The Experts below are selected from a list of 219 Experts worldwide ranked by ideXlab platform
Cheryl L. Holmes - One of the best experts on this subject based on the ideXlab platform.
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Vasopressin in the ICU.
Current Opinion in Critical Care, 2004Co-Authors: Cheryl L. Holmes, Keith R. WalleyAbstract:Purpose of the review Vasopressin is one of the most important endogenously released stress hormones during shock. In this review, studies published in the past year that add to our understanding of the use of Vasopressin in the ICU are discussed. Recent findings Endogenous Vasopressin levels are inappropriately low in adults with severe sepsis but not in children with meningococcal septic shock. Vasopressin but not norepinephrine improved renal blood flow and oxygen delivery and prolonged survival in animal models of septic shock. In human vasodilatory shock, the combination of low-dose Vasopressin and norepinephrine was found to be safe and effective. In humans, Vasopressin can cause gastrointestinal hypoperfusion and ischemic skin lesions. In hypodynamic animal models of sepsis Vasopressin compromised oxygen delivery and decreased systemic and gut blood flow.High-dose bolus Vasopressin appeared promising in animal studies of hemorrhagic shock and cardiopulmonary arrest and in a large, randomized clinical trial of Vasopressin versus epinephrine in human cardiopulmonary arrest with asystole. However, poor neurologic outcomes raised controversy in introducing Vasopressin into CPR guidelines. Summary There is growing evidence that Vasopressin infusion in septic shock is safe and effective. Several studies published this year support the hypothesis that Vasopressin should be used as a continuous low-dose infusion (between 0.01 and 0.04 U/min in adults) and not titrated as a single vasopressor agent. However, multiple studies highlight the clinical equipoise that exists regarding the use of Vasopressin in vasodilatory shock. Guidelines on management of septic shock recommend "cautious use of Vasopressin pending further studies."
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Science Review: Vasopressin and the cardiovascular system part 1 – receptor physiology
Critical Care, 2003Co-Authors: Cheryl L. Holmes, Donald W Landry, John T GrantonAbstract:Vasopressin is emerging as a rational therapy for vasodilatory shock states. Unlike other vasoconstrictor agents, Vasopressin also has vasodilatory properties. The goal of the present review is to explore the vascular actions of Vasopressin. In part 1 of the review we discuss structure, signaling pathways, and tissue distributions of the classic Vasopressin receptors, namely V_1 vascular, V_2 renal, V_3 pituitary and oxytocin receptors, and the P_2 class of purinoreceptors. Knowledge of the function and distribution of Vasopressin receptors is key to understanding the seemingly contradictory actions of Vasopressin on the vascular system. In part 2 of the review we discuss the effects of Vasopressin on vascular smooth muscle and the heart, and we summarize clinical studies of Vasopressin in shock states.
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science review Vasopressin and the cardiovascular system part 1 receptor physiology
Critical Care, 2003Co-Authors: Cheryl L. Holmes, Donald W Landry, John T GrantonAbstract:Vasopressin is emerging as a rational therapy for vasodilatory shock states. Unlike other vasoconstrictor agents, Vasopressin also has vasodilatory properties. The goal of the present review is to explore the vascular actions of Vasopressin. In part 1 of the review we discuss structure, signaling pathways, and tissue distributions of the classic Vasopressin receptors, namely V1 vascular, V2 renal, V3 pituitary and oxytocin receptors, and the P2 class of purinoreceptors. Knowledge of the function and distribution of Vasopressin receptors is key to understanding the seemingly contradictory actions of Vasopressin on the vascular system. In part 2 of the review we discuss the effects of Vasopressin on vascular smooth muscle and the heart, and we summarize clinical studies of Vasopressin in shock states.
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Science Review: Vasopressin and the cardiovascular system part 2 – clinical physiology
Critical Care, 2003Co-Authors: Cheryl L. Holmes, Donald W Landry, John T GrantonAbstract:Vasopressin is emerging as a rational therapy for vasodilatory shock states. In part 1 of the review we discussed the structure and function of the various Vasopressin receptors. In part 2 we discuss vascular smooth muscle contraction pathways with an emphasis on the effects of Vasopressin on ATP-sensitive K^+ channels, nitric oxide pathways, and interaction with adrenergic agents. We explore the complex and contradictory studies of Vasopressin on cardiac inotropy and coronary vascular tone. Finally, we summarize the clinical studies of Vasopressin in shock states, which to date have been relatively small and have focused on physiologic outcomes. Because of potential adverse effects of Vasopressin, clinical use of Vasopressin in vasodilatory shock should await a randomized controlled trial of the effect of Vasopressin's effect on outcomes such as organ failure and mortality.
