title: The pressure-flow relation in the canine coronary artery: combined effects of critical stenosis and intracoronary thrombosis.
abstract: OBJECTIVE
  To characterise the effect of coronary intra-arterial thrombosis upon the downstream vascular bed.
  
  
  BACKGROUND
  The vascular response downstream from a coronary intra-arterial thrombus has not previously been characterised. We postulated that downstream vasoconstriction might result from the presence of endothelial damage with consequent growth of platelet-rich thrombus.
  
  
  METHODS
  We measured the pressure gradient and flow across, and the pressure/flow ratio distal to, a canine left circumflex artery stenosis with and without endothelial damage causing intracoronary thrombosis. We also observed the effects of transient complete conclusions.
  
  
  RESULTS
  At occlusion, the pressure gradient was maximal; relief of occlusion caused a rapid increase flow and distal pressure with a rapid decrease in stenosis pressure gradient and resistance. Subsequently there was a period of stable stenosis resistance with pressure gradient and flow declining; distal pressure therefore increased at this time. Finally in the thrombus group only, stenosis resistance increased again towards re-occlusion. During occlusion, distal pressure averaged 49 +/- 18 mmHg in the presence of thrombus vs. 22 +/- 4 mmHg in its absence (P < 0.001). Following release of occlusion, the flow increased faster than distal pressure, so that the ratio (distal pressure/flow) fell rapidly. Subsequently, distal pressure continued to increase after flow had reached a peak and begun to decline, suggesting vasoconstriction. In the presence of thrombus, the distal pressure/flow ratio was higher than in the absence of thrombus, both at maximal vasodilation (P < 0.005) and at maximum vasoconstriction (P < 0.025).
  
  
  CONCLUSIONS
  During cyclic flow variations the stenosis resistance changes are exactly as expected from thrombus growth and embolisation. The distal pressure/flow ratio showed a time-dependent increase which appeared greater when conditions favoured intracoronary thrombosis.
authors.affiliation: Academic Unit of Cardiovascular Medicine, Charing Cross & Westminster Medical School, London, UK.
authors.forename: P R
authors.initials: PR
authors.lastname: Belcher
authors.forename: I
authors.initials: I
authors.lastname: Vergroesen
authors.forename: A J
authors.initials: AJ
authors.lastname: Drake-Holland
authors.forename: M I
authors.initials: MI
authors.lastname: Noble
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000503:physiopathology*; D003328:Coronary Thrombosis / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology*; D004285:Dogs; D013997:Time Factors; D014655:Vascular Resistance / Q000502:physiology