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Abstract
In laboratory investigations, vasopressin given during CPR resulted in improved vital
organ blood flow when compared with epinephrine. Given the profound and long lasting
vasopressor effects of vasopressin, we tested the hypothesis that vasopressin given
during CPR would result in renal and splanchnic hypoperfusion in the post-resuscitation
period when compared with epinephrine. After 4 min of ventricular fibrillation, 16
pigs were randomly assigned to receive either 0.045 mg x kg(-1) epinephrine or 0.4
U X kg(-1) vasopressin before defibrillation. Splanchnic and renal blood flow were
measured 30, 90, and 240 min after restoration of spontaneous circulation (ROSC) in
the epinephrine and vasopressin groups and in a control group of eight pigs using
radiolabeled microspheres. Hepatic blood flow was measured before arrest and 30, 90,
and 240 min after ROSC by means of indocyanine green infusion. Thirty minutes after
ROSC, renal and adrenal blood flow were significantly lower in the vasopressin group
(300 [273-334] and 256 [170-284] ml X min(-1) x 100 g(-1)) (median and 25th and 75th
percentile) as compared with the epinephrine group (370 [346-429] and 360 [326-420]
ml x min(-1) x 100 g(-1); P < 0.05). Pancreatic, intestinal, and hepatic blood flow
were not significantly different in animals after receiving epinephrine or vasopressin.
In comparison to epinephrine, vasopressin given during cardiac arrest impairs renal
and adrenal perfusion temporarily but does not lead to intestinal or hepatic hypoperfusion
in the post-resuscitation phase.