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  • 1
    Electronic Resource
    Electronic Resource
    Effects of vasoactive autacoids on the human umbilical-fetal placental vasculature (1984)
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 91 (1984), S. 0 
    Details
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Studies have been made of the effects of autacoids on vascular tone of the human perfused fetal umbilical vein and placental lobule. The thromboxane A2 (TxA2)-mimetic substance U46619, 5-hydroxytryptamine and bradykinin were powerful constrictors of the vein. Prostaglandins E2 (PGE2), F2α(PGF2α), adrenaline, noradrenaline, histamine and angiotensin II were much less potent. Venoconstriction caused by U46619, bradykinin and 5-hydroxytryptamine was reduced during inhibition of phospholipase A2 with mepacrine. Responses to U46619 were also reduced after inhibition of cyclo-oxygenase with indomethacin whereas those to bradykinin and 5-hydroxytryptamine were potentiated. In the placenta U46619 was the most potent vasoconstrictor, bradykinin, 5-hydroxytryptamine, angiotensin II, PGE2 and PGF2α being 10–100 times less active. Responses to U46619 were reduced by either mepacrine or indomethacin. Arachidonic acid caused umbilical venoconstriction but vasodilatation in the placenta. Both effects were reduced by indomethacin. Prostacyclin (PGI2) caused vasodilatation in both preparations. It is suggested that TxA2 in the placenta and TxA2, 5-hydroxytryptamine and bradykinin in the umbilical vein could contribute to control of vascular smooth muscle tone. Their vasoconstrictor effects are partly indirect and affected by the concomitant local release of eicosanoids. The results add suort to previous conclusions that these autacoids may normally have important influences on blood flow in the fetal extra-corporeal circulation. Agents inhibiting their synthesis, eg non-steroidal anti-inflammatory agents, should only be prescribed during pregnancy with these facts in mind.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-0528.1984.tb05890.x
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  • 2
    Electronic Resource
    Electronic Resource
    Adrenergic Neurone Blocking Agents (1965)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Pharmacology 5 (1965), S. 183-212 
    Details
    ISSN: 0362-1642
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.pa.05.040165.001151
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  • 3
    Electronic Resource
    Electronic Resource
    THROMBOXANE B2 INHIBITS PROSTAGLANDIN E2 INACTIVATION BY THE RAT ISOLATED PERFUSED LUNG (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 5 (1978), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effect of thromboxane B2 (T×B2) on inactivation of prostaglandin E2 (PGE2) by the rat isolated perfused lung has been studied.2. TxB2 when infused in low concentrations (100 ng/ml) into the pulmonary artery reduced PGE2 inactivation approximately two-fold.3. The rat isolated fundus strip was contracted by higher concentrations of TxB2 (1.0 Mg/ml) in the presence of hyoscine, mepyramine, methysergide, phenoxy-benzamine and propranolol. The size of contraction was reduced by indomethacin in concentrations known to inhibit prostaglandin synthetase.4. Thus, in circumstances in which T×B2 and PGE2 are released concomitantly by the lung, low concentrations of TxB2 may augment PGE2 release by reducing its inactivation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1978.tb00688.x
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  • 4
    Electronic Resource
    Electronic Resource
    AUTACOIDS AND CONTROL OF HUMAN PLACENTAL BLOOD FLOW (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Humans have a haemochorial, villous placenta. Uterine blood passes through maternal sinuses, bathing placental villi through which fetal blood circulates. Blood flow through each circulation is high and vascular resistance low. This haemodynamic situation is essential for efficient placental function.2. The low placental vascular resistance is due to a lack of nervous influences together with pregnancy-induced changes promoting vasodilatation. Increases occur in output of the vasodilators prostacyclin and nitric oxide and also in membrane sodium pump activity.3. Many autacoids are present in umbilical blood. Fetal vessels of the placenta develop intense vasoconstriction in the presence of some autacoids, such as thromboxane A2 and prostaglandins F2α and E2, and respond weakly to others, such as angiotensin II and 5-hydroxytryptamine. Nevertheless, vasodilator influences predominate.4. The diseases of pre-eclampsia and fetal growth retardation are associated with reduced output of nitric oxide and prostacyclin and with increased production of thromboxane A2 and endothelin-1. These changes promote vasoconstriction, increased vascular sensitivity to vasoconstrictor stimuli, platelet aggregation and intravascular coagulation, retarding blood flow and feto-placental growth.5. Aspirin and glyceryl trinitrate have been investigated for possible therapeutic use in pre-eclampsia and fetal growth retardation. Improved drug therapy is likely as knowledge increases of the importance of autacoids in normal placental function and in the changes that occur during disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02441.x
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  • 5
    Electronic Resource
    Electronic Resource
    RELEASE OF A SUBSTANCE FROM THE HUMAN PLACENTA HAVING DIGOXIN-LIKE IMMUNOREACTIVITY (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The human placental lobule, perfused with a constant flow (5 mL/min) of Krebs’ solution after delivery at term, released into the fetal perfusate a digoxin-like substance, as measured by a fluorescence polarization immunoassay.2. Initially the venous concentration was 360 ± 66.7 pmol/ L digoxin equivalents. This level did not change significantly during fetal vasoconstriction induced by prostaglandin F2α infusion and persisted for the duration of the experiment (1.5–2h).3. Infusion into the fetal circulation of Fab fragments of sheep antibodies to digoxin caused vasodilatation, indicated by a fall in perfusion pressure.4. Thus a digoxin-like immunoreactive substance, previously reported to be present in the placenta, is released into the fetal circulation and may play a role in placental control of fetal vascular tone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01747.x
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  • 6
    Electronic Resource
    Electronic Resource
    PREFACE (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00389.x
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  • 7
    Electronic Resource
    Electronic Resource
