Arginine vasopressin does not alter mucosal tissue oxygen tension and oxygen supply in an acute endotoxemic pig model

Knotzer, Hans; Maier, Stephan; Dünser, Martin W.; Hasibeder, Walter; Hausdorfer, Hans; Brandner, Julia; Torgersen, Christian; Ulmer, Hanno; Friesenecker, Barbara; Iannetti, Claudia; Pajk, Werner

doi:10.1007/s00134-005-2858-z

Cited by 47 publications

(33 citation statements)

References 18 publications

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“…While vasopressin is known to jeopardize splanchnic circulation (Knotzer et al 2005), this effect is abolished in the same model during endotoxemia (Knotzer et al 2006). Another study using terlipressin has shown even increased hepatic arterial blood flow with unaffected splanchnic DO 2 (Asfar et al 2005).…”

Section: Interpretation Of the Resultsmentioning

confidence: 95%

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Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Vollmer

Schwartges

Naber

et al. 2013

Journal of Endocrinology

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Hypercapnia (HC) improves systemic oxygen delivery (DO 2 ) and microvascular hemoglobin oxygenation of the mucosa (mHbO 2 ). Simultaneously, HC increases plasma levels of vasopressin. Although vasopressin is generally regarded a potent vasoconstrictor particularly in the splanchnic region, its effects on splanchnic microcirculation during HC is unclear. The aim of this study was to evaluate the role of endogenous vasopressin on gastric mucosal oxygenation and hemodynamic variables during physiological (normocapnia) and hypercapnic conditions. Five dogs were repeatedly anesthetized to study the effect of vasopressin V 1A receptor blockade ([Pmp 1 ,Tyr(Me) 2 ]-Arg 8 -Vasopressin, 35 mg/kg) on hemodynamic variables and mHbO 2 during normocapnia or HC (end-tidal CO 2 70 mmHg). In a control group, animals were subjected to HC alone. mHbO 2 was measured by reflectance spectrophotometry, systemic DO 2 was calculated from intermittent blood gas analysis, and cardiac output was measured by transpulmonary thermodilution. Data are presented as meanGS.E.M. for nZ5 animals. During HC alone, DO 2 increased from 12G1 to 16G1 ml/kg per min and mHbO 2 from 70G4 to 80G2%. By contrast, additional vasopressin V 1A receptor blockade abolished the increase in mHbO 2 (80G2 vs 69G2%) without altering the increase in DO 2 (16G1 vs 19G 2 ml/kg per min). Vasopressin V 1A receptor blockade (VB) during normocapnia neither affected DO 2 (13G1 vs 14G1 ml/kg per min) nor mHbO 2 (75G3 vs 71G5%). Vasopressin V 1A receptor blockade abolished the increase in mHbO 2 during HC independent of DO 2 . Thus, in contrast to its generally vasoconstrictive properties, the vasopressin V 1A receptors seem to mediate the increase in gastric microcirculatory mucosal oxygenation induced by acute HC.

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Section: Interpretation Of the Resultsmentioning

confidence: 95%

“…The expected negative effects of vasopressin could not be observed in a septic animal model (Knotzer et al 2006) and even an improvement of gut microcirculatory flow is possible (Asfar et al 2003). Furthermore, the effect seems to depend on flow.…”

Section: Introductionmentioning

confidence: 98%

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Vollmer

Schwartges

Naber

et al. 2013

Journal of Endocrinology

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“…Experimental animal studies reported neutral or even beneficial effects when low doses of AVP were used in endotoxemic shock [6,8]. On the other hand, van Haren et al demonstrated that vasopressin leads to gastrointestinal hypoperfusion in norepinephrine-dependent patients with septic shock [22].…”

Section: Discussionmentioning

confidence: 99%

Arginine-vasopressin in neonates with vasodilatory shock after cardiopulmonary bypass

et al. 2007

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“…A range of results are reported in animal models of sepsis and shock [55][56][57][58] , but, overall, vasopressin effects appear to be relatively minimal and hepatosplanchnic microcirculatory flow may also be maintained [58,59] . Indeed, vasopressin may have a beneficial effect on the gut microcirculation [60] .…”

Section: The Effects Of Vasopressin On Other Organ Dysfunctionmentioning

confidence: 99%

Vasopressin and Its Immune Effects in Septic Shock

Russell

Walley²

2010

J Innate Immun

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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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Arginine vasopressin does not alter mucosal tissue oxygen tension and oxygen supply in an acute endotoxemic pig model

Abstract: AVP administration did not further compromise mucosal tissue oxygen tension and oxygen supply in the acute phase of endotoxic pigs.

Cited by 47 publications

References 18 publications

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Arginine-vasopressin in neonates with vasodilatory shock after cardiopulmonary bypass

Vasopressin and Its Immune Effects in Septic Shock

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