Rapid communicationAdrenal-independent, anti-shock effect of ACTH-(1–24) in rats
References (5)
- et al.
The opiomelanotropineric neuronal and endocrine systems
Peptides
(1982) - et al.
Opioids and neuropeptides: mechanisms in circulatory shock
Cited by (57)
Melanocortins as potential therapeutic agents in severe hypoxic conditions
2012, Frontiers in NeuroendocrinologyCitation Excerpt :In these conditions, that in turn lead to the death of all saline-treated control animals within 30–35 min [15,16,18], conventional anti-shock drugs such as the glucocorticoid methylprednisolone, protease inhibitor aprotinin and sympathomimetic agent norepinephrine are ineffective [8]. Conversely, the intravenous bolus injection of nanomolar amounts of melanocortins [e.g., ACTH-(4–10), α-MSH, ACTH-(1–24), etc.] induces, within a few minutes, a dose-dependent restoration of arterial blood pressure and tissue blood flow, as well as a gradual normalization of blood gases, pH and lactate [12,15,16,18,89]. The melanocortin-induced shock reversal was found to be associated with a large increase in the volume of circulating blood, not due to hemodilution but as the consequence of the mobilization of the peripherally pooled residual blood that, in shock conditions, is trapped in capillaries and large blood reservoirs including liver and spleen [85,86,89].
Drug-induced activation of the nervous control of inflammation: A novel possibility for the treatment of hypoxic damage
2012, European Journal of PharmacologyCitation Excerpt :The minimum active dose [20 μg/kg in the case of ACTH-(1–24)] produces a 40% survival at 2 h after treatment; the maximum active dose (160 μg/kg) practically restores arterial pressure, pulse amplitude and respiratory rate to pre-bleeding values (Bertolini et al., 1986c), and produces a 100% survival – without reinfusion of the shed blood or infusion of blood substitutes – for more than 24 h (Bertolini et al., 1989). 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).
Brain effects of melanocortins
2009, Pharmacological ResearchNeuroprotection in focal cerebral ischemia owing to delayed treatment with melanocortins
2007, European Journal of PharmacologyCannabinoid CB<inf>1</inf> receptor blockade enhances the protective effect of melanocortins in hemorrhagic shock in the rat
2002, European Journal of Pharmacology