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


METHODS
Cardiac 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).


RESULTS
AVP 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 Finally, these effects were reversed 40 min after AVP was withdrawn.


CONCLUSIONS
Low 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.
Müller
Stig
S
Laboratory of Surgical Research, Institute of Clinical Medicine, University of Tromsø, N-9037 Tromsø, Norway.
How
Ole-Jakob
OJ
Hermansen
Stig Eggen
SE
Stenberg
Thor Allan
TA
Sager
Georg
G
Myrmel
Truls
T
D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology* / Q000627:therapeutic use; D001921:Brain / Q000098:blood supply*; D002302:Cardiac Output / Q000187:drug effects*; D003326:Coronary Circulation / Q000187:drug effects*; D007668:Kidney / Q000098:blood supply*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D017202:Myocardial Ischemia / Q000188:drug therapy; D015425:Myocardial Reperfusion; D013552:Swine; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
D014662:Vasoconstrictor Agents; D001127:Arginine Vasopressin