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  • 1
    Online Resource
    Online Resource
    Portland Press Ltd. ; 2002
    In:  Clinical Science Vol. 103, No. s2002 ( 2002-09-01), p. 336S-339S
    In: Clinical Science, Portland Press Ltd., Vol. 103, No. s2002 ( 2002-09-01), p. 336S-339S
    Abstract: This study compares the haemodynamic and hormonal responses during haemorrhage of conscious dogs pre-treated with an endothelin-A (ET-A) receptor inhibitor. The dogs were studied in two different randomized groups: the control group and a group that was given the ET-A receptor antagonist ABT-627 (as a bolus of 1mg·kg of body weight-1 followed by 0.01mg·kg body weight-1·min-1 intravenously). The time-course was the same for both groups: after a 1h baseline period (pre-haemorrhage), blood (25ml·kg of body weight-1) was withdrawn within 5min. Haemodynamics were continuously recorded and hormone levels measured after 1h (post-haemorrhage). Thereafter, the blood withdrawn was retransfused within 5min and haemodynamics again observed for 1h (post-retransfusion). In ABT-627-treated dogs, the decrease in mean arterial pressure from 87±3 to 64±3mmHg (P & lt;0.05 versus pre-haemorrhage), and cardiac output from 2.1±0.1 to 1.3±0.1l·min-1 (P & lt;0.05 versus pre-haemorrhage) and the increase in systemic vascular resistance from 3286±174 to 4211±230dyn·s·cm-5 (P & lt;0.05 versus pre-haemorrhage) during acute haemorrhage are comparable with controls. During haemorrhage in controls, vasopressin levels increased from 0±0 to 13±2pg·ml-1 (P & lt;0.05 versus pre-haemorrhage), angiotensin II levels increased from 9±1 to 28±9pg·ml-1 (P & lt;0.05 versus pre-haemorrhage) and adrenaline levels increased from 134±22 to 426±74pg·ml-1 (P & lt;0.05 versus pre-haemorrhage) whereas noradrenaline levels did not change (approx. 200 pg·ml-1). In ABT-627-treated dogs, vasopressin levels increased from 0.2±0.0 to 22.2±6.1pg·ml-1 (P & lt;0.05 versus pre-haemorrhage and P & lt;0.05 versus control), angiotensin II levels increased from 8±1 to 37±8pg·ml-1 (P & lt;0.05 versus pre-haemorrhage), noradrenaline levels increased from 147±16 to 405±116pg·ml-1 (P & lt;0.05 versus pre-haemorrhage) and adrenaline levels did not change (200 pg·ml-1) during haemorrhage. We conclude from our results that dogs receiving the selective ET-A inhibitor ABT-627 seem to show a different hormonal response after haemorrhage compared with controls, displaying considerably higher noradrenaline concentrations. Independent of ET-A receptor inhibition, cardiac output during haemorrhage was maintained within the control range. This may indicate that the organism is defending blood flow (cardiac output) over blood pressure during haemorrhage, and that this defence strategy is not compromised by ET-A receptor inhibition.
    Type of Medium: Online Resource
    ISSN: 0143-5221
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2002
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  • 2
    Online Resource
    Online Resource
    Portland Press Ltd. ; 1995
    In:  Clinical Science Vol. 89, No. 1 ( 1995-07-01), p. 19-25
    In: Clinical Science, Portland Press Ltd., Vol. 89, No. 1 ( 1995-07-01), p. 19-25
    Abstract: 1. We studied post-prandial changes in renal function in dogs adapted to either low or high sodium intake with and without concomitant post-prandial infusion of angiotensin II. Six trained dogs were exposed to diets containing either 0.5 or 14.5 mmol Na+ day−1 kg−1 body weight (low or high sodium respectively). They were studied from 20 min before to 4 h after food intake. In half of the experiments a physiological dose of angiotensin II (4 ng min−1 kg−1 body weight) was administered after food intake for four post-prandial hours. The water intake was high and equal on both diets (91 ml day−1 kg−1 body weight). 2. On a high-salt diet post-prandial sodium excretion and urine volume increased considerably above fasting values. This post-prandial increase was attenuated when angiotensin II was infused (post-prandial sodium excretion was 31% ± 3% of intake without versus 10% ± 1% with angiotensin II, post-prandial urine volume was 22% ± 2% without versus 8% ± 1% with angiotensin II, P & lt; 0.05). Post-prandial increases in glomerular filtration rate and fractional sodium excretion were attenuated during angiotensin II infusion in dogs on a high-salt diet. 3. On a low-salt diet post-prandial sodium excretion remained low with or without angiotensin II infusion, whereas urine volume increased post-prandially, and this increase was greater when angiotensin II was administered (40% ± 3% versus 34% ± 2% of intake, P & lt; 0.05). 4. Angiotensin II infusion increased mean arterial pressure by an average of 12 mmHg in dogs on a high-salt diet (P & lt; 0.05) and by 7 mmHg in dogs on a low-salt diet. In dogs on a high-salt diet, right atrial pressure was on an average 3 cmH2O higher with than without angiotensin II (P & lt; 0.05). In animals on a low salt intake post-prandial right atrial pressure decreased slightly, but remained in the range of fasting values, during angiotensin II infusion. 