Efeitos da dexmedetomidina sobre o sistema renal e sobre a concentração plasmática do hormônio antidiurético: estudo experimental em cães

Villela, Nivaldo Ribeiro; Júnior, Paulo do Nascimento; Carvalho, Lídia Raquel de; Teixeira, Andrey Borges

doi:10.1590/s0034-70942005000400007

Cited by 36 publications

(19 citation statements)

References 19 publications

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“…Studies performed on canines undergoing general anesthesia have shown that dexmedetomidine has a diuretic-like effect associated with a decreased urine osmolarity, increased free water clearance, and a reduction in plasma vasopressin levels. These studies suggest that dexmedetomidine may induce both vasopressin suppression and responsiveness [4-5]. In humans, it is currently unknown if dexmedetomidine causes an inadequate secretion of vasopressin (a central mechanism) or if it decreases the responsiveness of the renal tubules to vasopressin (a peripheral cause).…”

Section: Discussionmentioning

confidence: 99%

Intraoperative Dexmedetomidine-Induced Polyuric Syndrome

Granger

Ninan

2017

Cureus

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A 23-year-old male trauma patient with a cervical spine fracture underwent an anterior and posterior discectomy and spinal fusion surgery. The patient presented to the operating room with a stabilizing halo fixation device in place, and a fiberoptic intubation was performed with dexmedetomidine for sedation. During the surgical procedure, general anesthesia was maintained with a propofol and remifentanil infusion as the patient was monitored using somatosensory and motor evoked potentials. The patient's urine output increased gradually during the nine-hour surgical procedure from 150 mL/hour to over 700 mL/hour in the eighth hour of the procedure, where it remained until the end of the procedure. Postoperatively, the patient's laboratory values and urine output returned to baseline levels the following day. A search of the literature revealed few case reports of polyuria under similar conditions. Dexmedetomidine, being an alpha-2 agonist that blocks arginine-vasopressin release, may be responsible for inducing the polyuria noted in this patient case.

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Section: Discussionmentioning

confidence: 99%

Intraoperative Dexmedetomidine-Induced Polyuric Syndrome

Granger

Ninan

2017

Cureus

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“…In animal models propofol reduced markers of oxidative stress in the kidney [165, 166] and dexmedetomidine caused diuresis through reducing vasopressin secretion, enhancing renal blood flow and hence glomerular filtration [167] and showed renal protection [168–171]. …”

Section: Sedationmentioning

confidence: 99%

Prevention of acute kidney injury and protection of renal function in the intensive care unit: update 2017

et al. 2017

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BackgroundAcute kidney injury (AKI) in the intensive care unit is associated with significant mortality and morbidity.ObjectivesTo determine and update previous recommendations for the prevention of AKI, specifically the role of fluids, diuretics, inotropes, vasopressors/vasodilators, hormonal and nutritional interventions, sedatives, statins, remote ischaemic preconditioning and care bundles.MethodA systematic search of the literature was performed for studies published between 1966 and March 2017 using these potential protective strategies in adult patients at risk of AKI. The following clinical conditions were considered: major surgery, critical illness, sepsis, shock, exposure to potentially nephrotoxic drugs and radiocontrast. Clinical endpoints included incidence or grade of AKI, the need for renal replacement therapy and mortality. Studies were graded according to the international GRADE system.ResultsWe formulated 12 recommendations, 13 suggestions and seven best practice statements. The few strong recommendations with high-level evidence are mostly against the intervention in question (starches, low-dose dopamine, statins in cardiac surgery). Strong recommendations with lower-level evidence include controlled fluid resuscitation with crystalloids, avoiding fluid overload, titration of norepinephrine to a target MAP of 65–70 mmHg (unless chronic hypertension) and not using diuretics or levosimendan for kidney protection solely.ConclusionThe results of recent randomised controlled trials have allowed the formulation of new recommendations and/or increase the strength of previous recommendations. On the other hand, in many domains the available evidence remains insufficient, resulting from the limited quality of the clinical trials and the poor reporting of kidney outcomes.Electronic supplementary materialThe online version of this article (doi:10.1007/s00134-017-4832-y) contains supplementary material, which is available to authorized users.

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“…The α 2 -adrenoreceptors are widely distributed in the renal proximal and distal tubules, peritubular vasculature as well as in systemic tissues [15]. Dexmedetomidine treatment has been found to inhibit vasopressin secretion, enhance renal blood flow and glomerular filtration, and increase urine output [16-18]. Dexmedetomidine also has a cytoprotective effect against renal I/R injury.…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine protects against renal ischemia and reperfusion injury by inhibiting the JAK/STAT signaling activation

et al. 2013

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BackgroundThe α2-adrenoreceptor agonist dexmedetomidine is known to provide renoprotection against ischemia and reperfusion (I/R) injury. However the underlying molecular mechanisms remain unclear. The purpose of this study was to investigate whether the Janus kinase and signal transducer and activator of transcription (JAK/STAT) signaling pathway plays a role in dexmedetomidine’s renoprotection.MethodsI/R model was induced by bilateral renal pedicle clamping for 45 min followed by 48 h of reperfusion in male Wistar rat. Sham laparotomy served as controls. Animals received dexmedetomidine (50 μg/kg, i.p.) in the absence or presence of atipamezole (250 μg/kg, i.p.), or vehicle (DMSO) in the absence or presence of selective JAK2 inhibitor tyrphostin AG490 (10 mg/kg, i.p.) before ischemia. Renal function, histology, apoptosis, expression of cleaved caspase 3 protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and phosphorylations of JAK2, STAT1 and STAT3 were assessed.ResultsThe animals treated with either dexmedetomidine or AG490 exhibited an improved renal functional recovery, attenuated histological lesions and reduced number of apoptotic tubular epithelial cells. Either dexmedetomidine or AG490 inhibited the phosphorylations of JAK2 and its downstream molecule STAT1 and STAT3, accompanied by down-regulation the expression of cleaved caspase 3, ICAM-1 and MCP-1 proteins, and significantly ameliorated renal I/R injury.ConclusionsDexmedetomidine protects kidney against I/R injury, at least in part, through its inhibitory effects on injury-induced activation of JAK/STAT signaling pathway. If our data can be extrapolated to clinical setting, then dexmedetomidine may therefore serve as a clinical strategy to treat/prevent perioperative renal I/R injury.

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Efeitos da dexmedetomidina sobre o sistema renal e sobre a concentração plasmática do hormônio antidiurético: estudo experimental em cães

Abstract: In anesthetized dogs, low doses of dexmedetomidine inhibit vasopressin secretion, causing aqueous diuresis. These actions might protect kidneys during ischemic events.

Cited by 36 publications

References 19 publications

Intraoperative Dexmedetomidine-Induced Polyuric Syndrome

Intraoperative Dexmedetomidine-Induced Polyuric Syndrome

Prevention of acute kidney injury and protection of renal function in the intensive care unit: update 2017

Dexmedetomidine protects against renal ischemia and reperfusion injury by inhibiting the JAK/STAT signaling activation

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