Depletion of neurohypophyseal content of vasopressin in septic shock*

Sharshar, Tarek; Carlier, Robert; Blanchard, Anne; Feydy, A.; Gray, Françoise; Paillard, Michel; Raphaël, Jean-Claude; Gajdos, Philippe; Annane, Djillali

doi:10.1097/00003246-200203000-00001

Cited by 177 publications

(101 citation statements)

References 7 publications

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“…Cardiovascular collapse is associated with profound vasopressin release, with concentrations 100-fold greater than normal (52), presumably because greater vasopressin concentrations are needed to increase systolic BP than to regulate antidiuresis. Such high concentrations rapidly exhaust the pituitary vasopressin stores, and given the time-consuming nature of vasopressin production, vasopressin depletion is thought contributory to shock physiology (53). Subtle changes in body fluid volume modify the responsiveness of vasopressin release to osmolality.…”

Section: Vasopressinmentioning

confidence: 99%

Osmotic Homeostasis

Danziger

Zeidel

2015

Clinical Journal of the American Society of Nephrology

154

101

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Alterations in water homeostasis can disturb cell size and function. Although most cells can internally regulate cell volume in response to osmolar stress, neurons are particularly at risk given a combination of complex cell function and space restriction within the calvarium. Thus, regulating water balance is fundamental to survival. Through specialized neuronal "osmoreceptors" that sense changes in plasma osmolality, vasopressin release and thirst are titrated in order to achieve water balance. Fine-tuning of water absorption occurs along the collecting duct, and depends on unique structural modifications of renal tubular epithelium that confer a wide range of water permeability. In this article, we review the mechanisms that ensure water homeostasis as well as the fundamentals of disorders of water balance.

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Section: Vasopressinmentioning

confidence: 99%

Osmotic Homeostasis

Danziger

Zeidel

2015

Clinical Journal of the American Society of Nephrology

154

101

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“…20 A continuous infusion of AVP at 2 to 4 U/h restores AVP serum concentrations to values observed in other types of hypotension. 19 Therefore, infusion of AVP may reverse AVP deficiency and restore endogenous vasopressor effects in vasodilatory shock.…”

Section: Discussionmentioning

confidence: 90%

Arginine Vasopressin in Advanced Vasodilatory Shock

et al. 2003

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Background-Vasodilatory shock is a potentially lethal complication of severe disease in critically ill patients. Currently, catecholamines are the most widely used vasopressor agents to support blood pressure, but loss of catecholamine pressor effects is a well-known clinical dilemma. Arginine vasopressin (AVP) has recently been shown to be a potent vasopressor agent to stabilize cardiocirculatory function even in patients with catecholamine-resistant vasodilatory shock. Methods and Results-Forty-eight patients with catecholamine-resistant vasodilatory shock were prospectively randomized to receive a combined infusion of AVP and norepinephrine (NE) or NE infusion alone. In AVP patients, AVP was infused at a constant rate of 4 U/h. Hemodynamic, acid/base, single-organ, and tonometrically derived gastric variables were reported before the study and 1, 12, 24, and 48 hours after study entry. For statistical analysis, a mixed-effects model was used. AVP patients had significantly lower heart rate, NE requirements, and incidence of new-onset tachyarrhythmias than NE patients. Mean arterial pressure, cardiac index, stroke volume index, and left ventricular stroke work index were significantly higher in AVP patients. NE patients developed significantly more new-onset tachyarrhythmias than AVP patients (54.3% versus 8.3%). Gastrointestinal perfusion as assessed by gastric tonometry was better preserved in AVP-treated patients. Total bilirubin concentrations were significantly higher in AVP patients. Conclusions-The

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“…Proposed mechanisms to explain this phenomenon include depletion of neurohypophyseal stores, 30 baroreceptor and generalized autonomic dysfunction during prolonged shock, 31 and endogenous norepinephrine-induced inhibition of vasopressin release. 32 Vasopressin therapy may thus be effective in norepinephrine-resistant vasodilatory shock, improving MAP, cardiac index, and LV stroke work index and reducing the need for norepinephrine, resulting in decreased cardiotoxicity and malignant arrhythmias.…”

Section: Overgaard and Džavíkmentioning

confidence: 99%