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Biomedical subjects

D G Cooper

Publications and source records attributed to D G Cooper.

At least 19 recordsLinked to original sources
PubMed2004

Primary varicose veins: altered transcription of VEGF and its receptors (KDR, flt-1, soluble flt-1) with sapheno-femoral junction incompetence.

OBJECTIVE: Loss of regulation of vascular endothelial growth factor (VEGF) production and action disturbs vascular homeostasis leading to pathology. Primary varicose veins (VVs) demonstrate aberrant production/release of VEGF. Our aim was to examine transcription of genes for VEGF (VEGF(121)/VEGF(165)) and its receptors (KDR, flt-1, s.flt-1) in VVs, in relation to underlying venous incompetence. MATERIALS AND METHODS: Samples of varicose (n=83, 18 patients) or normal (n=14, five subjects) great saphenous vein were divided into segments, determined by anatomical position from the sapheno-femoral junction (SFJ). SFJ and segmental incompetence were determined from duplex scans. Gene transcripts were amplified by RT-PCR, analysed by scanning densitometry, and the levels of transcription determined by ratio to control gene GADPH-3 (GAP-3). RESULTS: VEGF(121)/(165), KDR and flt-1 transcription was elevated in VVs overall (p<0.001), and in VVs with an incompetent SFJ (p<0.001), but not when the SFJ was functional; s.flt-1 was unaltered. Notably, gene transcription was unaffected by segmental position, or incompetence. Position below the SFJ correlated with increased transcription of s.flt-1 when the SFJ was incompetent (p<0.04), and s.flt-1 and VEGF(121) when the segment was incompetent (p<0.03). CONCLUSIONS: SFJ incompetence is associated with altered transcription of VEGF and its receptors reflecting an aetiological mechanism or later stage of disease development. Altered VEGF(121) and s.flt-1 transcription may be an early event in varicogenesis.

Adult↗
PubMed2003

Primary varicose veins: the sapheno-femoral junction, distribution of varicosities and patterns of incompetence.

OBJECTIVE: to determine the patterns of long saphenous vein (LSV) disease in primary varicose veins (VVs). DESIGN: a retrospective analysis of venous duplex scans performed on patients referred for treatment of primary VVs. METHODS: analysis was made of sapheno-femoral junction (SFJ) incompetence, non-SFJ incompetence, segmental and perforating vein incompetence, distribution of varicosities, deep venous insufficiency, and short saphenous incompetence. RESULTS: four hundred and eighty-one patients were assessed (median age 50 (range 12-98) years; male:female ratio 1:1.95), comprising 706 limbs. Forty-six per cent of limbs had a competent SFJ, 64% of which had no incompetent perforating vessels associated. Disease was more widespread when the SFJ was incompetent. Varicosities were most common in the calf, occurring at or below the level of incompetence within the LSV. Incompetent segments occurred most commonly above-knee. There was no obvious correlation between incompetent perforators and distribution of varicosities, or incompetent segments. Short saphenous incompetence and non-SFJ groin recurrence were associated more with a competent SFJ, the converse being true for the Giacomini vein. CONCLUSION: primary VVs develop in isolated segments of the superficial venous system (without connection to the deep system) at, or distal to, the underlying main trunk incompetence, suggesting a process of "spreading incompetence" from one focal point, producing varicosities (mainly in tributaries).

Adolescent↗
PubMed2002

Biodegradation of plasticizers by Rhodococcus rhodochrous.

Rhodococcus rhodochrous was grown in the presence of one of three plasticizers: bis 2-ethylhexyl adipate (BEHA), dioctyl phthalate (DOP) or dioctyl terephthalate (DOTP). None of the plasticizers were degraded unless another carbon source, such as hexadecane, was also present. When R. rhodochrous was grown with hexadecane as a co-substrate, BEHA was completely degraded and the DOP was degraded slightly. About half of the DOTP was degraded, if hexadecane were present. In all of these growth studies, the toxicity of the media, which was assessed using the Microtox assay, increased as the organism degraded the plasticizer. In each case, there was an accumulation of one or two intermediates in the growth medium as the toxicity increased. One of these was identified as 2-ethylhexanoic acid and it was observed for all three plasticizers. Its concentration increased until degradation of the plasticizers had stopped and it was always present at the end of the fermentation. The other intermediate was identified as 2-ethylhexanol and this was only observed for growth in the presence of BEHA. The alcohol was observed early in the growth studies with BEHA and had disappeared by the end of the experiment. Both the 2-ethylhexanol and 2-ethylhexanoic acid were shown to be toxic and their presence explained the increase of toxicity as the fermentations proceeded. The appearance of these intermediates was consistent with similar degradation mechanisms for all three plasticizers involving hydrolysis of the ester bonds followed by oxidation of the released alcohol.

