Biomedical subjects

J H Rankin

Publications and source records attributed to J H Rankin.

At least 19 recordsLinked to original sources

PubMed1992

Differential effects of intravenous hydralazine on myoendometrial and placental blood flow in hypertensive pregnant ewes.

OBJECTIVE: The differential vasoactive effects of hydralazine on the uteroplacental vascular bed were studied. STUDY DESIGN: After control measurements were taken, near-term chronically prepared pregnant sheep were continuously infused with angiotensin II. Maternal arterial pressure was increased by 32 mm Hg. Hydralazine was then administered; the effects on regional resistance and blood flow were evaluated with a radionuclide-labeled microsphere technique. Analysis of variance for repeated measures was used to compare observations. RESULTS: When compared with the hypertensive state, hydralazine caused the following changes by 40 minutes (mean +/- SEM): Although maternal blood pressure fell 31% +/- 5% (p = 0.0005), placental blood flow was unchanged, total uteroplacental blood flow increased 24% +/- 8% (p = 0.03), total uteroplacental resistance decreased 43% +/- 4% (p = 0.0002), placental resistance decreased 19% +/- 9% (p = 0.01), myoendometrial blood flow increased 390% +/- 82% (p = 0.0005), and myoendometrial resistance decreased 82% +/- 4% (p = 0.0005). CONCLUSIONS: In angiotensin II-induced hypertensive ewes, hydralazine is an effective dilator of the uteroplacental vascular bed and can maintain placental blood flow while blood pressure.

Adrenal Glands↗

PubMed1992

Influence of terbutaline on ovine uterine response to prostaglandin E2 challenge.

OBJECTIVE: Our purpose was to test the effects of terbutaline on uterine electric and contractile responses to prostaglandin E2. STUDY DESIGN: In five late-gestation ewes, prostaglandin E2 (22.9 +/- 2.3 micrograms/min for 3 minutes) was given twice at 30-minute intervals during control. Terbutaline sulfate (2 micrograms/min) was then infused for 30 minutes. Prostaglandin E2 challenge was repeated 10 minutes after the onset of terbutaline infusion and thereafter at 30-minute intervals. Two-way analysis of variance for repeated measures revealed a significant main effect for time (p less than or equal to 0.0001) and between time and response (p less than or equal to 0.05). RESULTS: Both electric (p less than or equal to 0.0001) and intrauterine pressure (p less than or equal to 0.0001) responses were suppressed during terbutaline. The influence on intrauterine pressure persisted 10 minutes after terbutaline (p less than or equal to 0.01) while the electric response was not different from control. CONCLUSIONS: Terbutaline initially diminishes both uterine contractile and electric activity, but electric recovery precedes contractile recovery.

Animals↗

PubMed1992

Fetal heart rate variability and behavioral state: analysis by power spectrum.

OBJECTIVE: We attempted to determine the relationship between the fetal heart rate power spectrum and fetal state. STUDY DESIGN: Interbeat intervals, electrocortical activity, and fetal breathing movements were recorded from five near-term fetal lambs. Interbeat intervals were taken from epochs of low-voltage electrocortical activity with breathing, low-voltage electrocortical activity without breathing, and high-voltage electrocortical activity without breathing. Power spectral techniques were applied to determine the underlying frequencies contributing to fetal heart rate variability. Spectral analysis was also performed on fetal breathing data from three animals. RESULTS: Significant differences were found between low-voltage electrocortical activity with breathing and high-voltage electrocortical activity without breathing at 0.62 Hz and from 1.09 to 1.56 Hz. There was no clear relationship between the breathing and heart rate spectra. CONCLUSIONS: Fetal heart rate is mediated by both state and respiratory variables. The respiratory component is not strictly related to respiratory rate.

Animals↗

PubMed1991

Effects of severe reduction in maternal placental blood flow on blood flow distribution in the sheep fetus.