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physiology of Vasopressin relevant to management of septic shock
Chest, 2001Co-Authors: Cheryl L. Holmes, James A. Russell, Bhavesh M Patel, Keith R. WalleyAbstract:Vasopressin is emerging as a rational therapy for the hemodynamic support of septic shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal of this review is to understand the physiology of Vasopressin relevant to septic shock in order to maximize its safety and efficacy in clinical trials and in subsequent therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. In addition, Vasopressin, at low plasma concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Septic shock causes first a transient early increase in blood Vasopressin concentrations that decrease later in septic shock to very low levels compared to other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma Vasopressin levels to those observed in patients with hypotension from other causes, such as cardiogenic shock. Increased Vasopressin levels are associated with a lesser need for other vasopressors. Urinary output may increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of Vasopressin, clinical use of Vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality.
Keith R. Walley - One of the best experts on this subject based on the ideXlab platform.
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Vasopressin and its immune effects in septic shock.
Journal of Innate Immunity, 2010Co-Authors: James A. Russell, Keith R. WalleyAbstract:Vasopressin is a stress hormone. However, Vasopressin levels are inappropriately low in septic shock. Vasopressin stimulates AVPR1a, AVPR1b, AVPR2 and purinergic receptors. Vasopressin increases blood pressure by occupying AVPR1a receptors on vascular smooth muscle. An increase in ventricular afterload due to vasopressor administration limits ventricular systolic ejection, an effect that becomes increasingly important as systolic contractility is decreased. Stimulation of AVPR1a receptors may also decrease edemagenesis. Stimulation of AVPR1b by Vasopressin releases ACTH and cortisol. AVPR2 stimulation increases retention of water by increasing cyclic AMP. Yet, Vasopressin infusion may increase urine output, creatinine clearance and improve renal function in septic shock. Vasopressin has many effects on immune function such as altering cytokines, neuroimmunity, prostaglandins, humoral immunity and immune cells. For example, Vasopressin decreases sepsis-induced pulmonary inflammation, could have renal anti-inflammatory effects and may decrease prostaglandin levels in a dose-dependent manner. Vasopressin may also modulate responses to stress by expression and release from immune cells. Interestingly, there are Vasopressin receptors on immune cells. Many small clinical studies of Vasopressin infusion in septic shock have shown that Vasopressin infusion increases blood pressure, decreases requirements for norepinephrine and improves renal function. However, Vasopressin could decrease coronary, cerebral and mesenteric perfusion. A multicenter trial of Vasopressin versus norepinephrine in septic shock found no overall difference in mortality. Vasopressin may decrease mortality in patients with less severe septic shock. Vasopressin plus corticosteroid treatment may decrease mortality compared to corticosteroids plus norepinephrine. Potential mechanisms are that Vasopressin plus corticosteroids beneficially alter immunity in septic shock.
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Vasopressin in the ICU.
Current Opinion in Critical Care, 2004Co-Authors: Cheryl L. Holmes, Keith R. WalleyAbstract:Purpose of the review Vasopressin is one of the most important endogenously released stress hormones during shock. In this review, studies published in the past year that add to our understanding of the use of Vasopressin in the ICU are discussed. Recent findings Endogenous Vasopressin levels are inappropriately low in adults with severe sepsis but not in children with meningococcal septic shock. Vasopressin but not norepinephrine improved renal blood flow and oxygen delivery and prolonged survival in animal models of septic shock. In human vasodilatory shock, the combination of low-dose Vasopressin and norepinephrine was found to be safe and effective. In humans, Vasopressin can cause gastrointestinal hypoperfusion and ischemic skin lesions. In hypodynamic animal models of sepsis Vasopressin compromised oxygen delivery and decreased systemic and gut blood flow.High-dose bolus Vasopressin appeared promising in animal studies of hemorrhagic shock and cardiopulmonary arrest and in a large, randomized clinical trial of Vasopressin versus epinephrine in human cardiopulmonary arrest with asystole. However, poor neurologic outcomes raised controversy in introducing Vasopressin into CPR guidelines. Summary There is growing evidence that Vasopressin infusion in septic shock is safe and effective. Several studies published this year support the hypothesis that Vasopressin should be used as a continuous low-dose infusion (between 0.01 and 0.04 U/min in adults) and not titrated as a single vasopressor agent. However, multiple studies highlight the clinical equipoise that exists regarding the use of Vasopressin in vasodilatory shock. Guidelines on management of septic shock recommend "cautious use of Vasopressin pending further studies."