Alkanes↗
PubMed2001

Conformationally restricted indolopiperidine derivatives as potent CCR2B receptor antagonists.

The preparation and biological evaluation of a series of indolopiperidine CCR2B receptor antagonists possessing a conformationally restricted C-5 linker chain in combination with a restricted piperidine ring are described. Compared to the parent compound 1, analogue 8 shows a dramatic improvement in selectivity against a range of 5-HT and dopaminergic receptors.

Dopamine Antagonists↗
PubMed2000

Potent inhibition of a recombinant low voltage-activated Ca(2+) channel by SB-209712.

T-type Ca(2+) currents were recorded in 2 mM Ca(2+) from HEK293 cells stably expressing the low voltage-activated Ca(2+) channel sub-unit alpha(1I). These currents were inhibited by the known Ca(2+) channel antagonist mibefradil with an IC(50) close to 1 microM. SB-209712 (1,6,bis¿1-[4-(3-phenylpropyl)piperidinyl]¿hexane), a compound originally developed as a high voltage-activated Ca(2+) channel blocker, proved to be a more potent T-type channel antagonist, exhibiting an IC(50) in the region of 500 nM. The antagonism produced by SB-209712 was reversed following drug removal and the observed antagonism exhibited little or no voltage-dependence with respect to either holding or test potential. These data indicate that SB-209712 is amongst the most potent known non-peptide T-type channel antagonists and thus may have some use in understanding the role of these channels in cellular function.

Animals↗
PubMed2000

Modeling of biological processes using self-cycling fermentation and genetic algorithms.

Self-cycling fermentation (SCF) was coupled with a genetic algorithm (GA) to provide a simple system for evaluating biological models. The SCF provided the necessary system excitation and data "richness" required to completely define the fitted biological models. The solution scheme based on the GA avoided the computational difficulties often associated with calculus-based nonlinear regression techniques, resulting in rapid and accurate convergence. After validating the mathematical approach, data from the SCF obtained under denitrifying conditions were fitted successfully to an established model using the GA. Finally, data obtained in the SCF for the removal of phenol were used to compare multiple models. This work suggests that the SCF, in conjunction with the GA, provides a coherent system that can facilitate the characterization of biological systems.

Algorithms↗
PubMed1999

Alzheimer's disease: correlation of the suppression of beta-amyloid peptide secretion from cultured cells with inhibition of the chymotrypsin-like activity of the proteasome.

Peptide aldehyde inhibitors of the chymotrypsin-like activity of the proteasome (CLIP) such as N-acetyl-Leu-Leu-Nle-H (or ALLN) have been shown previously to inhibit the secretion of beta-amyloid peptide (A beta) from cells. To evaluate more fully the role of the proteasome in this process, we have tested the effects on A beta formation of a much wider range of peptide-based inhibitors of CLIP than published previously. The inhibitors tested included several peptide boronates, some of which proved to be the most potent peptide-based inhibitors of beta-amyloid production reported so far. We found that the ability of the peptide aldehyde and boronate inhibitors to suppress A beta formation from cells correlated extremely well with their potency as CLIP inhibitors. Thus, we conclude that the proteasome may be involved either directly or indirectly in A beta formation.

Aldehydes↗
PubMed1999

Propagating front in an excited granular layer.

A partial monolayer of approximately 20 000 uniform spherical steel beads, vibrated vertically on a flat plate, shows remarkable ordering transitions and cooperative behavior just below 1g maximum acceleration. We study the stability of a quiescent disordered or "amorphous" state formed when the acceleration is switched off in the excited "gaseous" state. The transition from the amorphous state back to the gaseous state upon increasing the plate's acceleration is generally subcritical: An external perturbation applied to one bead initiates a propagating front that produces a rapid transition. We measure the front velocity as a function of the applied acceleration. This phenomenon is explained by a model based on a single vibrated particle with multiple attractors that is perturbed by collisions. A simulation shows that a sufficiently high rate of interparticle collisions can prevent trapping in the attractor corresponding to the nonmoving ground state.

