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.

Acute Disease↗

PubMedDate not supplied

Induction of beta-lactamase in Gram-negative bacteria.

The induction of beta-lactamase in Gram-negative bacteria in vitro has been established. It is possible to distinguish between high and low beta-lactamase inducers in vitro. This differentiation is clinically irrelevant because induction has little effect on the treatment of a bacterial infection with beta-lactam antibiotics. Regardless of the amount of induced beta-lactamase, the kill kinetics are usually not affected. In mutated cells, the regulatory mechanism is destroyed by inactivation of the relevant genes with respect to their regulatory function, particularly by inactivation of the amp D gene. These mutants overproduce the beta-lactamase constitutively, which results in an enzyme level that significantly exceeds the induced level. The induction process is probably not the cause of clinical failures associated with the use of beta-lactam antibiotics. It is concluded that the selection of resistant mutants with constitutive overproduction of beta-lactamase is the reason for most of these treatment failures.

Anti-Bacterial Agents↗