To test the hypothesis that fetal lambs are able to maintain oxygen delivery to myocardial, brain and adrenal tissues during reduction in uterine blood flow to 25% of control, we performed experiments on five ewes and their fetuses. A snare occluder was placed around the maternal common hypogastric artery and catheters were placed for measurement of blood pressures, flows, blood gas tensions, pH and oxygen content. After a five day recovery period, control measurements were made. The snare occluder was then closed until the artery was fully occluded. The arterial occlusion caused uteroplacental blood flow to fall to 32 +/- 4% and maternal placental blood flow to fall to 25 +/- 3% of control values. This level of asphyxia was maintained for 19 +/- 3 minutes, when maternal and fetal blood flows were measured again. In response to occlusion, fetal ascending aortic PO2 fell from 21 +/- 2 (SEM) to 13 +/- 2 mmHg (P less than or equal to 0.01), oxygen content from 4.3 +/- 0.3 to 1.4 +/- 0.2 mM (P less than or equal to 0.01) and pH from 7.37 +/- 0.01 to 7.21 +/- 0.05 (P less than or equal to 0.01). PCO2 rose from 48 +/- 1 to 62 +/- 3 mmHg (P less than or equal to 0.01). Fetal arterial blood pressure increased from 51 +/- 3 to 61 +/- 3 mmHg (P less than or equal to 0.001) and heart rate decreased from 172 +/- 10 to 104 +/- 4 beats.min-1 (P less than or equal to 0.01). The heart, brain and adrenals showed vasodilation in response to the asphyxic stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

PubMed1990

The pathophysiology of the anophthalmic socket. Part I. Analysis of orbital blood flow.

A wide variety of complications of the anophthalmic socket develop in patients after enucleation, including enophthalmos, superior sulcus deformities, eyelid malpositions, implant migration and extrusion, poor prosthetic motility, and socket contraction. Changes in the orbital blood flow and metabolic activity of the socket tissues and atrophy of the orbital fat occurring after enucleation have been suggested as two theoretical mechanisms that result in the development of these clinical conditions. Lack of scientific evidence and a limited understanding of the pathophysiologic basis of the features of anophthalmos led us to evaluate the validity of these proposed mechanisms in an animal model. Selected parameters of the normal orbits were compared with the contralateral anophthalmic orbits at different time intervals after surgery. Orbital blood flow was studied with selective ophthalmic artery angiography and radioactive microsphere techniques. Ophthalmic arteriography demonstrated symmetric caliber and filling characteristics of the major orbital vessels of the control and experimental orbits, although their topographic course was slightly more tortuous in the anophthalmic socket. Results of radioactive microsphere analysis of capillary blood flow per weight of the different orbital tissue compartments of the animals in the long-term group showed no significant difference between the normal and anophthalmic sockets. These findings provide evidence that the circulation dynamics and blood flow to orbital tissues do not change after enucleation surgery.

Angiography↗

PubMed1990

The pathophysiology of the anophthalmic socket. Part II. Analysis of orbital fat.

The pathophysiologic mechanisms responsible for the clinical features of the anophthalmic socket are poorly understood. Atrophy of orbital fat has been thought to be a major contributing cause of enophthalmos and the superior sulcus deformities that develop after enucleation, but it has never been demonstrated histopathologically or confirmed by scientific analysis. This study was undertaken to investigate the changes that occur in the orbital fat compartment of the anophthalmic socket in an animal model by measuring orbital soft tissue mass and evaluating adipocyte cell size. Instead of reduction in the tissue mass, a statistically significant greater weight of the fat and connective tissue compartment was found in the anophthalmic orbit by nearly 13% compared to the control orbit in the animals in the long-term group. No significant change in the mean maximal diameter of adipocytes developed 7 months after enucleation. These analyses do not support the concept that orbital fat atrophy or a reduction of metabolic activity occurs in the anophthalmic socket in this animal model. From these results and our previous findings that the circulation dynamics and blood flow to orbital tissues do not change after enucleation, we propose that the pathophysiologic basis of the problems associated with anophthalmos is a disturbance in the spatial architecture and interrelationships of the multiple tissue components of the orbit, not a change in the orbital blood flow or development of fat atrophy.

Adipose Tissue↗

PubMed1990

High frequency differences between high and low voltage electrocorticograms in the ovine fetus.

