after 10 minutes of infusion. The procedural order was reversed in the remaining 4 animals. Resistance was calculated as mean arterial pressure divided by total flow to an organ. FPL 55712 decreased the blood pressure from 83 +/- 2 to 76 +/- 3 mmHg (P less than .001). Uterine resistance was not significantly changed (387 +/- 44 to 362 +/- 42 mmHg X ml-1 X min X gm), but renal resistance fell from 18.5 +/- 1.1 to 15.1 +/- 1.2 mmHg X ml-1 X min X gm (P less than .01). FPL 55712 induced maternal placental vasodilatation with resistance decreasing from 291 +/- 33 to 261 +/- 31 mmHg X ml-1 X min X gm (P less than .04). Vehicle administration did not cause dilation in any vascular bed. FPL 55712 appears to be a placental vasodilator whose action is most likely due to receptor blockade of the vasoconstrictive endogenous leukotrienes.

Animals↗
PubMed1985

Fetal insulin and placental 3-O-methyl glucose clearance in near-term sheep.

It is difficult, if not impossible, to measure the placental transfer of glucose directly because of placental glucose consumption and the low A-V glucose difference across the sheep placenta. We have approached the problem of quantifying placental hexose transfer by using a nonmetabolized glucose analogue (3-O-methyl glucose) which shares the glucose transport system. We have measured the clearance by using a multisample technique permitting least squares linear computing to avoid the errors implicit in the Fick principle. The placental clearance of 3-O-methyl glucose was measured in the control condition and after the administration of insulin to the fetal circulation. A glucose clamp technique was used to maintain constant transplacental glucose concentrations throughout the duration of the experiment. A control series was performed in which the only intervention was the infusion of normal saline. In these experiments the maternal and fetal glucose concentrations remained constant as did the volume of distribution of 3-O-methyl glucose in the fetus. The maternal insulin concentration remained constant and fetal insulin concentration changed from 11 +/- 2 microU/ml to 355 +/- 51 microU/ml (P less than 0.01). In the face of this large increase in fetal plasma insulin, there was no change in the placental clearance of 3-O-methyl glucose. In the control condition the clearance was 14.1 +/- 1.0 ml/min per kg and this was 13.8 +/- 1.0 ml/min per kg in the high insulin condition. Fetal insulin may change placental glucose flux by decreasing fetal plasma glucose concentrations but does not do so by changing the activity of the glucose transport system.

3-O-Methylglucose↗
PubMed1984

The effect of a leukotriene receptor antagonist, FPL 55712, on estrogen-induced uterine hyperemia in the nonpregnant rabbit.

Estrogen results in delayed uterine hyperemia. We postulate that the leukotrienes may be the mediators of the uterine vascular responses to estrogen. To test this hypothesis, we gave FPL 55712, a selective leukotriene antagonist, to estrogen-primed, nonpregnant rabbits and measured regional blood flows by the radioactive microsphere technique. In 10 chronically catheterized animals, blood flows were measured in the control condition (C), and again 2 hours after systemic administration of estradiol (EST). Thirty minutes before administration of estradiol, five animals received systemic FPL 55712, whereas five animals received vehicle only. The vehicle group showed the expected increase in uterine blood flow from 0.62 +/- 0.1 to 2.72 +/- 0.4 ml X min-1 X gm-1, and decrease in uterine resistance from 144 +/- 31 to 34 +/- 8 peripheral resistance units (PRU) X gm, with a resistance ratio (estradiol/C) of 0.23 +/- 0.01. Unexpectedly, the FPL 55712 group showed a further increase in uterine blood flow from 0.66 +/- 0.1 to 4.60 +/- 0.3 ml X min-1 X gm-1, and a decrease in resistance from 133 +/- 25 to 17 +/- 1 PRU X gm, with a resistance ratio of 0.13 +/- 0.02. The leukotriene antagonist FPL 55712 potentiates estrogen-induced uterine hyperemia by 77% (P less than 0.001). These data suggest that leukotrienes do not mediate, but rather inhibit, the uterine vascular responses to estrogen.

Animals↗
PubMed1983

Lack of harmful effects from simulated dives in pregnant sheep.

The purpose of the study was to determine if a near-maximum exposure to air at increased atmospheric pressure causes gross fetal malformations, decreased birth weight, or death when administered to pregnant sheep during peak development of the embryo. Twenty-eight timed-pregnant sheep were alternately assigned to a series of 25- or 30-minute exposures at either 4.6 atmospheres absolute or surface pressure between days 12 and 40 of gestation. About day 130 of pregnancy, 11 experimental and eight control fetuses were recovered, weighed, measured, fixed, and examined for defects. No major structural malformations were present. One minor variation, an undescended testis, occurred in a treated fetus. The results indicate that a series of short, marginally tolerated "dives" by pregnant sheep during peak development does not affect fetal health or survival.

