2011
DOI: 10.1007/s10354-010-0853-7
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The role of vasopressin and terlipressin in catecholamine-resistant shock and cardio-circulatory arrest in children: Review of the literature

Abstract: No firm recommendations on the use of AVP/TP in children with severe forms of cardio-circulatory failure can be issued.

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Cited by 17 publications
(8 citation statements)
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References 60 publications
(224 reference statements)
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“…Thereafter, hemodynamic support is achieved with vasopressors and inotropes [5, 7]. However, reduced vasoconstrictor sensitivity to vasopressors in shock can lead to vasodilation, severe hypotension, and vasoparalysis [8]. There is, therefore, a pressing need for agents which target other pathways involved in the development of shock.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Thereafter, hemodynamic support is achieved with vasopressors and inotropes [5, 7]. However, reduced vasoconstrictor sensitivity to vasopressors in shock can lead to vasodilation, severe hypotension, and vasoparalysis [8]. There is, therefore, a pressing need for agents which target other pathways involved in the development of shock.…”
Section: Introductionmentioning
confidence: 99%
“…AVP acts on V1 receptors located on vascular smooth muscle leading to an increase in mean arterial pressure (MAP). Patients with shock exhibit inappropriately low circulating AVP concentrations [7, 8, 10]. From a biologic perspective, the basic rationale behind the addition of AVP/TP in refractory shock is the depletion of endovascular AVP in states of shock [11].…”
Section: Introductionmentioning
confidence: 99%
“…Experience with AVP/TP in neonates has been more focused on term newborns with congenital heart disease who develop hypotension after surgery, newborns with PPHN or with septic shock all reporting increased blood pressure, most reporting increased urine output and some reporting decreased lactate levels coming from retrospective studies or case series [85,[90][91][92][93][94][95].…”
Section: Evidence and Pd Effectsmentioning
confidence: 99%
“…31 The postulated mechanism of action for this effect is that the stimulation of V1 receptors in vascular smooth muscle leads to an increase in cytoplasmic ionized calcium via the phosphatidylinositol biphosphate cascade. [31][32][33] In HRS type 1, the effect that terlipressin promulgates is mediated by vasoconstriction of the splanchnic arterial blood vessels reducing blood flow to the system, thereby providing indirect volume expansion. 3 Stimulation of V2 receptors responsible for an antidiuretic effect is less desirable in HRS.…”
Section: Discussionmentioning
confidence: 99%