Dawes (1986) has stated that, "The difference between high and low voltage activity depends solely on the presence in the latter of higher amplitude oscillations with relatively low frequency superimposed on the low voltage components as shown by spectral analysis". We have tested the constancy of the high frequency section of the power spectrum of the electrocorticogram in 7 near-term sheep fetuses. Under sterile conditions we implanted biparietal electrodes in the dura and a ground lead subcutaneously on the scalp. Five days after the surgery, with the animal standing quietly in the laboratory, we acquired the fetal electrocorticograms. Data were acquired during several high and low voltage electrocorticographic cycles in each animal. Two hundred power spectra were obtained during high and low voltage fetal electrocortical activity and statistically analyzed by paired t-test to discern differences in power between the high and low voltage pattern at each frequency (n = 7). We found that at all frequencies between 4 and 12 cycles/s the high voltage electrocorticogram had significantly more power than the low voltage electrocorticogram (P less than 0.05). This is in accordance with the established literature. We also observed that from 17 through 24 cycles/s the low voltage electrocorticogram is significantly higher than the high voltage electrocorticogram (P less than 0.05). In this frequency range the power of the high voltage expressed as a percentage of the power of the low voltage were respectively, 80, 74, 71, 66, 64, 64, 67, 64. These differences are of considerable magnitude and may be physiologically important.

Animals↗

PubMed1990

Adenosine causes a biphasic response in the ovine fetal placental vasculature.

We have reported in a previous study that adenosine infusion causes fetal placental vascular resistance to increase after 2 min. To determine whether this action is followed by a more prolonged vasodilation, we studied 7 mature fetal lambs. At surgery, catheters were inserted into the fetal hindlimb arteries and veins. After a five day recovery period, control blood flow measurements were made by radiolabeled microsphere technique immediately after an infusion of 0.9% NaCl, (vehicle, 1.03 ml.min-1) into a fetal vein for 2 min. Within 5 min of the control blood flow measurement, adenosine (10 mg/min) was infused for 2 min. Blood flow measurements were repeated 5, 10, 15, 20 and 30 min after the end of the infusion period. Fetal arterial blood pressure dropped from 50 +/- 1 to 34 +/- 5 mmHg immediately after the adenosine infusion and returned to the control value within 5 min after the infusion. No further blood pressure response was detected. However, placental vascular resistance fell from 0.334 +/- 0.040 to 0.269 +/- 0.027 (P less than 0.05) at the 15 min measurement, remained low through the 20 min measurement (P less than 0.001) and was not different from control levels 30 min after the adenosine infusion. We conclude that the fetal placental vasculature responds to systemic adenosine infusion in a biphasic manner. The immediate reaction to adenosine is a transient vasoconstriction in the fetal placental vasculature followed by vasodilation 15 to 20 min after the initial exposure to adenosine.

Adenosine↗

PubMed1990

Relationship between plasma catecholamine levels and electrocortical state in the mature fetal lamb.

In late pregnancy the electrocortical activity (ECoG) in the ovine fetus starts to cycle between high and low voltage states. During the high voltage states of this activity fetal regional blood flows are decreased, and heart rate and fetal arterial blood pressure are both increased. Jensen et al. (1986) have postulated that these changes may be mediated by changes in autonomic tone. To test this hypothesis we placed catheters in 6 near-term sheep fetuses (gestational age = 128 days) and implanted electrodes to measure electrocortical activity. Five days after the surgery, fetal arterial blood was withdrawn during the first 3-5 min of each high and low voltage ECoG for 5 full cycles in each fetus. Plasma samples were analyzed for epinephrine, norepinephrine, and dopamine. Dopamine levels were not different in high and low voltage electrocortical state. In the high voltage ECoG state, epinephrine levels were 75 +/- 7 pg/ml and fell to 34 +/- 4 pg/ml during low voltage ECoG (P less than 0.01). During the high voltage state plasma norepinephrine was 623 +/- 85 pg/ml and fell during the low voltage period to 462 +/- 99 pg/ml (P less than 0.01). These data demonstrate that in the near-term sheep fetus plasma catecholamine levels fluctuate with ECoG state.

Animals↗

PubMed1989

Uncoupling of excitation from contraction in uterine smooth muscle in near-term ewes.