Journal Article↗
PubMed1997

The effects of SB 206284A, a novel neuronal calcium-channel antagonist, in models of cerebral ischemia.

The effects of SB 206284A, 1-[7-(4-benzyloxyphenoxy)heptyl] piperidine hydrochloride, have been investigated in vitro on calcium and sodium currents in rat-cultured dorsal root ganglion (DRG) neurones and potassium-mediated calcium influx in rat synaptosomes. Cardiovascular hemodynamic effects in both anesthetized and conscious rats, and neuroprotective activity in in vivo cerebral ischemia models were also investigated. In the rat DRG cells, SB 206284A caused almost complete block of the sustained inward Ca2+ current (IC50 = 2.4 microM), suggesting that the compound is an effective blocker of slowly inactivating, high-voltage calcium current. SB 206284A reduced locomotor hyperactivity in the gerbil bilateral carotid artery occlusion model without affecting ischemia-induced damage in the hippocampal CA1 region. In the rat middle cerebral artery occlusion model, SB 206284A reduced lesion volume in the posterior forebrain, and in the rat photochemical cortical lesion model, lesion volume was reduced even when treatment was delayed until 4 hours after occlusion. At neuroprotective doses, SB 206284A had no cardiovascular effects. These findings show that SB 206284A is a novel calcium channel antagonist that shows neuroprotective properties.

Animals↗
PubMed1994

Structures of histamine H1-receptor antagonists derived from the cimetidine group of histamine H2-receptor antagonists.

The crystal and molecular structures of ten compounds with strong structural resemblances to the cimetidine group of histamine H2-receptor antagonists, but exhibiting selective H1-receptor antagonist activity, (1)-(7), or H1 and H2 activity (8)-(10), have been determined: (1) 2-[4-(5-Bromo-3-methyl-2-pyridyl)butylamino]-5- (6-methyl-3-pyridylmethyl)-4-pyrimidone trihydrobromide (temalastine), C21H27BrN5O3+.3Br-, M(r) = 685.09, triclinic, P1, a = 6.314 (2), b = 11.192 (2), c = 19.441 (5) A, alpha = 102.47 (2), beta = 92.77 (2), gamma = 103.28 (2) degrees, V = 1298.51 A3, Z = 2, Dx = 1.75 g cm-3, mu = 61.6 cm-1, F(000) = 672, R = 2.93% for 3208 independent reflexions. (2) 2-[4-(5-Bromo-3-methyl-2-pyridyl)butylamino]-4-pyrimidone, C14H19BrN4O2, M(r) = 355.23, monoclinic, I2/a, a = 16.359 (3), b = 10.469 (6), c = 18.339 (4) A, beta = 90.90 (2) degrees, V = 3140.49 A3, Z = 8, Dx = 1.503 g cm-3, mu = 26.0 cm-1, F(000) = 1176, R = 4.2% for 1872 independent reflexions. (3) 3-[4-(5-Bromo-3-methyl-2-pyridyl)butylamino]-4- amino-1,2,5-thiadiazole-1-oxide, C12H16BrN5OS, M(r) = 358.26, triclinic, P1, a = 14.295 (2), b = 12.447 (2), c = 9.917 (2) A, alpha = 95.77 (2), beta = 113.86 (2), gamma = 106.91 (1) degrees, V = 1495.18 A3, Z = 4, Dx = 1.59 g cm-3, mu = 50.96 cm-1, F(000) = 728, R = 5.98% for 5674 independent reflexions. (4) 3-[4-(5-Bromo-3-methyl-2-pyridyl)butylamino]-4- benzylamino-1,2,5-thiadiazole-1-oxide, C19H22BrN5OS, M(r) = 448.38, monoclinic, P2(1)/c, a = 36.293 (7), b = 4.826 (2), c = 11.528 (3) A, beta = 96.91 (2) degrees, V = 2004.27 A3, Z = 4, Dx = 1.49 g cm-3, mu = 39.2 cm-1, F(000) = 920, R = 12.1% for 1945 independent reflexions. (5) 2-[3-(N-Benzyl-N-2- pyridylamino)propylamino]-4-pyrimidone, C19H21N5O, M(r) = 335.4, orthorhombic, Pbna, a = 7.082 (1), b = 19.889 (3), c = 24.899 (3) A, V = 3507.16 A3, Z = 8, Dx = 1.27 g cm-3, mu = 6.24 cm-1, F(000) = 1424, R = 4.05% from 2470 independent reflexions. (6) 3-[3-(N-4-Fluorobenzyl-N-2- pyridylamino)propylamino]-4-ethylamino-1,2,5-thiadiazole-1-oxide, C19H23FN6OS, M(r) = 402.5, monoclinic, P2(1)/n, a = 6.686 (2), b = 14.717 (3), c = 20.850 (5) A, beta = 97.83 (2) degrees, V = 2032.47 A3, Z = 4, Dx = 1.32 g cm-3, mu = 16.41 cm-1, F(000) = 848, R = 8.5% from 2484 independent reflexions. (7) 5-(6-Methyl-3-pyridylmethyl)-2-[3-(5,6,7,8-tetrahydro-8- quinolyl)propylamino]-4-pyrimidone, C23H29N5O2, M(r) = 407.5, monoclinic, P2(1)/c, a = 14.966 (2), b = 16.075 (2), c = 9.1608 (9) A, beta = 99.158 (8) degrees, V = 2175.83 A3, Z = 4, Dx = 1.24 g cm-3, mu = 6.19 cm-1; F(000) = 872, R = 5.3% from 2784 independent reflexions. (8) 2-(4-Phenylbutylamino)-5-(3-pyridyl-methyl)-4-pyrimidone, C20H26N4O3, M(r) = 370.5, monoclinic, P2(1)/c, a = 8.040 (4), b = 21.279 (4), c = 11.404 (2) A, beta = 92.08 (5) degrees, V = 1949.68 A3, Z = 4, Dx = 1.26 g cm-3, mu = 0.93 cm-1, F(000) = 792, R = 4.05% from 3816 independent reflexions.(ABSTRACT TRUNCATED AT 400 WORDS)