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physiology of Vasopressin relevant to management of septic shock
Chest, 2001Co-Authors: Cheryl L. Holmes, James A. Russell, Bhavesh M Patel, Keith R. WalleyAbstract:Vasopressin is emerging as a rational therapy for the hemodynamic support of septic shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal of this review is to understand the physiology of Vasopressin relevant to septic shock in order to maximize its safety and efficacy in clinical trials and in subsequent therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. In addition, Vasopressin, at low plasma concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Septic shock causes first a transient early increase in blood Vasopressin concentrations that decrease later in septic shock to very low levels compared to other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma Vasopressin levels to those observed in patients with hypotension from other causes, such as cardiogenic shock. Increased Vasopressin levels are associated with a lesser need for other vasopressors. Urinary output may increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of Vasopressin, clinical use of Vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality.
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Sepsis: Is There Room for Vasopressin?
Sepsis, 2001Co-Authors: Cheryl L. Holmes, James A. Russell, Keith R. WalleyAbstract:Cardiovascular dysfunction contributes importantly to the high mortality of septic shock, which remains in excess of 50%. Non-survivors are characterized by an inadequate response to fluid resuscitation and catecholamine infusions. A number of recent reports suggest that Vasopressin, a non-catecholamine vasopressor, may contribute usefully to the cardiovascular management of septic shock and other forms of vasodilatory shock. Here we review the clinical studies to date of Vasopressin use in septic shock and other vasodilatory shock. We then review the known physiology of Vasopressin to help understand why Vasopressin may be beneficial in this setting. In general, humans having severe vasodilatory shock demonstrate low endogenous Vasopressin blood concentration. Low-dose Vasopressin infusion in this setting increases blood Vasopressin concentration to that observed in hypotension of other causes, results in an increase in mean arterial pressure, and reduces the need for additional α-adrenergic vasopressor infusions. Current studies in low numbers of patients suggest that low-dose Vasopressin may increase urine output in this setting. Vasopressin infusion increases blood pressure by V1 receptor stimulation on vascular smooth muscle. This vasoconstrictor effect is less pronounced in the cerebral, coronary, and renal circulations. Diminished vasoconstriction in some regional circulations may be contributed to by nitric oxide-mediated vasodilation resulting from oxytocin receptor stimulation by low-dose Vasopressin. Thus, low-dose Vasopressin infusion may be a useful adjunct to fluid resuscitation and catecholamine infusion in severe septic shock and other forms of vasodilatory shock.
John T Granton - One of the best experts on this subject based on the ideXlab platform.
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Science Review: Vasopressin and the cardiovascular system part 1 – receptor physiology
Critical Care, 2003Co-Authors: Cheryl L. Holmes, Donald W Landry, John T GrantonAbstract:Vasopressin is emerging as a rational therapy for vasodilatory shock states. Unlike other vasoconstrictor agents, Vasopressin also has vasodilatory properties. The goal of the present review is to explore the vascular actions of Vasopressin. In part 1 of the review we discuss structure, signaling pathways, and tissue distributions of the classic Vasopressin receptors, namely V_1 vascular, V_2 renal, V_3 pituitary and oxytocin receptors, and the P_2 class of purinoreceptors. Knowledge of the function and distribution of Vasopressin receptors is key to understanding the seemingly contradictory actions of Vasopressin on the vascular system. In part 2 of the review we discuss the effects of Vasopressin on vascular smooth muscle and the heart, and we summarize clinical studies of Vasopressin in shock states.
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science review Vasopressin and the cardiovascular system part 1 receptor physiology
Critical Care, 2003Co-Authors: Cheryl L. Holmes, Donald W Landry, John T GrantonAbstract:Vasopressin is emerging as a rational therapy for vasodilatory shock states. Unlike other vasoconstrictor agents, Vasopressin also has vasodilatory properties. The goal of the present review is to explore the vascular actions of Vasopressin. In part 1 of the review we discuss structure, signaling pathways, and tissue distributions of the classic Vasopressin receptors, namely V1 vascular, V2 renal, V3 pituitary and oxytocin receptors, and the P2 class of purinoreceptors. Knowledge of the function and distribution of Vasopressin receptors is key to understanding the seemingly contradictory actions of Vasopressin on the vascular system. In part 2 of the review we discuss the effects of Vasopressin on vascular smooth muscle and the heart, and we summarize clinical studies of Vasopressin in shock states.
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Science Review: Vasopressin and the cardiovascular system part 2 – clinical physiology
Critical Care, 2003Co-Authors: Cheryl L. Holmes, Donald W Landry, John T GrantonAbstract:Vasopressin is emerging as a rational therapy for vasodilatory shock states. In part 1 of the review we discussed the structure and function of the various Vasopressin receptors. In part 2 we discuss vascular smooth muscle contraction pathways with an emphasis on the effects of Vasopressin on ATP-sensitive K^+ channels, nitric oxide pathways, and interaction with adrenergic agents. We explore the complex and contradictory studies of Vasopressin on cardiac inotropy and coronary vascular tone. Finally, we summarize the clinical studies of Vasopressin in shock states, which to date have been relatively small and have focused on physiologic outcomes. Because of potential adverse effects of Vasopressin, clinical use of Vasopressin in vasodilatory shock should await a randomized controlled trial of the effect of Vasopressin's effect on outcomes such as organ failure and mortality.
