ONSET OF SEGMENTAL RELAXATION DYSFUNCTION WITH DECREASED MYOCARDIAL TISSUE PERFUSION - MODULATION BY PROPOFOL

Objectives: To estimate myocardial oxygen needs by studying the effect s of reduced coronary blood flow on segmental myocardial function. To study the tolerance of limited oxygen supply to a myocardial segment d uring propofol administration. Design: A prospective experimental stud y. Setting: An experimental animal laboratory in a university. Partici pants: Eighteen adult dogs, weighing 20 to 35 kg. Interventions: Open thorax open pericardium experiments were performed under standard anes thetic conditions. Segment length gauges were placed subendocardially in an anteroapical and in a basal segment. flow to the anteroapical se gment was reduced by tightening a micrometer-controlled snare placed a round the second diagonal coronary artery. Left ventricular pressure-l ength signals allowed for identification of onset of relaxation dysfun ction. Myocardial tissue flow at onset of relaxation dysfunction was d efined as critical flow. Tracer microspheres were used to measure sube picardial, midwall, and subendocardial flow at critical flow. Measurem ents and Main Results: Stability of the model and reproducibility of c ritical flow were studied in a first series of six dogs with the heart s paced at 110 beats/min. Hemodynamics, left ventricular, and segmenta l 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 bea ts/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, c ritical flow was measured during sufentanil, 0.6 mu g/kg/min, and incr easing 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 compare d with PD, hemodynamic and left ventricular contraction parameters wer e stable at P4 but were decreased at P8. At P0, critical flow was: 0.6 3 +/- 0.14, at P4: 0.34 +/- 0.09, and at P8: 0.25 +/- 0.07 mL/min/g (p < 0.05). Conclusion: Critical myocardial tissue flow was reproducible and sensitive for altered myocardial oxygen needs. The negative inotr opic properties of P decreased myocardial oxygen needs during unchange d hemodynamic and left ventricular contraction parameters. A higher P dose depressed left ventricular function. Copyright (C) 1995 by W.B. S aunders Company