Effect oflabetalol onlimbhaemodynamics inpatients following coronary artery bypass graft surgery

Labetalol isa competitive inhibitor ofa-andP-adrenergic receptors andhasan antihypertensive action. Todetermine limbhaemodynamic effects, wemeasured calf blood flowandvenous capacitance byvenous occlusion plethysmography before andafter orallabetalol in10patients 3-7daysfollowing coronary bypass surgery. Vascular resistance wascalculated astheratio ofmeanarterial pressure toarterial flow. Thepeak effect oflabetalol wastaken asthepoint ofmaximumblood pressure decline, andthis interval wasselected for evaluation ofthelimbhaemodynamic response. Ninety to120 minafter administration of100-200 mgoflabetalol themeanblood pressure fell from88± 3to79+ 3mm Hg;(P< 0.005). Themeanarterial blood flowregistered 5.1+ 1.0ml100 ml-' limbtissue min-' which wasnotsignificantly different fromthecontrol value of4.4+ 0.8ml100m-1' limbtissue min-.Thecalculated index oflimbvascular resistance wasnot affected bylabetalol administration, averaging 37± 12mm Hg100-1 mllimbtissue min-' before labetalol and30+ 11mm Hgm-1' 100mllimbtissue min-' atthetimeofpeak hypotensive effect. There wasaslight butstatistically significant increment inlimbvenous volumeto1.9+ 0.3from1.5+ 0.3ml100ml-1limbtissue (P< 0.025). Placebo administration produced noconsistent changes inbloodpressure, arterial bloodflow, vascular resistance orvenous capacitance. Thehypotensive action oflabetalol involved no arteriolar vasoconstriction inthelimbs ofthese patients, andmildvenodilatation developed. Thefindings maybeexplained bybalanced a-and0-adrenoceptor inhibitory effects on skeletal muscle arterioles andperipheral venouspooling. Unlike pure,3-adrenoceptor antagonists, labetalol doesnotdecrease perfusion ofresting skeletal muscle inpatients recovering fromcoronary surgery.