Animals↗
PubMed1983

Placental vascular responses to 6-keto-prostaglandin E1 in the near-term sheep.

6-Keto-prostaglandin E1 (6-keto-PGE1) is a biologically active, stable metabolite of prostaglandin I2 (PGI2). It has vasoactive properties similar to those of PGI2 and it has been shown to decrease the resistance of the renal, mesenteric, and pulmonary vascular beds. PGI2 is synthesized by the pregnant uterus and is vasoactive in the ovine placenta. The effects of 6-keto-PGE1 on uterine and placental blood flow in pregnant ewes were determined for comparison with those of PGI2. Near-term ewes and their fetuses were chronically catheterized to permit the measurement of regional blood flow by the radioactive microsphere method. In six sheep a 5-minute maternal jugular infusion of 3.25 micrograms/kg/min of 6-keto-PGE1 decreased mean arterial blood pressure from 89 +/- 4.8 to 63 +/- 7.1 mm Hg. Uterine vascular resistance decreased from 0.55 +/- 0.11 to 0.35 +/- 0.05 peripheral resistance units (PRU), but maternal cotyledonary resistance increased from 0.19 +/- 0.04 to 0.27 +/- 0.03 PRU. In five sheep a fetal intravenous infusion of 18 micrograms/min of 6-keto-PGE1 decreased mean fetal blood pressure from 43 +/- 2 to 29 +/- 2 mm Hg. Cotyledonary vascular resistance increased from 0.30 +/- 0.02 to 0.55 +/- 0.09 PRU . kg-1. In these sheep there were no significant changes in maternal uterine, renal, or cotyledonary blood flows. These results indicate that 6-keto-PGE1 is similar to PGI2 in that it produces maternal cotyledonary vasoconstriction, hypotension, and vasodilation in other organs.

Alprostadil↗
PubMed1983

Cardiovascular effects of induced decompression sickness in sheep fetus.

Ten chronically catheterized near-term sheep fetuses were used to study the effect of induced intravascular bubbling on fetal placental vascular dynamics and fetal regional blood flows. Fetal blood pressure and heart rate were measured, and radioactive microspheres were administered to fetuses before and 5, 10, 15, and 20 min after a simulated no-decompression dive to 100 fsw (4 ATA) for 25 min. A decrease in brain blood flow was the only effect observed 5 min after decompression. Fifteen minutes later arterial hypertension was evident. Eight fetuses displayed arrhythmia, but there was no significant change in heart rate, myocardial blood flow, or resistance. There was a reduction in blood flow, and a concomitant increase in vascular resistance, in the gut, kidneys, placental membranes, and skeletal muscle, as well as in the brain. Total placental blood flow was unchanged throughout the postdive period, although placental vascular resistance was elevated 20 min after surfacing. Analysis of the placental blood flow at the cotyledonary level in 6 animals revealed no uniform response to decompression. The results are consistent with the hypothesis that the instrumented fetus suffers widespread vascular embolization and disruption of organ blood flows. We conclude that the observed changes in the fetal cardiovascular system, however, are not precipitated by an initial effect of decompression on the fetal placental circulation.

Animals↗
PubMed1982

Carbon disulfide-induced neuropsychiatric changes in grain storage workers.

The clinical and neuropsychiatric features of seven workers from the grain storage industry are described. All were exposed to fumigants, especially carbon disulfide and malathion. Clinical manifestations included cogwheel rigidity, resting and action tremor, peripheral neuropathy, pyramidal tract signs, an EEG pattern of sleep apnea, and characteristic measurable neurobehavioral dysfunction. Similar signs and symptoms due to carbon disulfide exposure in the viscose rayon industry strongly supported the conclusion that these grain storage workers were suffering from carbon disulfide poisoning. Malathion exposure probably had a contributing role. We conclude that exposure to these fumigants poses a serious occupational risk to the nervous system.

Aged↗
PubMed1982

Effect of PGI2 on the response of the ovine placenta to norepinephrine.

We have examined the effects of PGI2, 50 microgram/kg, on norepinephrine induced placental vasoconstriction in 6 chronically catheterized near-term sheep. Regional blood flows were measured with radioactive microspheres. Control flows were measured. Norepinephrine was than infused at 50 microgram/min throughout the experiment. After 15 min the blood flows were again measured and PGI2 was then added to the infusate at 50 microgram/min. In 15 min regional blood flows were again measured and the PGI2 infusion was stopped. Regional blood flows were measured for the last time 15 min later. The renal and nonplacental uterine vasculatures behaved in a predictable manner. There was constriction with norepinephrine but PGI2 opposed the effects of norepinephrine and decreased the resistance towards the normal levels. The placenta did not behave as did the other organs. Norepinephrine increased placental resistance but PGI2 did not decrease the resistance and severely depress the placental blood flows. PGI2 does not appear to oppose norepinephrine induced placental vasoconstriction.

Animals↗