RESUMO
The objective of this study was to determine the role of adrenergic tone on the peripheral vascular decompensation reported to occur during systemic endotoxemia. An in situ constant-flow double-canine gracilis muscle (GM) preparation allowed one GM to serve as an innervated control (GMc) for the contralateral denervated muscle (GMe). Group I (n = 9): normal inherent vascular tone; Group II (n = 7): adrenergic tone elevated by bilateral common carotid artery ligation. The GMc Group II vascular conductance was significantly lower than GMe at .0485 +/- .004 ml/min/100 g/mm Hg and .0636 +/- .005 ml/min/100 g/mm Hg respectively. GM denervation had no significant effect on Group I conductance suggesting a low level of baseline intrinsic adrenergic tone; however, denervation did increase the vascular conductance by more than 30% from .0485 +/- .004 to .0638 +/- .008 ml/min/100 g/mm Hg in Group II. A 2 mg/kg dose of endotoxin was infused i.v. over 30 min and data collected over an additional 60 min. The endotoxin caused a decrease in MAP from 129 +/- 5 to 73 +/- 6 mm Hg in Group I and from 177 +/- 16 to 92 +/- 14 mm Hg in Group II. both the GMc and GMe Group I GMs showed an initial increase in conductance to 115 +/- 9 and 117 +/- 8% respectively at 5 min followed by a reduction to 82 +/- 9 and 101 +/- 10% at 60 min. Group II (GMe) showed a significantly increased conductance following denervation to 125% which increased insignificantly to 140 +/- 15% at 60 min, while conductances either remained at about 100% or decreased slightly to 88 +/- 7% in the innervated Group II GMc. The data suggest that the baseline level of vascular tone may not be an important factor when evaluating the effect of systemic endotoxemia on the skeletal muscle peripheral vasculature.