5. Neither plasma osmolality nor plasma sodium concentration changed in any of the four protocols. 6. We conclude that the post-prandial effects of angiotensin II in dogs on a high water intake depend on the amount of concomitant sodium intake. Angiotensin II reduces the post-prandial diuresis and natriuresis when given to sodium-loaded dogs, whereas angiotensin II does not reduce post-prandial urine flow and sodium excretion rates in dogs on a low sodium intake and may even augment water excretion in this condition.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1995
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Anesthesiology Vol. 100, No. 4 ( 2004-04-01), p. 885-893
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 4 ( 2004-04-01), p. 885-893
    Abstract: The objective of this study was to determine whether endothelin-A receptor blockade (ETAB) impairs hemodynamic and hormonal regulation compared with controls and angiotensin II receptor blockade (AT1B) during hypotensive hemorrhage in dogs under isoflurane-nitrous oxide anesthesia. Methods Six dogs were studied in four protocols: (1) control experiments (controls); (2) ETA blockade using ABT-627 (ETAB); (3) AT1 blockade using losartan (AT1B); and (4) combined AT1B and ETAB (AT1B + ETAB). After a 30-min awake period, isoflurane-nitrous oxide anesthesia was established (1.3 minimum anesthetic concentration). After 60 min of anesthesia, 20 ml blood/kg body weight was withdrawn within 5 min, and the dogs were observed for another hour. Thereafter, the blood was retransfused, and the dogs were observed for a final hour. Results Anesthesia: Cardiac output decreased in all protocols, whereas mean arterial pressure decreased more in AT1B and AT1B + ETAB than in controls and ETAB. Hemorrhage: After 60 min, cardiac output had decreased less in controls than in all other protocols. Mean arterial pressure decreased more during ETAB than in controls, but most severely during AT1B and AT1B + ETAB. Angiotensin II increased further only in controls and ETAB, whereas vasopressin and catecholamines increased similarly in all protocols. Retransfusion: Mean arterial pressure remained below controls in all protocols but was lowest when the AT1 receptor was blocked. Cardiac output fully recovered in all but the ETAB protocol. Conclusions ETAB impairs long-term hemodynamic regulation after hemorrhage and retransfusion during anesthesia despite an activation of vasoconstrictive hormones. This suggests that endothelins have a role in long-term cardiovascular regulation. AT1B impairs both short- and long-term blood pressure regulation during anesthesia and after hemorrhage.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 2016092-6
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  • 4
    In: Kidney and Blood Pressure Research, S. Karger AG, Vol. 18, No. 1 ( 1995), p. 35-48
    Abstract: The diurnal time course of urinary flow rate (UV), urinary sodium (U 〈 sub 〉 Na 〈 /sub 〉 V), and potassium (U 〈 sub 〉 K 〈 /sub 〉 V) excretion, and of hormones such as atrial natriuretic peptide (ANP) and aldosterone, was investigated during 5 days of continuous captopril infusion (15 µg · kg body weigth 〈 sup 〉 -1 〈 /sup 〉 · min 〈 sup 〉 -1 〈 /sup 〉 ) in 4 conscious dogs on a high sodium diet (14.5 mmol Na·kg body weigth 〈 sup 〉 -1 〈 /sup 〉 24 h 〈 sup 〉 -1 〈 /sup 〉 ). All food and water was given once daily at 8.30 a.m. On the control day and on days 1, 3, and 5 of·captopril infusion, urine was collected by an automated system at 20-min intervals over 24 h, blood was taken every 4 h. Mean arterial blood pressure (MABP) and heart rate were evaluated as 5-min averages. Time courses of U 〈 sub 〉 Na 〈 /sub 〉 V, UV, and UKV were compared with the individual control day without captopril. With captopril, 24-hour balances for Na and H 〈 sub 〉 2 〈 /sub 〉 0 were slightly negative, while the K balance was slightly positive for 2-3 days. Thereafter, all 24-hour balances were restored. MABP continued to decrease even after Na and water intake and output had come into balance again. Captopril treatment changed the diurnal excretion pattern for U 〈 sub 〉 Na 〈 /sub 〉 V and UV characteristically. In the postprandial period until 5 p.m., less Na and urine were excreted than on the control day, whereas during the evening and night more Na and urine were excreted. The changes in the excretion pattern persisted for the entire observation period. The results indicate that disturbances in the regulating systems, induced by converting-enzyme blockade, bring about complex reactions of, e.g., MABP ANP and aldosterone that finally restore Na and water 24-hour input/output balances.