Yukimasa Kohda - One of the best experts on this subject based on the ideXlab platform.
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Vasopressin regulates the renin angiotensin aldosterone system via v1a receptors in macula densa cells
American Journal of Physiology-renal Physiology, 2008Co-Authors: Toshinori Aoyagi, Yuichiro Izumi, Masami Hiroyama, Takanobu Matsuzaki, Yukiko Yasuoka, Atsushi Sanbe, Hiroki Miyazaki, Yoko Fujiwara, Yushi Nakayama, Yukimasa KohdaAbstract:The neuropeptide hormone arginine-Vasopressin (AVP) is well known to exert its antidiuretic effect via the Vasopressin V2 receptor (V2R), whereas the role of the Vasopressin V1a receptor (V1aR) in ...
Gilles Guillon - One of the best experts on this subject based on the ideXlab platform.
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Synthetic rat V1a Vasopressin receptor fragments interfere with Vasopressin binding via specific interaction with the receptor.
Journal of Biological Chemistry, 1997Co-Authors: Christiane Mendre, Marie Noëlle Dufour, Sylvie Roux, René Seyer, Laurent Guillou, Bernard Calas, Gilles GuillonAbstract:To study the Vasopressin receptor domains involved in the hormonal binding, we synthesized natural and modified fragments of V1a Vasopressin receptor and tested their abilities to affect hormone-receptor interactions. Natural fragments mimicking the external loops one, two, and three were able to inhibit specific Vasopressin binding to V1a receptor. In contrast, the natural N-terminal part of the V1a Vasopressin receptor was found inactive. One fragment, derived from the external second loop and containing an additional C-terminal cysteine amide, was able to fully inhibit the specific binding of both labeled Vasopressin agonist and antagonist to rat liver V1a Vasopressin receptor and the Vasopressin-sensitive phospholipase C of WRK1 cells. The peptide-mediated inhibition involved specific interactions between the V1a receptor and synthetic V1a Vasopressin receptor fragment since 1) it was dependent upon the Vasopressin receptor subtype tested (Ki(app) for the peptide: 3.7, 14.6, and 64.5 microM for displacing [3H]Vasopressin from rat V1a, V1b, and V2 receptors, respectively; 2) it was specific and did not affect sarcosin 1-angiotensin II binding to rat liver membranes; 3) it was not mimicked by Vasopressin receptor unrelated peptides exhibiting putative detergent properties; and 4) no direct interaction between [3H]Vasopressin and synthetic peptide linked to an affinity chromatography column could be observed. Such an inhibition affected both the maximal binding capacity of the V1a Vasopressin receptor and its affinity for the labeled hormone, depending upon the dose of synthetic peptide used and was partially irreversible. Structure-activity studies using a serie of synthetic fragments revealed the importance of their size and cysteinyl composition. These data indicate that some peptides mimicking extracellular loops of the V1a Vasopressin receptor may interact with the Vasopressin receptor itself and modify its coupling with phospholipase C.
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molecular and functional characterization of v1b Vasopressin receptor in rat adrenal medulla
Endocrinology, 1996Co-Authors: E Grazzini, Anne Marie Lodboerer, Antonia Perezmartin, Dominique Joubert, Gilles GuillonAbstract:In rat adrenal medulla, PCR experiments reveal the expression of messenger RNA encoding the gene for the V1b Vasopressin receptor. Complementary DNA amplified sequences corresponded to the cloned rat pituitary V1b Vasopressin receptor. Video microscopy experiments performed on fura-2-loaded adrenal medullary or adrenal glomerulosa cell primary cultures showed that Vasopressin dose dependently mobilized intracellular calcium, suggesting that functional Vasopressin receptors are expressed in these tissues. The use of d[D-3-Pal]Vasopressin, a specific V1b Vasopressin agonist, and SR 49059, a specific V1b Vasopressin antagonist, revealed that V1b receptors are exclusively expressed in adrenal medulla. Using an indirect immunological approach (plasma membrane localization of dopamine-beta-hydroxylase), we demonstrated that stimulation of rat adrenal medulla V1b receptor leads to catecholamine secretion. More interestingly, PCR experiments performed on rat adrenal medulla RNA revealed that the arginine vasopres...
