EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY
1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In s...
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| Autor*in: |
Kingsford, Nicola M. [verfasserIn] Lumbers, Eugenie R. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1989 |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2007 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: Clinical and experimental pharmacology and physiology - Oxford [u.a.] : Wiley-Blackwell, 1974, 16(1989), 11, Seite 0 |
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volume:16 ; year:1989 ; number:11 ; pages:0 |
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| DOI / URN: |
10.1111/j.1440-1681.1989.tb01527.x |
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| 245 | 1 | 0 | |a EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY |
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| 520 | |a 1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. | ||
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10.1111/j.1440-1681.1989.tb01527.x doi (DE-627)NLEJ238609723 DE-627 ger DE-627 rakwb Kingsford, Nicola M. verfasserin aut EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY Oxford, UK Blackwell Publishing Ltd 1989 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| fetus Lumbers, Eugenie R. verfasserin aut In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 16(1989), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:16 year:1989 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1989.tb01527.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 1989 11 0 |
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10.1111/j.1440-1681.1989.tb01527.x doi (DE-627)NLEJ238609723 DE-627 ger DE-627 rakwb Kingsford, Nicola M. verfasserin aut EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY Oxford, UK Blackwell Publishing Ltd 1989 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| fetus Lumbers, Eugenie R. verfasserin aut In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 16(1989), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:16 year:1989 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1989.tb01527.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 1989 11 0 |
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10.1111/j.1440-1681.1989.tb01527.x doi (DE-627)NLEJ238609723 DE-627 ger DE-627 rakwb Kingsford, Nicola M. verfasserin aut EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY Oxford, UK Blackwell Publishing Ltd 1989 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| fetus Lumbers, Eugenie R. verfasserin aut In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 16(1989), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:16 year:1989 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1989.tb01527.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 1989 11 0 |
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10.1111/j.1440-1681.1989.tb01527.x doi (DE-627)NLEJ238609723 DE-627 ger DE-627 rakwb Kingsford, Nicola M. verfasserin aut EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY Oxford, UK Blackwell Publishing Ltd 1989 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| fetus Lumbers, Eugenie R. verfasserin aut In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 16(1989), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:16 year:1989 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1989.tb01527.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 1989 11 0 |
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10.1111/j.1440-1681.1989.tb01527.x doi (DE-627)NLEJ238609723 DE-627 ger DE-627 rakwb Kingsford, Nicola M. verfasserin aut EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY Oxford, UK Blackwell Publishing Ltd 1989 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| fetus Lumbers, Eugenie R. verfasserin aut In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 16(1989), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:16 year:1989 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1989.tb01527.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 1989 11 0 |
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effects of autonomic blockade on the hypertensive response of the fetus to hyperosmolality |
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EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY |
| abstract |
1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. |
| abstractGer |
1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. |
| abstract_unstemmed |
1. Infusions of hyperosmotic mannitol to the ewe caused a rise in fetal arterial pressure in 17 chronically catheterized fetal sheep aged 120–140 days. The fetal heart slowed in 13 out of 17 of these fetuses. The rise in pressure occurred before there was any rise in fetal urinary osmolality.2. In seven fetal sheep combined α- and β-adrenoceptor and muscarinic blockade delayed the onset of the rise in blood pressure and no bradycardia was observed. It is concluded that the hypertension was due in part to increased activity of the sympatho-adrenal system, and that any reflex bradycardia that occurred was mediated by the vagus.3. In three other fetal sheep aged 125–131 days, the cardiovascular responses elicited by infusion of hyperosmotic mannitol to the ewe were not blocked by a specific vasopressin antagonist. Thus vasopressin could not be responsible for either the initial rise in pressure nor the delayed hypertensive response that was not blocked by α- and β-adrenoceptor blockade.4. Fetal blood volume was maintained even though the changes in plasma osmolality and electrolytes were indicative of a fall in blood volume. Thus changes that threaten maintenance of fetal blood volume seem to induce increased solute and water transport across the placenta or from the extracorporeal fluid compartments. |
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EFFECTS OF AUTONOMIC BLOCKADE ON THE HYPERTENSIVE RESPONSE OF THE FETUS TO HYPEROSMOLALITY |
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10.1111/j.1440-1681.1989.tb01527.x |
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