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Departments of Anesthesiology, Neurosurgery, Neurology, and General Clinical Research Center, Mayo Clinic and Mayo Medical School, Rochester, Minnesota 55905
To determine whether endothelial
function is altered by chronic surgical sympathectomy, we infused ACh,
isoproterenol, nitroprusside (NTP), and the nitric oxide synthase
inhibitor NG-mono-methyl-L-arginine
(L-NMMA) into the brachial arteries of nine patients
5-64 mo after thoracic sympathectomy for hyperhidrosis. Age- and
gender-matched controls were also studied. Forearm blood flow (FBF) was
measured by venous occlusion plethysmography. Lower body negative
pressure was used to assess reflex vasoconstrictor responses. Tyramine,
which acts locally and causes norepinephrine release from sympathetic
nerves, was also administered via the brachial artery. FBF at rest was
2.5 ± 0.4 ml · dl
1 · min1 in the
patients and 2.5 ± 0.3 ml · dl1 · min1 in the
controls (P = 0.95). The normal vasoconstrictor
responses to lower body negative pressure were abolished in the
patients. By contrast, tyramine produced dose-dependent
vasoconstriction in the patients that was identical to that of
controls. The dose-response curves to ACh were similar in patients and
controls, with maximum values of 19.3 ± 4.4 vs. 25.5 ± 2.8 ml · dl1 · min1,
respectively. L-NMMA reduced baseline FBF similarly and
reduced the maximal FBF response to ACh in both groups (patients
8.9 ± 3.5 vs. controls 9.7 ± 2.5 ml · dl1 · min1). The
vasodilation to isoproterenol was similar and blunted to the same
extent in both groups by L-NMMA. The responses to NTP in
patients and controls were similar and not affected by
L-NMMA. We conclude that, in humans, chronic surgical
sympathectomy does not cause major disruptions in vascular function in
the forearm. The normal vasoconstrictor responses to tyramine indicate
that there were viable sympathetic nerves in the forearm that were not
engaged by LBNP.
forearm blood flow; endothelium; vasodilation; nitric oxide; tyramine
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