We infused forskolin in 30% ethanol or 30% ethanol systemically in seven chronically catheterized near-term sheep to determine the response of ovine uterine musculature to cyclic adenosine monophosphate stimulation. Maternal and fetal arterial pressure, fetal venous pressure, intrauterine pressure, and uterine electromyogram activity were monitored continuously. Prostaglandin E2 was infused at a delivery rate that caused a minimal 5 mm Hg increase in intrauterine pressure with definite contraction-like pressure spikes and associated uterine electromyogram activity. Forskolin (10 mg in 30% ethanol) or ethanol (vehicle) was then infused for 20 minutes. The prostaglandin E2 challenge was repeated 3 minutes later and again every 30 minutes over a 2 1/2-hour period. Data were analyzed by repeated measures analysis of variance. Infusion of ethanol (n = 2) had no apparent effect on either the intrauterine pressure or the uterine electromyogram response to prostaglandin E2 challenge. Forskolin infusion (n = 5) caused an attenuation of the intrauterine pressure response to prostaglandin E2 for 93 minutes. This effect was greatest 33 minutes after the infusion ended when the integrated pressure signal was 37% of the initial prostaglandin E2 response. The forskolin infusion had no effect on uterine electromyogram response to prostaglandin E2. We conclude that forskolin causes an uncoupling of excitation from contraction in the intact near-term ovine uterus.

Animals↗

PubMed1989

Effects of atrial natriuretic factor on maternal ovine vascular resistance.

Atrial natriuretic factor (ANF) is a potent endogenous vaso-dilator and diuretic peptide of uncertain physiologic relevance. In this study, the effects of ANF on normal and angiotensin II constricted placental, uterine and renal vessels were examined in pregnant sheep. Ewes were equipped with catheters to monitor vascular pressures, infuse drugs and measure blood flow by the microsphere technique. An electromagnetic flow sensor was placed around the middle uterine artery and electromyogram electrodes were attached to the uterus. ANF was administered into a branch of the uterine artery to minimize its systemic effects. The experiment included two protocols. First, blood flows and pressures were measured after a 5-min period of saline infusion into the uterine artery. These measurements were repeated at the end of a 5-min infusion of ANF (6.25 micrograms.min-1) into the uterine artery. During the second protocol, angiotensin II (AII) was infused via the jugular vein at 5 micrograms.min-1 for 10 min and ANF (6.25 micrograms.min-1) was infused through the uterine artery during the second half of the AII infusion. In the absence of AII, ANF lowered blood pressure from 97 +/- 6 to 90 +/- 6 mmHg (P less than 0.05); and placental resistance from 67.8 +/- 11.3 to 57.3 +/- 10.4 mmHg.min.ml-1 per g (P less than 0.01). Uterine resistance did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1989

Ovine fetal coronary and cerebral vascular responses to forskolin.

The time related hemodynamic responses to forskolin-elicited increases in cAMP were studied in the near-term fetus. Catheters and electrodes were inserted into 6 fetal sheep to measure arterial, venous and thoracic pressures, electrocorticogram, and electrocardiogram. At gestational day 134, experiments were performed to determine the effect of forskolin infusion (400 micrograms/ml at 1.03 ml/min for 5 min) on fetal blood pressure, coronary and cerebral blood flow and resistance. Blood flow measurements were made using 15 microns microspheres labelled with radioactive isotopes during the control period and at 0, 5, 10, 15, and 45 min after forskolin infusion. Forskolin infusion was always initiated during a high-voltage electrocortical epoch and was given twice in each animal. In each case, forskolin caused electrocortical activity to change from high-voltage state to an intermediate voltage state. Blood pressure fell significantly by the end of the infusion period and returned to control levels 10 min later. Fetal heart rate and coronary blood flow were immediately elevated by forskolin (P less than 0.01) whereas cerebral blood flow did not increase until 5 min later (P less than 0.01). Cerebral blood flow was still elevated (P less than 0.05) 45 min after the end of forskolin infusion, whereas coronary blood flow had returned to control levels. Both cerebral and coronary vascular resistance fell significantly in response to forskolin infusion (P less than 0.01). This effect lasted at least 15 min and had returned to control levels 45 min after forskolin had been terminated.

Animals↗

PubMed1989

Effects of antipyrine on electrocortical state and regional blood flows in the mature sheep fetus.