Cimetidine↗
PubMed1993

SB 201823-A, a neuronal Ca2+ antagonist is neuroprotective in two models of cerebral ischaemia.

We have characterised the Ca2+ channel blocking properties of a new non-peptide Ca2+ channel antagonist, SB 201823-A, in cultures of rat sensory neurones. The IC50 for SB 201823-A against total Ca2+ current in sensory neurones was 4.9 microM. SB 201823-A showed little selectivity for sub-types of neuronal Ca2+ channel but was selective for Ca2+ channels over Na+ and K+ channels. Efficacy against other types of cation channel such as agonist gated channels was not assessed. SB 201823-A was neuroprotective in vivo when administered post-ischaemia in one focal and one global model of neuronal ischaemia. In the rat photothrombotic focal lesion model, SB 201823-A administered i.p. 10 min post-ischaemia resulted in a dramatic reduction in lesion volume. In the gerbil bilateral carotid artery occlusion global model, SB 201823-A dosed i.p. 30 min post-occlusion resulted in both histological and functional improvements when compared to vehicle treated animals. These data suggest that such novel neuronal Ca2+ channel antagonists may have potential in ameliorating both the pathological and functional consequences of stroke in man.

Animals↗
PubMed1992

The human pattern ERG: alteration of response properties with aging.

The influence of aging on both the amplitude and the latency of transient and steady-state pattern electroretinograms (PERG's) was studied in 80 healthy participants ranging from 25 to 77 years of age (mean age, 55.3 years). Responses to counterphasing checkerboard patterns were recorded for each of 7 test conditions in which the spatial (i.e., check sizes 0.25, 0.50, 1.00, and 2.00 degrees) and temporal characteristics (i.e., counterphasing at either 2, 4, 8, or 16 rps) of the stimuli were varied. For both the transient and steady-state PERG's amplitude was inversely related to age (p less than 0.05 for each test condition). In general, PERG latency directly correlated with age, but this effect was less robust (p less than 0.05 for one transient condition and three of the four steady-state conditions). The influence of age on the spatial tuning of the PERG was minimal; the decrease in PERG amplitude and the increase in PERG latency as a function of age were essentially the same for all test conditions. However, the magnitude of the age-related reduction in PERG amplitude was observed to vary with temporal frequency, being largest for the steady-state condition (16 rps). The results from an experiment in which young subjects were tested while wearing opaque contact lenses with 2-mm artificial pupils suggest that senile miosis is a significant factor contributing to the age-related PERG amplitude and latency changes, but it does not fully account for the observed changes.

