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  • 1
    Electronic Resource
    Electronic Resource
    Plasma catecholamines, plasma renin activity and haemodynamics during sodium nitroprusside-induced hypotension and additional beta-blockade with bunitrolol (1981)
    Springer
    European journal of clinical pharmacology 19 (1981), S. 317-322 
    Details
    ISSN: 1432-1041
    Keywords: hypotension ; nitroprusside ; bunitrolol ; plasma catecholamines ; plasma renin activity ; haemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of β-blockade on certain physiological and haemodynamic responses to sodium nitroprusside-induced hypotension have been studied in 5 patients, aged 18–54 years, undergoing inner ear surgery. Samples of blood were collected unter premedication, following induction of anaesthesia, during neuroleptanalgesia, during a sodium nitroprusside infusion adjusted to produce a 40% fall in blood pressure, during superimposed β-blockade with bunitrolol and under stable haemodynamic conditions after discontinuation of sodium nitroprusside. The sodium nitroprusside-induced reduction in blood pressure led to a massive increase in plasma noradrenaline and adrenaline and in plasma renin activity. β-blockade with bunitrolol did not affect the increased catecholamine concentrations, the increase in plasma renin activity was significantly reduced, the increase in heart rate was reversed, and total peripheral resistance and diastolic blood pressure were further reduced. These changes can be attributed to the intrinsic β-sympathomimetic activity of bunitrolol in addition to its β-blocking effect. Since no adverse effect was observed in this study, combined therapy with sodium notroprusside and β-receptor blockade should be employed if the effects of increased sympathetic tone are considered to be undesirable.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00544580
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  • 2
    Electronic Resource
    Electronic Resource
    Acute effects of alinidine on heart rate and blood pressure in healthy subjects and patients with hyperkinetic heart syndrome (1983)
    Springer
    European journal of clinical pharmacology 24 (1983), S. 31-34 
    Details
    ISSN: 1432-1041
    Keywords: hyperkinetic heart syndrome ; alinidine ; bradycardia ; blood pressure ; sympatho-inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of a single dose of alinidine (0.5 mg/kg i.v.), the N-allyl-derivative of clonidine, on heart rate and blood pressure were investigated in healthy volunteers and in patients with hyperkinetic heart syndrome, at rest and during bicycle exercise. In healthy volunteers plasma catecholamine levels were also determined. Alinidine did not change heart rate at rest in the healthy volunteers but it did significantly reduce exercise-induced tachycardia, whereas blood pressure and plasma catecholamine levels were not significantly affected by alinidine, either at rest or during exercise. In patients with hyperkinetic heart syndrome, alinidine reduced heart rate at rest and during exercise to a similar extent as propranolol (0.1 mg/kg i.v.). The blood pressure did not change with alinidine but it was significantly reduced by propranolol. The observation that an alinidine-induced reduction of heart rate occurs without a concomitant fall in blood pressure, and without a clonidine-like symphatho-inhibitory action, is in line with experimental findings suggesting a specific bradycardic action of alinidine under short-term conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00613923
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  • 3
    Electronic Resource
    Electronic Resource
    Sympatho-adrenal response to hypoglycaemia in infants (1988)
    Springer
    European journal of pediatrics 148 (1988), S. 253-256 
    Details
    ISSN: 1432-1076
    Keywords: Noradrenaline ; Adrenaline ; Hypoglycaemia ; Infants
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10–189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a β-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29±0.03 to 0.61±0.09 ng/ml (P〈0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00441414
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of captopril on renin and blood pressure in cirrhosis (1987)
    Springer
    European journal of clinical pharmacology 33 (1987), S. 249-254 
    Details
    ISSN: 1432-1041
    Keywords: liver cirrhosis ; captopril ; renin-angiotensin system ; blood pressure ; aldosterone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction. Captopril caused an increase in plasma renin activity (p〈0.005) and a decrease in plasma aldosterone (p〈0.025) from an elevated baseline, and a moderate drop in systolic (p〈0.025) and diastolic (p〈0.05) blood pressure. Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r=−0.66,p〈0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r=0.49,p〈0.05 for systolic andr=0.71,p〈0.01 for diastolic blood pressure). No change occurred in heart rate or in stimulated plasma noradrenaline and vasopressin levels. The data suggest that in these cirrhotic patients the reactivity of the renin-angiotensin-aldosterone system was still intact, although it occurred at a higher level. They confirm the importance of the renin-angiotensin-aldosterone system in arterial blood pressure regulation in cirrhosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00637557