Antipyrine has recently been shown to decrease prostaglandin production in mature fetuses. Prostaglandins are important in the regulation of blood flow, and electrocortical state has been shown to influence regional blood flows. To assess the effect of antipyrine on blood flow, it is important to take electrocortical state into account. We therefore examined the effect of antipyrine infusion on placental, renal, and cerebral blood flow during periods of high and low voltage electrocortical activity. Six mature sheep fetuses were equipped with electrodes for determination of electrocortical state. Intravascular catheters were inserted into the fetal forelimb and hindlimb arteries and vein and an additional catheter was placed in the maternal femoral artery. After a five day recovery period, pressures were recorded and electrocorticogram was monitored for 3 full cycles of electrocortical activity. Antipyrine infusion (30 mg.min-1) was then started. After 1 h, blood flow measurements were made by microsphere method in the first 5 min of each subsequent electrocortical state for the next three full cycles. Blood flows are expressed as ml.min-1 per g (mean +/- SEM). Cerebral blood flow was 1.587 +/- 0.272 during low and 1.209 +/- 0.171 during high voltage periods (P less than 0.05). Placental blood flow was 2.103 +/- 0.294 during low and 2.047 +/- 0.325 during high voltage electrocortical activity. Renal blood flow was 2.394 +/- 0.330 during low and 2.360 +/- 0.386 during high voltage periods of electrocortical activity. Blood pressure was 50.8 +/- 1.8 mmHg during low and 52.8 +/- 2.3 mmHg during periods of high voltage activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Relationship between fetal electrocorticographic changes and umbilical blood flow in the near-term sheep fetus.

Local blood flow was measured with radioactive microspheres in 9 near-term ewes 2 min into successive high and low voltage electrocortical activity states. In an additional 8 animals the umbilical blood flow was measured using an electromagnetic flow-probe on the common umbilical vein. The microsphere data indicated that the blood flow during low and high voltage electrocortical activity was 185 +/- 22 ml/min per kg of fetus (SEM) and 165 +/- 22 ml/min per kg of fetus (P less than 0.01) respectively. Using the electromagnetic flowprobe the average flow during low and high voltage electrocortical activity was 203 +/- 14 ml/min per kg of fetus and 196 +/- 13 ml/min per kg of fetus (P less than 0.05) respectively. We observed that the decrease in the umbilical blood flow preceded the change from low to high voltage electrocortical activity by approximately 1 min. In that time the flow is significantly lower than it was during the preceding measurements taken during the low voltage electrocortical activity periods. This depression was still significantly lower at 3 min into the high voltage electrocortical activity whereas at 5 min into the high voltage state it was elevated to near average values. We conclude that the umbilical blood flow, on the average, is lower in high voltage states than it is in low voltage states and that this change precedes the switch from low to high voltage electrocortical activity.

Animals↗

PubMed1989

Matching of maternal and fetal flow ratios in the sheep placenta.

Local interaction of maternal and fetal placental blood flows was studied in two groups of unanaesthetized near-term sheep. Five sheep were exposed to a simulated dive to 100 feet of seawater (4.03 atmospheres) for 25 min. Six fetuses received an infusion of noradrenaline (6.8 micrograms/[kg x min]). Radioactive microspheres were administered simultaneously to mother and fetus before (control) and after (test) the experimental manipulation. Maternal and fetal relative activities, defined as % of total placental radioactivity divided by % of total placental weight, were calculated for 1-g pieces of cotyledonary tissue under control and test conditions. Pieces of cotyledons were defined as matched if the direction of change in relative activity from control to test was the same for mother and fetus. In the absence of an interaction between the maternal and fetal placental circulations, the probability of a piece of cotyledon being matched is 0.5. In each series of experiments the proportion of all cotyledon pieces having maternal and fetal relative activities that changed in the same direction was significantly greater than 0.5. Thus, the majority of the placental mass responds to a physical or chemical perturbation of the fetus in such a way that changes in relative perfusion are qualitatively matched in the adjacent maternal and fetal placental circulations.

Animals↗

PubMed1989

Cardiovascular responses to forskolin in the ovine fetus.