Adult↗
PubMed1992

Development and clinical evaluation of a computerized limb volume measurement system (CLEMS).

Limb edema is a common problem in both rehabilitation and acute care settings. In the past, attempts to determine an optimal management strategy for limb edema have been limited by the lack of accurate, noninvasive, rapid, clinical tools for quantifying limb volumes. The water displacement method is slow and difficult to use in the clinical setting. Furthermore, water displacement requires that the limb be in a dependent position. The tape measure method is unreliable because it is difficult to position the tape measure on a swollen limb. The development and evaluation of a new tool called the computerized limb volume measurement system (CLEMS) is described. The shape and volume of a limb or limb segment can be rapidly measured by CLEMS, independent of limb position. The limb volumes generated by CLEMS were compared to volumes determined by water displacement and by a tape measure. Volumes of eighteen legs (plaster, nonedematous and edematous) were measured using CLEMS, water displacement, and the tape measure. In all cases, the CLEMS and water displacement methods showed close agreement. CLEMS was found to be a reliable and valid new method of determining limb volume; whereas, the tape measure method was found to be invalid. This new tool allows clinicians to measure the efficacy of different treatment strategies in the management of limb edema.

Edema↗
PubMed1991

Ionic channels induced by surfactin in planar lipid bilayer membranes.

Surfactin is a lipopeptide produced by certain strains of Bacillus subtilis and has potent surface activity. Here, we present the first results showing that ion-conducting pores can be formed by surfactin in artificial lipid membranes. With a low aqueous concentration of surfactin (1 microM) and a restricted membrane area (5.10(-5) cm2) we observed conductance jumps that indicate the formation of individual ionic channels in the presence of K+, Rb+, Cs+, Na+ or Li+ chlorides. Although for every salt concentration (Ci), the distribution in amplitude of the conductance steps (lambda i) may be rather broad, there is always a step amplitude which is more frequent than the others. In addition, the channels corresponding to this most frequent step amplitude are the longest in duration. For Ci = 1 M, the cationic selectivity sequence deduced from these most frequent events is K+ greater than Rb+ greater than Na+ greater than Cs+ = Li+ with respective values for lambda Mi: 130, 110, 80 and 30 pS. In KCl solutions lambda MKCl increases as a function of Ci for low Ci, and shows a plateau for Ci greater than 0.5 M. When measured on larger area membranes (10(-2)cm2) with 1 M solutions of the monovalent salts KCl, NaCl, RbCl and CsCl or the divalent salt CaCl2, the macroscopic low voltage conductance (G0) increases with a slope of 2 on a log-log plot as a function of surfactin concentration. These results demonstrate that surfactin produces selective cationic channels in lipid bilayer membranes and suggest that at higher salt concentration, a dimer is involved in this functional channel-forming process.

Bacillus subtilis↗
PubMed1991

Octimibate, a potent non-prostanoid inhibitor of platelet aggregation, acts via the prostacyclin receptor.