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  • 5
    Electronic Resource
    Electronic Resource
    The effect of repeated intravenous and oral doses of molsidomine (N-carboxy-3-morpholino-sydnonimine-ethylester) on plasma renin activity and plasma catecholamine levels in conscious dogs (1983)
    Springer
    Basic research in cardiology 78 (1983), S. 193-202 
    Details
    ISSN: 1435-1803
    Keywords: molsidomine ; renin angiotensin aldosterone system ; plasma catecholamines ; counterregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Wirkung intravenöser und peroraler Gaben von Molsidomin auf die Plasmareninaktivität (PRA) und die Plasmakatecholaminspiegel wacher Hunde wurde untersucht. Intravenöse Verabreichung von Molsidomin in einer Dosierung bis zu 0,4 mg/kg bei einem gleichbleibenden Dosisintervall von 4 Stunden führte zu keinem langanhaltenden Anstieg der PRA. Im Gegensatz dazu war nach peroraler Verabreichung von 0,4 mg/kg Molsidomin nach 4 Stunden die PRA noch deutlich erhöht. Der relativ stärkere Anstieg der PRA auf orale Gabe wird mit Bezugnahme auf den Abbau von Molsidomin zu einem aktiven Metaboliten in der Leber diskutiert. Verkürzung des Dosisintervalls auf 3 Stunden und weniger führte zu einem kumulativen PRA-Anstieg. Es ist anzunehmen, daß Substanzen, die venöses Pooling verursachen, zu einer andauernden Aktivierung des Renin-Angiotensin-Aldosteron-Systems (RAA-System) führen, welche dem ursprünglichen therapeutischen Effekt entgegenwirkt. Der geringe Anstieg der Plasmanoradrenalinwerte, der nach peroraler Gabe von 0,4 mg/kg Molsidomin bei einem Dosisintervall von 2 Stunden beobachtet wurde, deutet die Mitbeteiligung des Sympathischen Nervensystems bei der Gegenregulation an.
    Notes: Summary The responses of plasma renin activity (PRA) and plasma catecholamine levels to molsidomine, administered both intravenously and orally, were investigated in conscious trained dogs. Intravenous administration of molsidomine at increasing dosage up to 0.4 mg/kg with a constant dose interval of 4 hours did not lead to a sustained increase in PRA. By contrast, a significant increase in PRA was still present after 4 hours on administration of 0.4 mg/kg molsidomine by the oral route. This longer-lasting increase in PRA following oral administration is discussed in relation to the conversion of molsidomine to an active metabolite in the liver. A reduction of dose interval to 3 hours or less led to a marked cumulative increase in PRA. It appears that substances acting via venous pooling lead to persistent activation of the renin angiotensin aldosterone system (RAA system), which counteracts its primary therapeutic effect. A slight increase in plasma noradrenaline levels was observed in response to repeated oral administration of 0.4 mg/kg molsidomine at a dose interval of 2 hours, indicating participation of the sympathetic nervous system in the counterregulatory process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01906672
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  • 6
    Electronic Resource
    Electronic Resource
    Prostaglandin E1 bridge to heart transplantation – methods, technique, results (1999)
    Springer
    Zeitschrift für Kardiologie 88 (1999), S. S033 
    Details
    ISSN: 1435-1285
    Keywords: Key words Prostaglandin E1 – dobutamine – heart transplantation – bridging agent – heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Heart transplantation (HTx) candidates who remain severely symptomatic despite optimal therapy are normally hospitalized. Continuous infusion of intravenous drugs from a portable pump may allow such patients to live fairly active life until a donor heart is found. Among the current potential bridging agents the synthetic β-agonist dobutamine is preferred for inotropic support. Prostaglandin E1 (PGE1), a naturally occurring substance with an eicosanoid structure and potent pulmonary and systemic vasodilator action, is another candidate for this indication. It was shown in a double-blind trial that PGE1 lowers pre- and afterload in patients with left ventricular failure who are already stabilized on catecholamines. In addition, an open pilot study of 54 patients suggested that chronic infusions with PGE1 at reduced dosages is a feasible and safe therapeutic approach to bridge end-stage heart failure patients and may yield desirable effects in a subset of patients in the absence of intropic support with dobutamine. Meanwhile, we have demonstrated in a recent prospective randomized trial that PGE1 is superior to dobutamine as a single bridging drug with regard to improving event-free survival rates in this high-risk patient population.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003920050584
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