    Type of Medium: Online Resource
    ISSN: 1420-4096 , 1423-0143
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1995
    detail.hit.zdb_id: 1482922-8
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  • 5
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2008
    In:  Critical Care Vol. 12, No. 3 ( 2008), p. 303-
    In: Critical Care, Springer Science and Business Media LLC, Vol. 12, No. 3 ( 2008), p. 303-
    Type of Medium: Online Resource
    ISSN: 1364-8535
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2008
    detail.hit.zdb_id: 2051256-9
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  • 6
    In: Journal of Visualized Experiments, MyJove Corporation, , No. 115 ( 2016-09-07)
    Type of Medium: Online Resource
    ISSN: 1940-087X
    Language: English
    Publisher: MyJove Corporation
    Publication Date: 2016
    detail.hit.zdb_id: 2259946-0
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  • 7
    In: Canadian Journal of Physiology and Pharmacology, Canadian Science Publishing, Vol. 86, No. 6 ( 2008-06), p. 373-379
    Abstract: The effects of endothelin receptor subtype A (ET A ) blockade on hemodynamics and hormonal adaptation during hemorrhage were studied in xenon/remifentanil-anesthetized dogs (n = 6) pretreated with an angiotensin II type 1 (AT 1 )-receptor blocker. Controls: after a baseline awake period, anesthesia was induced in the dogs with propofol and maintained with xenon/remifentanil (baseline anesthesia). Sixty minutes later, 20 mL·kg –1 of blood was withdrawn within 5 min and the dogs observed for another hour (hemorrhage). AT 1 group followed the same protocol as controls except the AT 1 -receptor blocker losartan (i.v. 100 μg·kg –1 ·min –1 ) was started at the beginning of the experiment. AT 1 +ET A group was the same as AT 1 group but with the addition of the ET A -receptor blocker atrasentan (i.v. 1 mg·kg –1 , then 0.01 mg·kg –1 ·min –1 ). In controls, mean arterial pressure (MAP) remained unchanged during baseline anesthesia, whereas systemic vascular resistance (SVR) increased from 3282 ± 281 to 7321 ± 803 dyn·s·cm –5 , heart rate (HR) decreased from 86 ± 4 to 40 ± 3 beats·min –1 , and cardiac output (CO) decreased from 2.3 ± 0.2 to 0.9 ± 0.1 L·min –1 (p  〈 0.05), with no further changes after hemorrhage. In AT 1 -inhibited dogs, MAP (71 ± 6 mm Hg) and SVR (5939 ± 611 dyn·s·cm –5 ) were lower during baseline anesthesia and after hemorrhage, but greater than those in AT 1 +ET A (66 ± 7 mm Hg, 5034 ± 658 dyn·s·cm –5 ) (p  〈 0.05). HR and CO were not different between groups. Plasma concentration of vasopressin was highest with AT 1 +ET A inhibition after hemorrhage. Combined AT 1 +ET A -receptor blockade impaired vasoconstriction more than did AT 1 -receptor blockade alone, both during baseline xenon anesthesia and after hemorrhage. Even a large increase in vasoconstrictor hormones could not prevent the decrease in blood pressure and the smaller increase in SVR. Thus, endothelin is an important vasoconstrictor during hemorrhage, and both endothelin and angiotensin II are essential hormones for cardiovascular stabilization after hemorrhage.
    Type of Medium: Online Resource
    ISSN: 0008-4212 , 1205-7541
    Language: English
    Publisher: Canadian Science Publishing
    Publication Date: 2008
    detail.hit.zdb_id: 2004356-9
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  • 8
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Journal of Cardiovascular Pharmacology Vol. 44, No. Supplement 1 ( 2004-11), p. S151-S155
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. Supplement 1 ( 2004-11), p. S151-S155
    Type of Medium: Online Resource
    ISSN: 0160-2446
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 9
    Online Resource
    Online Resource
    Georg Thieme Verlag KG ; 2007
    In:  Intensivmedizin up2date Vol. 3, No. 1 ( 2007-2), p. 53-68
    In: Intensivmedizin up2date, Georg Thieme Verlag KG, Vol. 3, No. 1 ( 2007-2), p. 53-68
    Type of Medium: Online Resource
    ISSN: 1614-4856 , 1614-6697
    Language: German
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2007
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  • 10
    In: Pediatric Anesthesia, Wiley, Vol. 16, No. 1 ( 2006-01), p. 95-96
    Type of Medium: Online Resource
    ISSN: 1155-5645 , 1460-9592
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2008564-3
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