1. Octimibate, 8-[(1,4,5-triphenyl-1H-imidazol-2-yl)oxy]octanoic acid, is reported to have antithrombotic properties. This is in addition to its antihyperlipidaemic effects which are due to inhibition of acylCoA:cholesterol acyltransferase (ACAT). The aim of this study was to investigate the mechanism of the antithrombotic effect of octimibate, and to determine whether the effects of octimibate are mediated through prostacyclin receptors. 2. In suspensions of washed (plasma-free) human platelets, octimibate is a potent inhibitor of aggregation; its IC50 is approx. 10 nM for inhibition of aggregation stimulated by several different agonists, including U46619 and ADP. The inhibitory effects of octimibate on aggregation are not competitive with the stimulatory agonist; the maximal response is suppressed but there is no obvious shift in potency of the agonist. In platelet-rich plasma, octimibate inhibits agonist-stimulated aggregation with an IC50 of approx. 200 nM. 3. Octimibate also inhibits agonist-stimulated rises in the cytosolic free calcium concentration, [Ca2+]i, in platelets. Both Ca2+ influx and release from intracellular stores are inhibited. The effects of octimibate on aggregation and [Ca2+]i are typical of agents that act via elevation of adenosine 3':5'-cyclic monophosphate (cyclic AMP). Similar effects are seen with forskolin, prostacyclin (PGl2) and iloprost (a stable PGl2 mimetic). 4. Octimibate increases cyclic AMP concentrations in platelets and increases the cyclic AMP-dependent protein kinase activity ratio. Octimibate stimulates adenylyl cyclase activity in human platelet membranes, with an EC50 of 200 nM. The maximal achievable activation of adenylyl cyclase by octimibate is 60% of that obtainable with iloprost. Octimibate has no effect on the cyclic GMP-inhibited phosphodiesterase (phosphodiesterase-ITI), which is the major cyclic AMP-degrading enzyme in human platelets.5. Octimibate inhibits, apparently competitively, the binding of [3H]-iloprost (a stable PGl2 mimetic) to platelet membranes; the estimated Ki is 150 nm. 6. The platelets of different species show considerable differences in the apparent potency of their inhibition of aggregation by octimibate; platelets from cynomolgus monkeys are 3 fold more sensitive than those from humans, while rat, cat and cow platelets are 50, 100, and 250 fold less sensitive than human platelets. The sensitivity of these different species to iloprost, however, varies over a range of only 10 fold with no obvious difference between primates and non-primates. 7. Octimibate appears to be a potent agonist (aggregation), or partial agonist (adenylyl cyclase), at prostacyclin receptors and is the first non-prostanoid agent of this type to be identified. The species differences in relative potency of octimibate and iloprost may reflect the existence of receptor subtypes.

Adenylyl Cyclases↗
PubMed1991

Primate vascular responses to octimibate, a non-prostanoid agonist at the prostacyclin receptor.

1. Octimibate is a potent inhibitor of human platelet aggregation, and appears to act (at least in part) through the prostacyclin receptor, as described in the preceding paper. Here, the vascular effects, both in vitro and in vivo, of octimibate have been compared to those of the stable prostacyclin (PGI2) mimetic, iloprost. Since octimibate shows extensive species variation and is potent at inhibiting platelet aggregation in primates, all of the experiments reported here have been carried out with primate tissue or in vivo in cynomolgus monkeys. 2. Activation of adenylyl cyclase in human lung membranes appears to involve stimulation of the vascular PGI2 receptor. Octimibate, as well as iloprost, stimulates adenylyl cyclase in this preparation. The EC50 values for iloprost and octimibate are 50 nM and 340 nM respectively. These values are similar to those seen with human platelet membranes. As with platelets, the maximal activation achievable with octimibate is 60% of that seen with iloprost. This result suggests that octimibate is a partial agonist for stimulation of adenylyl cyclase. 3. Iloprost (10-100 nM) relaxes human coronary and mesenteric artery precontracted with KCl, and also relaxes cynomolgus monkey aorta precontracted with phenylephrine. Octimibate appears to be a partial agonist for relaxation of human coronary artery precontracted with KCl; the intrinsic activity of octimibate (10 microM) is 0.15 compared to iloprost, and octimibate surmountably antagonizes the relaxant effects of iloprost with a Kp of 200 nM. Octimibate (up to 10 microM) evokes only weak relaxation of human mesenteric artery (precontracted with KCl) and cynomolgus monkey aorta (precontracted with phenylephrine). 4. The effects of iloprost and octimibate were compared in vivo in cynomolgus monkeys. In addition to inhibiting ex vivo platelet aggregation, both compounds cause hypotension with little effect on heart rate. The dose-response curves for inhibition of ex vivo platelet aggregation and a fall in mean arterial blood pressure were compared. The dose-separation (i.e., the relative differences in effective concentrations) for the two responses is similar with both iloprost and octimibate. 5. Since the pern; beral resistance vessels are intimately involved in regulation of systemic arterial blood pressure, the effects of both agents were tested on human peripheral resistance vessels (150-400pm diameter) in vitro. These vessels are relaxed by both iloprost and octimibate following precontraction with KCI. The IC50 value for iloprost is 44nM, and 1.7 microM octimibate evokes 50% of the maximal relaxation obtained with iloprost. Thus, the relative potencies of the two compounds in relaxing human subcutaneous resistance vessels are similar to their relative potencies in inhibiting platelet responses. This result correlates with the lack of platelet versus vascular selectivity seen with the in vivo monkey studies. 6. These results suggest that octimibate, a partial agonist at the prostacyclin receptor, is unable to discriminate between platelet and vascular prostacyclin receptors in primates.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