    CHARACTERIZATION OF THROMBOXANE A2 RECEPTORS IN THE HUMAN FETAL PLACENTAL VESSELS AND UMBILICAL VEIN (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 13 (1986), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. An in vitro examination has been made of the thromboxane A2 receptors in human fetal placental villous vessels and umbilical veins utilizing the TxA2 agonist U46619 and its competitive antagonist AH22921.2. U46619 was a potent constrictor of both preparations. The EC50 were 25.3 nmol/1 (s.e.m. =2.5, n= 8) for causing constriction of perfused villous vessels and 22 nmol/1 (s.e.m. = 5, n= 17) for contraction of the venous longitudinal strip.3. AH22921 competitively antagonized responses to U46619 in both preparations. The pA2 values were not significantly different and their 95% confidence limits, obtained for its ability to antagonize responses to U46619 in villous vessels and the umbilical vein, were 8.0 (7.3-8.8) and 7.1 (6.3-7.9) respectively.4. It is concluded that TxA2 receptors in both the human fetal placental villous vessels and umbilical vein may be similar. They also may be similar to those in human platelets and pulmonary blood vessels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1986.tb00319.x
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  • 8
    Electronic Resource
    Electronic Resource
    SYNERGISTIC POTENTIATION BY CAPTOPRIL AND PROPRANOLOL OF BRADYKININ-INDUCED BRONCHOCONSTRICTION IN THE GUINEA-PIG (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 16 (1989), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Captopril (30 or 100 μg/kg intravenous (i.v.)) in anaesthetized artificially ventilated guinea-pigs potentiated bronchoconstrictor responses to bradykinin, but not those to histamine or the thromboxane A2-mimetic U46619.2. Propranolol (5 mg/kg, i.v.) potentiated bradykinin-induced bronchoconstriction. The potentiated responses were further augmented by captopril.3. The captopril-potentiated responses to bradykinin were inhibited during cyclo-oxygenase inhibition with indomethacin. Bronchoconstrictor responses to bradykinin, but not those to histamine or U46619, were reduced after thromboxane synthase inhibition with dazoxiben. The thromboxane A2 antagonist AH23848 inhibited bronchoconstrictor responses to bradykinin, arachidonic acid or U46619 whereas it did not affect those to histamine.4. A kininase I inhibitor dl-2-mercaptomethyl-3-guanidinoethyl thiopropanoic acid caused no change in bronchoconstriction caused by bradykinin and did not alter the potentiated responses occurring after captopril.5. Thus, confirmation has been obtained that bradykinin causes bronchoconstriction in the guinea-pig indirectly, by release of eicosanoids. Thromboxane A2 is likely to be the major eicosanoid released, since the bronchoconstrictor effect of bradykinin was blocked by indomethacin, dazoxiben and AH23848. The intensity of the bronchoconstriction appears dependent on sympathetic influences mediated by β-adrenoceptors. Kininase I, in contrast to kininase II apparently has little role in terminating the effects of bradykinin in the lung.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1989.tb01524.x
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  • 9
    Electronic Resource
    Electronic Resource
    The Influence of Drugs and Other Factors on Inactivation of Prostaglandin E2 by the Rat Isolated Perfused Lung (1979)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 6 (1979), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The mechanisms responsible for inactivating prostaglandin E2 (PGE2) in the rat isolated lung were saturated by high rates of arterial presentation of the prostaglandin.2. Lungs from normotensive females, and from males of the New Zealand hypertensive strain, inactivated PGE2 less readily than did those from normotensive males.3. Increasing the perfusion rate or pre-treating animals with probenecid or cycloheximide reduced inactivation of PGE2. Treatment with cycloheximide plus probenecid did not however reduce inactivation to a greater extent than did cycloheximide alone.4. Pregnancy or administration of hydrocortisone increased pulmonary removal of PGE2 whereas adrenalectomy reduced it.5. Thus the rate of inactivation of PGE2 in this species may depend both on the activity of an initial active transport process and also on the levels of catabolising enzymes. The latter may be of greatest importance when pulmonary artery concentrations of PGE2 are low with the transport mechanism assuming greater significance when they are high. The rate of removal is also dependent on sex, genotype, steroidal status, pregnancy and pulmonary flow.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1979.tb00025.x
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  • 10
    Electronic Resource
    Electronic Resource
    HUMAN PLACENTAL ACETYLCHOLINE CONTENT AND RELEASE AT PARTURITION (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 15 (1988), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Measurements were made of human placental acetylcholine (ACh) content and release into maternal and fetal circulations from placenta obtained before, during and after labours of both spontaneous and induced onsets. ACh content was determined in ex vivo placental biopsies using a radio-enzymatic assay. ACh release was determined by bioassay of the effluent from placental lobules perfused with amniotic fluid-like Kreb's containing physostigmine (2.4 μmol/1).2. ACh content of placentae obtained after labour (spontaneous onset of labour, normal vaginal delivery) and during labour (spontaneous onset of labour, Caesarean section delivery) was significantly less than before labour (no labour onset, Caesarean section delivery).3. Mean ACh output into maternal vessels 1.5–4.0 h after commencement of perfusion of placentae obtained after labour (spontaneous onset of labour, normal vaginal delivery) was significantly less than from those obtained before labour (no labour onset, Caesarean section delivery). No differences were found in ACh output into fetal vessels of placentae obtained before, during or after labour.4. These results suggest a role for placental ACh in the events of human labour. The decrease in ACh content and maternal vascular release in placenta obtained after labour is consistent with a depletion of placental ACh during labour which may indicate ACh release at this time. The lack of any significant change in fetal vascular release of ACh in placenta obtained before, during or after labour, raises the possibility of different roles for ACh released into fetal and maternal vasculature.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1988.tb01131.x
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