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(The FASEB Journal. 2007;21:751.22)
© 2007 FASEB
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751.22

Isoflurane abolishes purinergic receptor mediated restraint of skeletal muscle blood flow

Darren DeLorey, John Buckwalter, Maria Anton, Heidi Kluess and Philip Clifford

Anesthesiology, Medical College of Wisconsin, Anesthesia Research 151, 5000 W National Ave, Milwaukee, WI, 53295

ABSTRACT

Blood pressure (BP) declines during isoflurane anesthesia. The decrease in BP has been partially attributed to an attenuation of alpha-adrenergic receptor mediated vasoconstriction. The effect of isoflurane on non-adrenergic receptor mediated vasoconstriction has not been investigated. Therefore, the purpose of this study was to investigate the effect of isoflurane on purinergic receptor (P2X) mediated vasoconstriction in the skeletal muscle vasculature. The P2X receptor agonist {alpha}-ß-methylene ATP (0.1 ug · ml · min–1of hindlimb blood flow) and antagonist pyridoxal-phosphate-6-azophenyl-2'4'-disulfonic acid (PPADS; 40 mg bolus) were infused into the hindlimb circulation in anesthetized (n=8) and conscious (n=8) canines instrumented with transit-time flow probes on the external iliac arteries and an indwelling catheter in a branch of the femoral artery. Infusion of {alpha}-ß-methylene ATP produced a similar vasoconstriction in conscious and anesthetized canines (54 ± 5 % vs. 45 ± 12 %; p > 0.05). P2X receptor blockade increased (P < 0.05) iliac vascular conductance by 117 ± 21 % in conscious dogs, whereas no increase (P > 0.05) in iliac vascular conductance was observed in anesthetized dogs (6 ± 17 %). These data demonstrate that P2X receptor mediated restraint of skeletal muscle blood flow is abolished by isoflurane anesthesia. Furthermore, the similar vascular response to infusion of exogenous P2X agonist suggests that the abolition of P2X mediated vasoconstriction is due to a change in muscle sympathetic nerve activity which effects neural ATP release.

Supported by NHLBI and NSERC, Canada





This Article
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Right arrow Articles by Clifford, P.