Regular paperACTH-(1–24) blocks the decompensatory phase of the haemodynamic response to acute hypovolaemia in conscious rabbits
References (45)
- et al.
Adrenal-independent, anti-shock effect of ACTH-(1–24) in rats
Eur. J. Pharmacol.
(1986) - et al.
Adrenocorticotropin reversal of experimental hemorrhagic shock is antagonized by morphine
Life Sci.
(1986) - et al.
The adrenocorticotropic hormone (ACTH)-induced reversal of hemorrhagic shock
Resuscitation
(1989) - et al.
Sympathetic terminal mediation of the acute cardiovascular response of γ2-MSH
J. Auton. Nerv. Sys.
(1988) - et al.
The hemodynamic effects of γ2-melanocyte-stimulating hormone and related melanotropins depend on the arousal potential of the rat
Eur. J. Pharmacol.
(1993) - et al.
Intracisternal naloxone and cardiac nerve blockade prevent vasodilatation during simulated haemorrhage in awake rabbits
J. Physiol. (London)
(1989) - et al.
Pressor and cardioaccelerator effects of gamma-MSH and related peptides
Life Sci.
(1985) - et al.
Selective manipulation of neurohumoral control of the cardiac pacemaker by drugs given intrapericardially
J. Pharmacol. Methods
(1987) - et al.
The decompensatory phase of acute hypovolaemia in rabbits involves a central δ1-opioid receptor
Eur. J. Pharmacol.
(1994) - et al.
ACTH-(1–24) and hemorrhagic shock: preliminary clinical results
Resuscitation
(1989)
Haemorrhagic shock in cardiac surgery
Pharmacological treatment with ACTH (1–24)
Resuscitation
Preliminary data on the use of ACTH-(1–24) in human shock conditions
Resuscitation
Facilitation of the release of noradrenaline: an extra-adrenal effect of adrenocorticotropic hormone
Resuscitation
Heterogeneity of brain melanocortin receptors suggested by differential ligand binding in situ
Brain Res.
Selective opiate modulation of the physiological responses to hemorrhage in the cat
Endocrinology
Adrenocorticotropin response to graded blood loss in the cat
Am. J. Physiol.
Effect of rate of hemorrhage on release of ACTH in cats
Am. J. Physiol.
ACTH-(1–24) restores blood pressure in acute hypovolaemia and haemorrhagic shock in humans
Eur. J. Clin. Pharmacol.
Influence of endogenous opiates and cardiac afferents on renal nerve activity during haemorrhage in conscious rabbits
J. Physiol. (London)
Functional organization of central pathways regulating the cardiovascular system
Physiol. Rev.
Responses of ACTH, epinephrine, norepinephrine, and cardiovascular system to hemorrhage
Am. J. Physiol.
Effects of -like peptides on blood pressure, heart rate, and blood flow: structure-activity relationship
Can. J. Physiol. Pharmacol.
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Melanocortins as potential therapeutic agents in severe hypoxic conditions
2012, Frontiers in NeuroendocrinologyCitation Excerpt :Patients with respiratory arrest and cardiac arrest consequent to various insults [70,78], including overdose of opioid peptides, could take advantage from an early treatment with melanocortins. It is of note that melanocortins for many years have been considered among the main physiological antagonists of endogenous opioids [19]; consistently, morphine and an enkephalin analog antagonized the anti-shock effect of ACTH-(1–24) in rats and rabbits, with the overcoming of such antagonism by a higher dose of ACTH-(1–24) [16,130]. Heart ischemia/reperfusion injury is still considered a major problem in patients with acute coronary occlusion and in patients undergoing coronary artery bypass grafting [108].
Drug-induced activation of the nervous control of inflammation: A novel possibility for the treatment of hypoxic damage
2012, European Journal of PharmacologyCitation Excerpt :Adrenal glands are not involved, because the effect is the same either in intact or in adrenalectomized animals (Bertolini et al., 1986a) and is independent of the corticotropic activity of the melanocortin injected (Bertolini et al., 1986c). The resuscitating effect of melanocortins has been confirmed also in other shock conditions: the hypovolemic shock produced in rabbits by the graded occlusion of the inferior vena cava (Ludbrook and Ventura, 1995) and the rat model of splanchnic ischemia/reperfusion-induced shock (splanchnic artery occlusion shock, SAO shock) (Squadrito et al., 1999), and also in a pre-terminal condition produced in rats by prolonged asphyxia (Guarini et al., 1997). The reversal of shock by melanocortins occurs through activation of melanocortin MC4 receptors in the brain.
Brain effects of melanocortins
2009, Pharmacological ResearchNeuroprotection in focal cerebral ischemia owing to delayed treatment with melanocortins
2007, European Journal of Pharmacology