Angiotensin II for the emergency physician

Wallis, Marianne; Chow, Jonathan H.; Winters, Michael E.; McCurdy, Michael T.

doi:10.1136/emermed-2019-209062

Cited by 2 publications

(2 citation statements)

References 29 publications

(37 reference statements)

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“…Collectively, these actions result in increased circulatory volume and MAP. 5 Numerous studies have examined the use of bovine Ang-2 since the 1930s. [6][7][8] Since the ATHOS and ATHOS-3 trials, several subgroup analyses have been performed of ATHOS-3, which demonstrated mortality benefit in particular patient populations.…”

Section: Introductionmentioning

confidence: 99%

A Multicenter Observational Cohort Study of Angiotensin II in Shock

Smith

Newsome

Guo

et al. 2020

J Intensive Care Med

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Introduction: Angiotensin II (Ang-2) is a non-catecholamine vasopressor that targets the renin-angiotensin-aldosterone system by agonism of the angiotensin type 1 receptor. Its utility as a vasopressor and a catecholamine-sparing agent was demonstrated in the pivotal ATHOS-3 trial, and numerous post-hoc analyses have shown reduced mortality in certain subsets of the population. Methods: Consecutive adult patients at 5 centers who received Ang-2 from 2017-2020 were included in this multicenter, retrospective observational cohort study. Patient demographics, hemodynamics, and adverse events were collected. The primary outcomes of the study were the mean difference in MAP and norepinephrine (NEpi)-equivalent dose at hours 0 and 3 following initiation of Ang-2 therapy. Results: One hundred and sixty-two patients were included in this study. The primary outcomes of an increase in MAP (mean difference 9.3 mmHg, 95% CI 6.4-12.1, p < 0.001) and a reduction in NEpi equivalent dose (mean difference 0.16 µg/kg/min, 95% CI 0.10-0.22, p < 0.001) between hours 0 and 3 were statistically significant. The median time to reach a MAP ≥65 was 16 minutes (IQR 5-60 min). After stratifying patients by the NED dose and number of vasopressors administered prior to the initiation of Ang-2, those with a NED dose < 0.2 µg/kg/min, NED dose < 0.3 µg/kg/min, or those on ≤ 3 vasopressors had a significantly greater reduction in NED by hour 3 than those patients above these thresholds. Conclusion: Ang-2 is an effective vasopressor and reduces catecholamine dose significantly. Its effect is rapid, with target MAP obtained within 30 minutes in most patients. Given the critical importance of adequate blood pressure to organ perfusion, Ang-2 should be considered when target MAP cannot be achieved with conventional vasopressors. Ang-2 should be utilized early in the course of shock, before the NED dose exceeds 0.2-0.3 µg/kg/min and before the initiation of the fourth-line vasopressor.

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Section: Introductionmentioning

confidence: 99%

A Multicenter Observational Cohort Study of Angiotensin II in Shock

Smith

Newsome

Guo

et al. 2020

J Intensive Care Med

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“…The main effects of Ang-2 include vasoconstriction, water and sodium retention, and aldosterone release [10]. As one of the strongest vasoconstrictor substances known up to now, Ang-2 can bind to angiotensin receptors on vascular smooth muscle, thereby constricting arterioles throughout the body and raising blood pressure [11]. ACE2, a major component of the RAS reaction axis, is a homologue of ACE [12] and mainly expressed in renal vascular endothelial and tubular epithelium.…”

Section: Discussionmentioning

confidence: 99%

Experimental Study on the Mechanism of Cinnamaldehyde Ameliorate Proteinuria Induced by Adriamycin

et al. 2022

BioMed Research International

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Objective. Cinnamaldehyde (CA) is the main active component of Guizhi (Cinnamomi ramulus) to ameliorate adriamycin- (ADR-) induced proteinuria in rats. However, the underlying mechanism of CA against proteinuria remains unclear. The aim of this study was to investigate the action mechanisms of CA to treat proteinuria. Methods. 13 rats were randomly selected from 78 SD rats as control group, and the other rats were injected with ADR (3 mg/kg/time) twice through tail vein on day 1 and day 8 for modeling. After modeling, the rats were randomly divided into 5 groups as follows: ADR group, ADR+CA low-dose group, ADR+CA middle-dose group, ADR+CA high-dose group and Benazepril group with 13 rats in each group. The urine of SD rats was collected for 24 h, urine protein, creatinine and urea nitrogen were detected, renal index was calculated, and HE staining and western blot were performed. Results. The 24 h urine volume and urine protein, renal function, and renal histopathology got worse significantly in the ADR group. To western blot, CA downregulated the protein expression of ACE and Ang-2 and upregulated the protein expression of ACE2 in RAS signaling pathway. Conclusion. The underlying action mechanism of CA to treat NS might mainly be achieved by regulating RAS signaling pathway.

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Angiotensin II for the emergency physician

Cited by 2 publications

References 29 publications

A Multicenter Observational Cohort Study of Angiotensin II in Shock

A Multicenter Observational Cohort Study of Angiotensin II in Shock

Experimental Study on the Mechanism of Cinnamaldehyde Ameliorate Proteinuria Induced by Adriamycin

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