title: Inhibition of nitric oxide synthase attenuates cutaneous vasodilation during warm moxibustion-like thermal stimulation in humans.
abstract: OBJECTIVE
  This study investigated if nitric oxide (NO) and/or prostaglandin (PG) are responsible for cutaneous vasodilation during warm moxibustion-like thermal stimulation (WMTS).
  
  
  METHODS
  For two protocols, two microdialysis membranes were placed in the medial forearm skin. In the first protocol (n=8), the sites were randomly assigned and perfused with N(G)-nitro-l-arginine methyl ester hydrochloride (l-NAME), an NO synthase inhibitor or Ringer's solution (control site). Similarly, two microdialysis membranes were placed in the medial forearm skin in the second protocol (n=6). One site was perfused with ketorolac (Keto), the cyclo-oxygenase (COX) pathway inhibitor, and the other site was perfused with Ringer's solution (control site). In both protocols, cutaneous vasodilation was induced using WMTS with an electronic warm moxibustion treatment appliance. After 10 minutes of baseline recording, WMTS was applied to the forearm skin for 20 minutes and recovery was monitored over a period of 20 minutes. Skin blood flow (SkBF) at each site was measured using laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was calculated as laser-Doppler flux/mean arterial blood pressure (BP).
  
  
  METHODS
  The study was conducted in a laboratory at the Kansai University of Health Sciences.
  
  
  METHODS
  The subjects were 14 healthy male volunteers.
  
  
  METHODS
  WMTS was applied to the medial forearm skin using an electronic warm moxibustion treatment appliance.
  
  
  METHODS
  SkBF, skin temperature (Tsk), core body temperature (Tc), heart rate (HR), and BP were outcome measures.
  
  
  RESULTS
  In the first protocol, peak CVC values during WMTS at the site perfused with l-NAME were significantly decreased, compared to those at the control site (p<0.05). In the second protocol, peak CVC values during WMTS did not differ between the control site and the Keto site (p>0.05).
  
  
  CONCLUSIONS
  These data demonstrate that NO is involved in the mechanism of cutaneous vasodilation induced by WMTS. Furthermore, increases in CVC despite inhibition of the COX pathway suggest that PG does not contribute to cutaneous vasodilation during WMTS.
authors.affiliation: Department of Health Sciences, Kansai University of Health Sciences, Osaka, Japan. k.kimura@kansai.ac.jp
authors.forename: Kenichi
authors.initials: K
authors.lastname: Kimura
authors.forename: Hayato
authors.initials: H
authors.lastname: Takeuchi
authors.forename: Kuniko
authors.initials: K
authors.lastname: Yuri
authors.forename: Ikuro
authors.initials: I
authors.lastname: Wakayama
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001794:Blood Pressure; D005542:Forearm; D006358:Hot Temperature; D006801:Humans; D020910:Ketorolac; D017078:Laser-Doppler Flowmetry; D008297:Male; D008875:Middle Aged; D009071:Moxibustion / Q000379:methods*; D019331:NG-Nitroarginine Methyl Ester; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D017063:Outcome Assessment, Health Care; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D011453:Prostaglandins; D012016:Reference Values; D012039:Regional Blood Flow; D015398:Signal Transduction; D012867:Skin / Q000098:blood supply*; D012879:Skin Physiological Phenomena; D014664:Vasodilation / Q000502:physiology*; D055815:Young Adult
chemical_list: D011453:Prostaglandins; D019001:Nitric Oxide Synthase; D011451:Prostaglandin-Endoperoxide Synthases; D019331:NG-Nitroarginine Methyl Ester; D020910:Ketorolac