title: Myocardial oxygenation and transmural lactate metabolism during experimental acute coronary stenosis in pigs.
abstract: Measurement of surface tissue pO2 (ptO2) with surface electrodes is increasingly applied in experimental medicine. Its use on the beating heart may seem to be problematic because transmural gradients of tissue pO2 would reduce the validity of pO2 determinations in the epicardial layers. This study attempted to determine whether ptO2 may be a valid and sensitive indicator of transmural myocardial oxygenation. In order to measure ptO2, two eight-channel Clark-type electrodes were placed on a beating porcine left ventricle (n = 13). Measurements were made at different degrees of acute stenosis of the left anterior descending artery (LAD). A 24-F cannula was inserted into the great cardiac vein, draining the poststenotic myocardium to obtain coronary venous blood samples. Transmural metabolic changes were detected simultaneously by coronary venous blood gas parameters and lactate levels. Epicardial tissue pO2 was 49 +/- 2 mm Hg (mean +/- SEM) before stenosis and decreased to a mean value of 25 +/- 2 mm Hg during stenosis. Different degrees of LAD stenosis (ptO2 range: 12-35 mm Hg) were substantial enough to alter arterio-coronary venous lactate difference (avd lactate) from +0.31 +/- 0.07 mmol/l (control) to -0.62 +/- 0.15 mmol/l (stenosis). A significant linear correlation between changes of ptO2 (delta ptO2) and changes of avd lactate (delta avd lactate) resulted (y = 0.59 + 0.62x; r = 0.86; p less than or equal to 0.001). However, linear regression analysis between delta ptO2 correlated with the corresponding data from coronary venous pO2 (delta pO2cv) oxygen content (delta O2contcv), and oxygen saturation (delta O2satcv) showed no significant correlations. We conclude that measurement of ptO2 is a sensitive and valuable indicator of transmural oxygenation in ischemic myocardium, whereas pO2cv, O2contcv and O2satcv do not seem to be valid predictors of ischemia in myocardial oxygenation.
authors.affiliation: Med. Dept. I, Klinikum Grosshadern, Munich, FRG.
authors.forename: P
authors.initials: P
authors.lastname: Gonschior
authors.forename: G M
authors.initials: GM
authors.lastname: Gonschior
authors.forename: P F
authors.initials: PF
authors.lastname: Conzen
authors.forename: J
authors.initials: J
authors.lastname: Hobbhahn
authors.forename: A E
authors.initials: AE
authors.lastname: Goetz
authors.forename: K
authors.initials: K
authors.lastname: Peter
authors.forename: W
authors.initials: W
authors.lastname: Brendel
mesh_terms: D000208:Acute Disease; D000818:Animals; D003251:Constriction, Pathologic; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics; D007773:Lactates / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D013552:Swine
chemical_list: D007773:Lactates