[Bilateral endocrinically inactive cancer of the adrenal cortex].
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Adrenal Cortex↗
Biomedical subjects
O Okazaki
Publications and source records attributed to O Okazaki.
Exercise-induced ST-segment changes permit prediction of improvement in left ventricular ischemic dysfunction after revascularization: evaluation with positron emission tomographic measurements of regional myocardial blood flow and cardiac output.
BACKGROUND: Prediction of the recovery of left ventricular (LV) ischemic dysfunction after revascularization is important in patients with coronary artery disease (CAD). We investigated whether the improvement in LV ischemic dysfunction after revascularization could be predicted preoperatively by exercise-induced ST-segment changes. METHODS AND RESULTS: Regional myocardial blood flow (RMBF) and cardiac output were measured with nitrogen 13-ammonia positron emission tomography at rest and during low-level exercise in 28 patients with angiographically proven CAD before and after successful revascularization and in 9 normal subjects. Before revascularization, exercise-induced upsloping ST-segment depression <1 mm 80 msec after the J-point was observed in 11 patients (group 1), horizontal depression of 1 to 1.5 mm was observed in 9 patients (group 2), and downsloping depression > or =1.5 mm was observed in 8 patients (group 3). The number of regions of critical CAD was greater in group 3 than in groups 1 and 2 (3.6 +/- 1.4 vs 1.6 +/- 0.7 and 2.2 +/- 1.1, p < 0.001, p < 0.02). Increase of RMBF in regions of critical CAD with exercise was lower in group 3 than in groups 1 and 2 (0.15 +/- 0.01 vs 0.22 +/- 0.01 and 0.18 +/- 0.02 ml/min per gram, p < 0.0001, p < 0.01). After revascularization, RMBF in regions of critical CAD both at rest and during exercise improved in groups 1 (0.49 +/- 0.15 to 0.60 +/- 0.18, 0.70 +/- 0.26 to 0.86 +/- 0.33 ml/min per gram, both p < 0.05) and 2 (0.50 +/- 0.15 to 0.62 +/- 0.19, 0.67 +/- 0.26 to 0.89 +/- 0.31 ml/min per gram, both p < 0.02), but was unchanged in group 3 (0.47 +/- 0.09 to 0.47 +/- 0.15, 0.62 +/- 0.17 to 0.64 +/- 0.23 ml/min per gram, both p = NS). Cardiac output at rest improved in groups 1 (4.98 +/- 0.43 to 5.35 +/- 0.50 L/min, p < 0.02) and 2 (5.08 +/- 0.52 to 5.53 +/- 0.28 L/min, p < 0.02), but was unchanged in group 3 (4.76 +/- 0.48 to 4.88 +/- 0.82 L/min, p = NS). CONCLUSIONS: Our results suggest that marked downsloping ST-segment depression induced by preoperative low-level exercise may predict a lack of improvement in LV ischemic dysfunction after revascularization.
Ammonia↗
N-nitroso-N-methylvinylamine: reaction of the epoxide with guanyl and adenyl moieties to yield adducts derived from both parts of the molecule.
N-Nitroso-N-methylvinylamine was synthesized and treated with dimethyldioxirane to produce 1-(N-nitrosomethylamino)oxirane. 1-(N-Nitrosomethylamino)oxirane had a t1/2 of < 5 s in buffer at neutral pH and 23 degrees C. This epoxide reacted with Ado to form 1,N6-etheno(epsilon-)Ado. It also reacted with DNA to form products arising from the oxirane portion of the molecule [N7-(2-oxoethyl)Gua,N2,3-epsilon-Gua, and 1,N6-epsilon-dAdo] and the methyl group (N7-methylGua). NADPH-fortified rat liver microsomes oxidized N-nitroso-N-methylvinylamine to form 1,N6-epsilon-Ado in the presence of Ado. Further, 1,N6-epsilon-Ado was also formed in microsomal incubations containing N-nitroso-N-methylethylamine, indicating that desaturation of the ethyl moiety occurs to form a vinyl group and then an epoxide. When NADPH-fortified microsomes were incubated with N-nitroso-N-methylvinylamine, HCHO was formed, and when DNA was included in incubations, 1,N6-epsilon-dAdo and N7-methylGua were isolated from DNA. In the cases of both HCHO and N7-methylGua, product formation was similar to the levels seen with N-nitroso-N,N-dimethylamine and N-nitroso-N-methylethylamine.
Adenine↗
Stereoselective glucuronidation of ofloxacin in rat liver microsomes.
The stereoselective glucuronidation of ofloxacin [(+/-)-OFLX], a new quinolone antibacterial agent, was studied in vitro using rat liver microsomes. OFLX glucuronidation exhibited Michaelis-Menten kinetics in rat liver microsomes. Stereoselective glucuronidation of the optical enantiomers occurred. S-(-)-OFLX glucuronide was produced 7-fold more than R-(+)-OFLX glucuronide with little or no difference in the values of KM of the enantiomers. The value of Vmax/KM for the glucuronide conjugate of S-(-)-OFLX was 8-fold greater than for the conjugate of R-(+)-OFLX. These results demonstrate that OFLX undergoes stereoselective glucuronidation in vitro. Moreover, we studied the in vivo interaction between enantiomers of OFLX in rats to clarify the effects of R-(+)-OFLX on the metabolism and disposition of S-(-)-OFLX. When the racemate [(+/-)-OFLX (20 mg/kg)] or single enantiomer [S-(-)-OFLX (10 mg/kg)] is administered iv to the rat, the serum concentrations of S-(-)-OFLX were higher after racemate administration than those after enantiomer administration, although the dose of S-(-)-OFLX was identical in both cases. These results indicate that R-(+)-OFLX may compete with S-(-)-OFLX in the in vivo glucuronidation. Furthermore, the results of the enantiomeric inhibition study showed that R-(+)-OFLX competitively inhibited S-(-)-OFLX glucuronidation in vitro with a Ki value of 2.92 mM.
Animals↗