title: Muscle microvascular oxygenation in chronic heart failure: role of nitric oxide availability.
abstract: OBJECTIVE
  To test the hypothesis that diminished vascular nitric oxide availability might explain the inability of individuals with chronic heart failure (CHF) to maintain the microvascular PO(2)'s (PO(2mv) proportional, variant O(2) delivery-to-uptake ratio) seen in healthy animals.
  
  
  METHODS
  We superfused sodium nitroprusside (SNP; 300 microm), Krebs-Henseleit (control, CON) and L-nitro arginine methyl ester (L-NAME; 1.5 mM) onto the spinotrapezius muscle and measured PO(2mv) by phosphorescence quenching in female Sprague-Dawley rats (n = 26) at rest and during twitch contractions (1 Hz). Seven rats served as controls (Sham) while CHF was induced by myocardial infarction. CHF rats were grouped as moderate (MOD; n = 15) and severe CHF (SEV; n = 4) according to morphological data and baseline PO(2mv).
  
  
  RESULTS
  In contrast to Sham and MOD, L-NAME did not affect the PO(2mv) response (dynamics and steady-state) of SEV when compared with CON. SNP restored the PO(2mv) profile of SEV to that seen in Sham animals during CON. Specifically, the effect of L-NAME expressed as Delta(L-NAME - CON) were: Baseline PO(2mv) [in mmHg, DeltaSham = -7.0 +/- 1.6 (P < 0.05); DeltaSEV =-1.2 +/- 2.1], end-contractions PO(2mv) [in mmHg, DeltaSham = -5.0 +/- 1.0 (P < 0.05); DeltaSEV = -2.5 +/- 0.5] and time constant of PO(2mv) decrease [in s, DeltaSham = -6.5 +/- 3.0 (P < 0.05); DeltaSEV = -3.2 +/- 1.8].
  
  
  CONCLUSIONS
  These data provide the first direct evidence that the pathological profiles of PO(2mv) associated with severe CHF can be explained, in part, by a diminished vascular NO availability.
authors.affiliation: Clarenburg Research Laboratory, Department of Anatomy and Physiology, and Department of Kinesiology, Kansas State University, Manhattan, KS 66506-5802, USA.
authors.forename: L F
authors.initials: LF
authors.lastname: Ferreira
authors.forename: K S
authors.initials: KS
authors.lastname: Hageman
authors.forename: S A
authors.initials: SA
authors.lastname: Hahn
authors.forename: J
authors.initials: J
authors.lastname: Williams
authors.forename: D J
authors.initials: DJ
authors.lastname: Padilla
authors.forename: D C
authors.initials: DC
authors.lastname: Poole
authors.forename: T I
authors.initials: TI
authors.lastname: Musch
mesh_terms: D000818:Animals; D001808:Blood Vessels / Q000378:metabolism*; D017079:Exercise Tolerance; D006333:Heart Failure / Q000378:metabolism*; D008297:Male; D008833:Microcirculation; D018482:Muscle, Skeletal / Q000098:blood supply*; D009203:Myocardial Infarction / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D010100:Oxygen; D019331:NG-Nitroarginine Methyl Ester