Six near-term ewes were instrumented to measure regional blood flows in the maternal and fetal subthoracic structures and allowed to recover for 5 days. Control blood flows were measured and 10(-3) molar forskolin was infused in the fetal hindlimb vein at 1 ml/min. After 10 min of infusion, maternal and fetal regional blood flows were measured. The fetal blood pressure was 44 +/- 3 mmHg in the control state and 40 +/- 4 mmHg after forskolin, P less than 0.056. The fetal renal vascular resistance changed from 24.4 +/- 2.4 to 17.5 +/- 1.7 mmHg.ml-1.min.g, P less than 0.005. The placenta had a control resistance of 27.7 +/- 5.0 and 25.6 +/- 5.1 mmHg.ml-1.min.g after forskolin, P less than 0.05. The placental membranes showed vasodilation: control resistance was 261 +/- 49 and 168 +/- 39 mmHg.ml-1.min.g after forskolin, P less than 0.02. The generalized vasodilation of the fetal circulation was paralleled in the maternal circulation. Forskolin, a lipid soluble diterpene, apparently had a placental clearance close to the theoretical maximum. Vasodilation was seen in the maternal renal, placental and uterine vasculatures. Maternal blood pressure was unchanged. Maternal placental vascular resistance was 47.4 +/- 3.0 mmHg.ml-1.min.g in the control state and 40.6 +/- 3.3 mmHg.ml-1.min.g after forskolin, P less than 0.02. Forskolin is a vasodilator in both the fetal and maternal circulations. The maintenance of a relatively normal blood pressure in the face of regional vasodilation shows that forskolin may have a positive inotropic effect on the fetal heart. These results indicate that neither the fetal nor the maternal ovine placental vasculature is maximally dilated in the control state.

Animals↗

PubMed1988

Dose-response curves of the uterine and placental vascular beds to prostaglandin I2.

Local infusion of prostaglandin I2 (PGI2) has been reported to dilate the uteroplacental vasculature in a dose-dependent manner. In this experiment we attempted to distinguish the placental and nonplacental (uterine) components of this response over four concentrations of PGI2. Eleven near-term sheep were chronically instrumented for determination of regional blood flows by the use of radioactive microspheres. PGI2 was administered in a retrograde manner via a branch of the middle uterine artery at 1, 3, 10, and 20 micrograms/min. Flows were measured before (control) and after 5-minute infusions at each of the four concentrations (test). The uterine vasculature vasodilated in response to local PGI2 infusion. The 10 micrograms/min dose, for example, produced a mean (+/- SEM) flow of 0.70 +/- 0.07 ml/min/gm; the control value was 0.41 +/- 0.03 ml/min/gm (p less than 0.001). At 20 micrograms/min the test and control flows were 0.75 +/- 0.16 and 0.36 +/- 0.06 ml/min/gm (p less than 0.05), respectively. Uterine vascular resistance fell in a dose-dependent manner as well. There was no evidence of placental vasodilation at any of the doses tested. Renal vasodilation and decreased systemic arterial pressure at higher PGI2 doses suggest a recirculation effect. We conclude that PGI2 does not dilate the placental vasculature over the dose range of 1 to 20 micrograms/min and that the reported vasodilation of the uteroplacental vasculature is a result of decreased resistance in the uterine vasculature alone.

Animals↗

PubMed1988

Effects of forskolin on placental vascular resistance in rabbits.

Forskolin is a direct stimulant of adenylate cyclase and increases cAMP production. It also acts as a vasodilator. To study the effect of forskolin infusion on rabbit maternal vascular resistance, we instrumented 11 pregnant rabbits with catheters in the left ventricle, jugular vein, and left and right femoral arteries. After a 2-day recovery period, one of two protocols was performed. In the control period of the first protocol (N = 6), 50% ethanol in saline was infused at 0.103 ml.min-1 for 5-min. Forskolin (10(-3) M) in 50% ethanol was then infused for 5 min at 0.103 ml.min-1. After each infusion period, regional blood flows were measured by microsphere injection. Data are expressed as means +/- SEM. Blood pressure decreased from 81 +/- 3 to 79 +/- 3 mm Hg, (P less than 0.05, N = 10) during forskolin infusion. Total placental resistance fell from 180.3 +/- 10.7 to 133.8 +/- 12.0 mm Hg.min.ml-1 per gram, P less than 0.05. Cerebral, coronary, and renal vascular resistance fell significantly. During the second protocol (N = 5), angiotensin II (0.05 microgram.min-1) was infused for 5 min followed by the addition of forskolin (10(-3) M at 0.103 ml.min-1) to the infusate. Regional blood flows, vascular resistances and blood pressures were determined. Blood pressure fell from 99 +/- 6 to 92 +/- 7 mm Hg (P less than 0.05) when forskolin was added to the infusate. Placental resistance fell from 202.5 +/- 21.6 to 158.0 +/- 29.0 mm Hg.min.ml-1 per gram (P less than 0.05). While cerebral vascular resistance did not change, renal and coronary resistances fell in response to forskolin. This study demonstrates that forskolin is able to dilate rabbit placental vessels alone and in the presence of the vasoconstrictive agent angiotensin II.

Angiotensin II↗