Onset of segmental relaxation dysfunction with decreased myocardial tissue perfusion: Modulation by propofol

Abstract

To estimate myocardial oxygen needs by studying the effects of reduced coronary blood flow on segmental myocardial function. To study the tolerance of limited oxygen supply to a myocardial segment during propofol administration. A prospective experimental study. An experimental animal laboratory in a university. Eighteen adult dogs, weighing 20 to 35 kg. Open thorax open pericardium experiments were performed under standard anesthetic conditions. Segment length gauges were placed subendocardially in an anteroapical and in a basal segment. Flow to the anteroapical segment was reduced by tightening a micrometer-controlled snare placed around the second diagonal coronary artery. Left ventricular pressure-length signals allowed for identification of onset of relaxation dysfunction. Myocardial tissue flow at onset of relaxation dysfunction was defined as critical flow. Tracer microspheres were used to measure subepicardial, midwall, and subendocardial flow at critical flow. Stability of the model and reproducibility of critical flow were studied in a first series of six dogs with the hearts paced at 110 beats/min. Hemodynamics, left ventricular, and segmental myocardial function during critical flow were stable. Subendocardial critical flow was identical with each flow reduction (45% +/- 5, 44% +/- 8, and 43% +/- 5 of baseline myocardial tissue flow). In a second series of six dogs, critical flow was measured at pacing rates 100 beats/min, 150 beats/min, and 100 beats/min with propranolol, 0.1 mg/kg, pretreatment. Critical flows were 38% +/- 5, 55% +/- 6, and 17% +/- 2 of baseline, respectively (p < 0.05). In a third series of six dogs, critical flow was measured during sufentanil, 0.6 microgram/kg/min, and increasing doses of propofol (P0: 0.0 mg/kg/h, P4: 4.0 mg/kg/h and P8: 8.0 mg/kg/h). Heart rate was kept constant at 110 beats/min. When compared with P0, hemodynamic and left ventricular contraction parameters were stable at P4 but were decreased at P8. At P0, critical flow was: 0.63 +/- 0.14, at P4: 0.34 +/- 0.09, and at P8: 0.25 +/- 0.07 mL/min/g (p < 0.05). Critical myocardial tissue flow was reproducible and sensitive for altered myocardial oxygen needs. The negative inotropic properties of P decreased myocardial oxygen needs during unchanged hemodynamic and left ventricular contraction parameters. A higher P dose depressed left ventricular function.