Vasopressin impairs brain, heart and kidney perfusion: an experimental study in pigs after transient myocardial ischemia

Stig Müller,Georg Sager,Thor Stenberg,Truls Myrmel,Ole-Jakob How,Stig Hermansen

doi:10.1186/cc6794

Stig Müller, Georg Sager + Show 4 more

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https://doi.org/10.1186/cc6794

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Abstract

IntroductionArginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.MethodsCardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs using transit-time flow probes. Left ventricular pressure-volume catheter and central arterial and venous catheters were used for haemodynamic recordings and blood sampling. Transient left ventricular ischemia was induced by intermittent left coronary occlusions resulting in a 17% reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg (p < 0.001). A low-dose therapeutic level of AVP (0.005 U/kg/min) was used to restore MAP to pre-ischemic values (93 ± 4 mmHg).ResultsAVP further impaired systemic perfusion (CO and brain, heart and kidney blood flow reduced by 29, 18, 23 and 34%, respectively) due to a 2.0-, 2.2-, 1.9- and 2.1-fold increase in systemic, brain, heart and kidney specific vascular resistances. The hypoperfusion induced by AVP was associated with an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 29 ± 1 to 21 ± 3% (p = 0.01). Finally, these effects were reversed 40 min after AVP was withdrawn.ConclusionLow dose AVP induced a pronounced reduction in vital organ blood flow in pigs after transient cardiac ischemia. This indicates a potentially deleterious effect of AVP in patients with heart failure or cardiogenic shock due to impaired coronary perfusion.

Highlights

Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes
The association found between low plasma AVP levels and advanced vasodilatory shock has given a rationale for administrating this hormone in septic shock and in systemic inflammatory response syndrome (SIRS) [1,2,3,4]
Post-ischemic circulation The repetitive ischemia/reperfusion (IR) protocol was characterised by a 17% reduction in cardiac output (Figure 1)

Summary

Introduction

Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is known to reduce cardiac output by increasing vascular resistance. Synthetic arginine vasopressin (AVP) has been increasingly used to restore systemic blood pressure in low pressure shock states unresponsive to conventional inotropes [1,2]. The response in vital organ perfusion, that is, pulmonary, coronary and cerebral circulation, to AVP-infusions is still insufficiently clarified [14]. Infusion of the drug has been found to dilate the coronary, pulmonary and vertebrobasilary arteries [14,15]

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