title: Transcutaneous electrical nerve stimulation induces vasodilation in healthy controls but not in refractory angina patients.
abstract: BACKGROUND
  Transcutaneous electrical nerve stimulation (TENS) is an effective treatment option to relieve ischemic pain in refractory angina pectoris (RAP). In healthy persons, TENS enhances local blood flow, but the mechanism responsible for the anti-ischemic effect in RAP seems to be different.
  
  
  OBJECTIVE
  The aim of the present investigation was to compare the difference in blood flow and vasodilatory response to TENS between angina patients and healthy controls and evaluate how vascular response in these groups is affected by amperage dosage above and below motor threshold levels.
  
  
  METHODS
  Our study evaluated upper limb vascular responses to low- and high-dose TENS (below and above motor threshold) in RAP patients compared with healthy controls. TENS was applied on the nondominating forearm. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. Forearm vascular resistance (FVR) was determined (mean arterial pressure [MAP]/FBF). Measurements were done during baseline, low-dose TENS, high-dose TENS, and during recovery.
  
  
  RESULTS
  A significant dose-dependent increase in FBF in response to TENS stimulation was seen in controls (n=18) but not in RAP (n=23) (P=0.008). There was no significant difference in FVR ratio (FVR(stim)/FVR(ctrl)) between control (n=7) and RAP (n=23) groups at low dose (controls, 5.7+/-21%; RAP, 9.7+/-20%) or recovery (controls, -4.6+19%; RAP, 5.9+25%). High-dose TENS resulted in a significantly reduced FVR ratio (-16.8+/-11%) in controls (n=7) compared with RAP (1.6+/-32%, n=23) (P=0.02).
  
  
  CONCLUSIONS
  High-dose TENS induces forearm vasodilation in healthy subjects but not in patients with RAP. These findings suggest that TENS has different vascular effects in patients with severe coronary artery disease compared with healthy controls.
authors.affiliation: Department of Anesthesia and Intensive Care, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
authors.forename: Katarina
authors.initials: K
authors.lastname: Hallén
authors.forename: Thórdís
authors.initials: T
authors.lastname: Hrafnkelsdóttir
authors.forename: Sverker
authors.initials: S
authors.lastname: Jern
authors.forename: Björn
authors.initials: B
authors.lastname: Biber
authors.forename: Clas
authors.initials: C
authors.lastname: Mannheimer
authors.forename: Smita
authors.initials: S
authors.lastname: DuttaRoy
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000787:Angina Pectoris / Q000503:physiopathology* / Q000628:therapy; D001794:Blood Pressure / Q000502:physiology; D004351:Drug Resistance; D005260:Female; D005542:Forearm / Q000098:blood supply; D006801:Humans; D007511:Ischemia / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D004561:Transcutaneous Electric Nerve Stimulation; D014664:Vasodilation / Q000502:physiology*