Vasopressin: Mechanisms of action on the vasculature in health and in septic shock

Barrett, Lucinda; Singer, Mervyn; Clapp, Lucie H.

doi:10.1097/01.ccm.0000251127.45385.cd

Cited by 197 publications

(136 citation statements)

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“…The mainstays of prevention and treatment include avoidance of nephrotoxins and ensuring adequate renal perfusion. In addition to its potent vasoconstrictor effects, vasopressin may also have specific beneficial effects on renal function secondary to its binding to a family of vasopressin receptors [8]. In several small studies of vasodilatory shock, vasopressin increased glomerular filtration rate, urine output and creatinine clearance [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

The effects of vasopressin on acute kidney injury in septic shock

et al. 2009

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Kidney injury was present in 464 patients (59.6%) at study entry. In patients in the RIFLE "Risk" category (n=106) vasopressin as compared with norepinephrine was associated with a trend to a lower rate of progression to renal "Failure" or "Loss" categories (20.8% v 39.6% respectively, p=0.03), and a lower rate of use of renal replacement therapy (17.0% v 37.7%, p=0.02). Mortality rates in the "Risk" category patients treated with vasopressin compared to norepinephrine were 30.8% v 54.7%, p=0.01, but this did not reach significance in a multiple logistic regression analysis (OR=0.33, 99%CI 0.10-1.09, p=0.02). The interaction of treatment group and RIFLE category was significant in predicting mortality. Conclusions:Vasopressin may reduce progression to renal failure and mortality in patients at risk of kidney injury who have septic shock.

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Section: Introductionmentioning

confidence: 99%

The effects of vasopressin on acute kidney injury in septic shock

et al. 2009

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“…Vasopressin (or synthetic analogues such as terlipressin) is not recommended as a first line treatment, but can be considered as a salvage therapy [118,119]. Vasopressin infusion rates up to 0.01-0.04 U/min are generally considered safe when norepinephrine infusion rate exceeds 0.5 µg/kg/min.…”

Section: Inotropes For Contractilitymentioning

confidence: 99%

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer

2013

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Septic shock is characterized by circulatory compromise, microcirculatory alterations and mitochondrial damage, which all reduce cellular energy production. In order to reduce the risk of major cell death and a diminished likelihood of recovery, adaptive changes appear to be activated. As a result, cells and organs may survive in a non-functioning hibernation-like condition. Sepsis-induced cardiac dysfunction may represent an example of such functional shutdown. Sepsis-induced myocardial dysfunction is common, corresponds to the severity of sepsis, and is reversible in survivors. Its mechanisms include the attenuation of the adrenergic response at the cardiomyocyte level, alterations of intracellular calcium trafficking and blunted calcium sensitivity of contractile proteins. All these changes are mediated by cytokines. Treatment includes preload optimization with sufficient fluids. However, excessive volume loading is harmful. The first line vasopressor recommended at present is norepinephrine, while vasopressin can be started as a salvage therapy for those not responding to catecholamines. During early sepsis, cardiac output can be increased by dobutamine. While early administration of catecholamines might be necessary to restore adequate organ perfusion, prolonged administration might be harmful. Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine reduces myocardial oxygen expenditure and ameliorates diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. All these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice. While early administration of catecholamines might be necessary to restore adequate organ perfusion and pressure, prolonged administration might be harmful.Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine will reduce myocardial oxygen expenditure and ameliorate diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. However, all these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice.-3 -Alain Rudiger & Mervyn Singer: The heart in sepsis

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“…The pressor effect of vasopressin is due to its action on the V1-receptors in vascular smooth muscle, and it is more predominant in the peripheral systemic arteriolar vasculature than in venous or pulmonary circulation 13,18 . Additionally, vasopressin leads to the potentiation of catecholamine action on vascular smooth 23,24 .…”

Section: Discussionmentioning

confidence: 99%

“…Despite considerable research attention, the mechanisms for vasopressin deficiency and hypersensitivity in vasodilatory shock remain unclear 9,12,13,[16][17][18][19][20] . Moreover, the clinical experience with vasopressin, as well as its hemodynamic effects in continuous infusions with progressive doses has been limited.…”

mentioning

confidence: 99%

“…In the last decade, vasopressin has been broadly used as an adjunct vasopressor agent for the management of catecholamine-resistant vasodilatory shock 9,[11][12][13] , and is also recommended to increase peripheral vascular tone during cardiopulmonary resuscitation as an alternative to epinephrine 14,15 . Despite considerable research attention, the mechanisms for vasopressin deficiency and hypersensitivity in vasodilatory shock remain unclear 9,12,13,[16][17][18][19][20] .…”

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confidence: 99%

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