Minimal effects of nitric oxide on spatial blood flow heterogeneity of the dog heart.
Eleven Beagle dogs were studied to elucidate the possible role of L-arginine-derived nitric oxide on local blood flow distribution in left and right ventricular myocardium. Local blood flow was determined in 256 samples from the left and 64 samples from the right ventricle per heart using the tracer microsphere technique (mean sample mass 319 +/- 131 mg). Nitric oxide production was effectively inhibited by intravenous infusion of 20 mg/kg nitro-L-arginine methylester (L-NAME) as evidenced by a shift of the dose/response curve for the effect of intracoronary administration of bradykinin (0.004-4.0 nmol/min) on coronary blood flow. L-NAME enhanced left and right ventricular systolic pressures from 132 +/- 18 to 155 +/- 15 mm Hg and from 26 +/- 3 to 29 +/- 3 mm Hg respectively (both P = 0.043). Mean left ventricular blood flow was 1.14 +/- 0.38 before and 0.99 +/- 0.28 ml min-1 g-1 after L-NAME (P = 0.068), while right ventricular blood flow fell from 0.72 +/- 0.28 to 0.53 +/- 0.20 ml min-1 g-1 (P = 0.043). Coronary conductance of left and right ventricular myocardium fell by 31 and 43% respectively (both P = 0.043). The coefficient of variation of left ventricular blood flow was 0.26 +/- 0.07 before and 0.29 +/- 0.07 after L-NAME (P = 0.068), that of right ventricular blood flow was 0.27 before and after L-NAME. Skewness (0.51) and kurtosis (4.23) of left ventricular blood flow distribution were unchanged after L-NAME, while in the right ventricle skewness decreased from 0.54 to 0.09 (P = 0.043) and kurtosis (3.68) tended to decrease after L-NAME (P = 0.080). The fractal dimension (D = 1.20-1.27) and the corresponding nearest-neighbor correlation coefficient (rn = 0.37-0.53) of left and right ventricular myocardium remained unchanged after infusion of L-NAME. From these results it is concluded that firstly, local nitric oxide release does not explain the higher perfusion of physiological high flow samples and secondly, that spatial myocardial blood flow coordination is not dependent on nitric oxide.
Deussen
A
A
Institut für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
Sonntag
M
M
Flesche
C W
CW
Vogel
R M
RM
D000818:Animals; D001120:Arginine / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001920:Bradykinin / Q000494:pharmacology; D003326:Coronary Circulation / Q000502:physiology*; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D016276:Ventricular Function
D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D001920:Bradykinin; D019331:NG-Nitroarginine Methyl Ester