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1 diameter, volumetric coronary blood flow, or coronary vascular resistance.
2   CAB-2 also retarded the onset of increased coronary vascular resistance.
3 brillation and the accompanying increases in coronary vascular resistance.
4 t percent changes in coronary blood flow and coronary vascular resistance (-31 +/- 4% versus -7 +/- 3
5                               A reduction in coronary vascular resistance and a decrease in coronary
6 ects on energy metabolism without effects on coronary vascular resistance and coronary blood flow.
7 fic antagonist of nitric oxide synthesis, on coronary vascular resistance and epicardial coronary art
8 MA, the 13 +/- 4% (mean +/- SEM) increase in coronary vascular resistance and the 4 +/- 1% lumen diam
9 h a higher coronary effluent PCO2, increased coronary vascular resistance, and development of ischemi
10 elopment of ischemic contracture, increasing coronary vascular resistance, and favoring the developme
11  length area, coronary artery blood flow and coronary vascular resistance, and myocardial oxygen cons
12  [*p < 0.05 vs. baseline value]) and reduced coronary vascular resistance (baseline, 1.6 +/- 0.3 mm H
13 -8%, P<.05, respectively) and an increase in coronary vascular resistance (CVR) (242+/-18% versus 110
14 (13)N]ammonia PET imaging to measure MBF and coronary vascular resistance (CVR) at rest and during a
15 ET-derived myocardial flow reserve (MFR) and coronary vascular resistance (CVR) for risk stratificati
16 and Doppler flow velocity were measured, and coronary vascular resistance (CVR) was calculated during
17 ood flow (MBF), myocardial flow reserve, and coronary vascular resistance (CVR), were assessed from b
18                                              Coronary vascular resistance (CVR; mean arterial pressur
19 mulation was performed, measuring changes in coronary vascular resistance (% delta CVR) before and af
20                    We measured the change in coronary vascular resistance (DeltaCVR) and epicardial d
21                                    Change in coronary vascular resistance (DeltaCVR) was measured as
22 Hg/s; P < .01) and coronary vasoconstrictor (coronary vascular resistance: first dose, +38 +/- 9% fro
23  decreased coronary blood flow and increased coronary vascular resistance in normal dogs; this effect
24 unction, determined as the percent change in coronary vascular resistance in response to ACH (P=0.009
25 e percent changes in coronary blood flow and coronary vascular resistance in the TIVCC compared with
26                                            A coronary vascular resistance index (CVR) was calculated
27          Cardiac pacing-induced reduction in coronary vascular resistance of 27+/-4% (p < 0.001) rema
28 ompromised by other mechanisms that increase coronary vascular resistance or reduce coronary driving
29 o significant effect on coronary blood flow, coronary vascular resistance, or coronary artery diamete
30 5) as the result of a 44 +/- 13% increase in coronary vascular resistance (p < 0.05).
31  (+15 +/- 4 from 41 +/- 4 ml/min), while the coronary vascular resistance response was greater in bab
32 stemic pressor, inotropic, chronotropic, and coronary vascular resistance responses to cocaine (1 mg/
33 ry artery diameter, coronary blood flow, and coronary vascular resistance were calculated on the basi
34 sclerotic patients (32.2 +/- 9% reduction in coronary vascular resistance with 10(-6) mol/liter acety