Phenylephrine Does Not Reduce Cerebral Perfusion During Canine Cardiopulmonary Bypass

Abstract

Gaseous microemboli during cardiopulmonary bypass (CPB) could injure the blood-brain barrier so that cerebral vasoconstriction would result from infusing alpha-agonist drugs, such as phenylephrine. Cerebral blood flow (radioactive microspheres) and metabolism were measured in seven dogs after rewarming from 150 min hypothermic CPB with bubble oxygenators used to produce gaseous microemboli. Phenylephrine (40 micrograms/min) was infused directly into the brachiocephalic artery so that aortic pressure before (80 +/- 2 mm Hg) and during (79 +/- 3 mm Hg) the infusion did not change. Neither blood flow to the cerebral hemispheres (P = 0.960), cerebellum (P = 0.854), and brainstem (P = 0.694) nor the cerebral metabolic rate for oxygen (P = 0.862) differed when values obtained before and after 30 min of phenylephrine infusion were compared. Cerebral vascular resistance was also unchanged by phenylephrine, being 1.22 +/- 0.10 mm Hg.mL-1.min-1 x 100 g-1 before infusion and 1.25 +/- 0.17 mm Hg.mL-1.min-1 x 100 g-1 during infusion (P = 0.849). Phenylephrine does not cause cerebral vasoconstriction after rewarming from hypothermic CPB, a finding which suggests that the blood-brain barrier is preserved during bypass.

Cerebral oxygenation and vascular resistance changes during cardiopulmonary bypass – where is the proof?

“…We agree with Grocott that a 1-2% decrease in rSO 2 is small and will probably not directly lead to worsened clinical outcome. However, the finding that phenylephrine causes a reduction in rSO 2 confirms earlier work in awake [2,3] and anaesthetised patients [4], as well as studies in patients during bypass [5]. Indeed, to the best of our knowledge, no study exists that shows an increase in rSO 2 after phenylephrine administration.…”

“…Whereas they suggest that this is a direct effect on the cerebral vasculature, with cerebral vasoconstriction reducing cerebral blood flow (CBF) and thus rSO 2 , their selective citing of the literature supporting a vasoconstrictive effect [3,4] fails to address other wellconducted studies that showed no effect of phenylephrine on CBF [5]. Indeed, a vasoconstrictive effect on rSO 2 is far more likely a manifestation of the inherent extracranial contamination that variably occurs with cerebral oximeters, particularly the one that they used in their study (INVOS 5100 cerebral oximeter; Somanetics Company, Troy, MI, USA) [6].…”

Cerebrovascular Regulation During Transient Hypotension and Hypertension in Humans

“…Previous studies have shown that intra-arterial phenylephrine (␣ 1 -adrenoreceptor agonist) does not cause any relevant MCA vasoconstriction. 25,26 Likewise, nitroprusside administered during craniotomy in humans did not affect MCA vessel diameter. 27 Therefore, it seems reasonable to assume that changes in MCAv measured via transcranial Doppler ultrasound were proportional to changes in CBF.…”

Dynamic cerebral autoregulation during and following acute hypoxia: role of carbon dioxide

“…It is possible that infusion of the vasoactive drugs had a direct effect on the diameter of the MCA. However, previous studies have demonstrated that intra-arterial infusion of nitroprusside or phenylephrine does not cause any relevant change in MCA diameter (9,15). It has been suggested that the integrity of the blood-brain barrier eliminates a possible influence of these drugs on cerebral vessels of different sizes (9,15).…”