A. Banic et al., Effects of sodium nitroprusside and phenylephrine on blood flow in free musculocutaneous flaps during general anesthesia, ANESTHESIOL, 90(1), 1999, pp. 147-155
Citations number
31
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Background: Hypoperfusion and necrosis in free flaps used to correct tissue
defects remain important clinical problems. The authors studied the effect
s of two vasoactive drugs, sodium nitroprusside and phenylephrine, which ar
e used frequently in anesthetic practice, on total blood now and microcircu
latory now in free musculocutaneous flaps during general anesthesia.
Methods: In a porcine model(n = 9) in which clinical conditions for anesthe
sia and microvascular surgery were simulated, latissimus dorsi free naps we
re transferred to the lower extremity. Total blood flow in the flaps was me
asured using ultrasound flowmetry and microcirculatory flow was measured us
ing laser Doppler flowmetry. The effects of sodium nitroprusside and phenyl
ephrine were studied during local infusion through the feeding artery of th
e flap and during systemic administration.
Results: Systemic sodium nitroprusside caused a 30% decrease in mean arteri
al pressure, but cardiac output did not change. The total flow in the flap
decreased by 40% (P < 0.01), and microcirculatory flow decreased by 23% in
the skin (P < 0.01) and by 30% in the muscle (P < 0.01) of the flap. Sodium
nitroprusside Infused locally into the flap artery increased the total fla
p now by 20% (P < 0.01). Systemic phenylephrine caused a 30% increase in me
an arterial pressure, whereas heart rate, cardiac output, and nap blood now
did not change. Local phenylephrine caused a 30% decrease (P < 0.01) in th
e total flap flow.
Conclusions: Systemic phenylephrine in a dose increasing the systemic vascu
lar resistance and arterial pressure by 30% appears to have no adverse effe
cts on blood flow in free musculocutaneous flaps. Sodium nitroprusside, how
ever, in a dose causing a 30% decrease in systemic vascular resistance and
arterial pressure, causes a severe reduction in free flap blood flow despit
e maintaining cardiac output.