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M Okada

Publications and source records attributed to M Okada.

At least 1,495 records · Page 83Linked to original sources

[Human adult left atrial volume estimated by M-mode echocardiography].

There are few systematic reports of the regression equation for humans, for estimating left atrial volumes from the anteroposterior left atrial dimensions measured by M-mode echocardiography (LADAP). In addition, several pitfalls were inherent in the M-mode method. In view of these pitfalls, we estimated the anteroposterior left atrial dimensions by directing the ultrasonic beam toward the "center" of the left atrium under the guidance of two-dimensional echocardiography. Simultaneously, we estimated left atrial volumes from anteroposterior and left lateral biplane left atrial angiocardiograms using a film changer at three frames per sec. The maximum elapsed time between the echocardiographic and angiocardiographic studies was two days. Left atrial volumes were calculated using the method of Sauter et al. Maximum left atrial volume was calculated at the end of the T wave. The results were as follows: For phantom experiments, a cylindrical container with varying amounts of contrast material was tested by biplane angiography using a film changer. The actual volume (x) and the calculated volume (y) were in good agreement with the regression equation; y = 1.05x-0.1 (r = 0.99, p less than 0.001, n = 6). The anteroposterior left atrial dimension in M-mode echocardiography (LADAP: x axis) and left atrial volume (ml) angiocardiographically obtained (y axis) showed the curvilinear regression equation; y = 1.4x3+23 (r = 0.83, p less than 0.01, n = 19). The relation between the left atrial cross-sectional area (cm2) obtained from the left ventricular long-axis view by two-dimensional echocardiography (x axis) and the left atrial volume (ml) by angiocardiography using a film changer (y axis) showed the regression equation; y = 1.2x1.5+17 (r = 0.82, p less than 0.01, n = 14). As a preliminary study, we calculated left atrial volume (LAVcine) for five patients by performing biplane cineangiocardiography at 50 frames per sec. The results were nearly the same as those obtained using a film changer. In summary, the derived equation predicts left atrial volume using M-mode echocardiography with considerable accuracy.

Adolescent↗

[Evaluation of the atrial contribution to ventricular filling in patients with DDD pacemakers].

To evaluate the usefulness of physiologic cardiac pacing, the trasmitral flow velocity was recorded using the pulsed Doppler method combined with 2-D echocardiography in 14 patients in whom a DDD pacemaker was implanted. DDD pacemakers were programmed to atrioventricular (AV) sequential pacing with AV intervals of 50, 100, 150, 200 and 250 msec, and VVI pacing modes at a heart rate of 70 bpm. The time-velocity integral (TVI) of the left ventricular (LV) inflow curve was obtained by digitizing the outline of the tracings and expressed in the percentage of that of AV sequential pacing with AV interval of 150 msec (the percent LV filling volume). The percent LV filling volume was 75% for 50 msec, 89% for 100 msec, 96% for 200 msec and 90% for 250 msec of an AV interval in AV sequential pacing. It was significantly smaller at AV intervals of 50, 100 and 250 msec than at an AV interval of 150 msec. It was significantly smaller (68%) in VVI pacing than at AV intervals of 100, 150, 200 and 250 msec in AV sequential pacing. The left atrial (LA) contribution to LV filling was assessed in terms of the fraction of TVI during LA contraction to that during total LV filling at the optimal AV interval (A/Fmax). The optimal AV interval was defined as the interval at which the maximum LV filling volume was achieved in individual patients. The A/Fmax showed a positive correlation with the percent increase of LV inflow volume, with conversion from VVI to AV sequential pacing with the optimal AV interval. It also showed a positive correlation with age. These results suggested that the LV inflow volume was greater in AV sequential pacing with the optimal AV interval than in VVI pacing, especially in patients with a large A/Fmax. In conclusion, pulsed Doppler echocardiography could be a useful, non-invasive technique to determine the indications for implanting a DDD pacemaker and the optimal AV interval in patients in whom DDD pacemakers are implanted.

Adult↗

In vitro metabolism of N-nitrodialkylamines.

The in vitro metabolism of N-nitramines was investigated in order to compare it with that of N-nitrosamines and to elucidate the mode of mutagenic action. N-Nitrodibutylamine (NO2DBA) and N-nitrodiethylamine (NO2DEA) were incubated with liver microsomes and hepatocytes prepared from rats treated with phenobarbital, and the products were analyzed by high-performance liquid chromatography and gas-liquid chromatography. The in vitro metabolic pattern of these nitramines was similar to that of the corresponding nitrosamines, except that N-nitro-N-alkylamines (produced via alpha-hydroxylation) were identified after incubation of the nitrodialkylamines. In the case of NO2DBA, besides N-nitro-N-butylamine, several nitramines produced by omega, omega-1, and omega-2 oxidations were identified as metabolites. NO2DBA and NO2DEA were mutagenic to Escherichia coli WP2 hcr- but not to Salmonella typhimurium TA1535. They were mutagenic only in the presence of hepatic microsomes, whereas their metabolites, N-nitro-N-butylamine and N-nitro-N-ethylamine, were direct mutagens. Thus, N-nitrodialkylamines are also metabolically activated to mutagens through alpha-hydroxylation.

Aniline Compounds↗

Metabolic fate of omega-1 and omega-2 oxidized N-nitrosodibutylamines in the rat.

Of the three metabolic oxidation pathways of N-nitrosodibutylamine (NDBA) demonstrated in vivo, omega oxidation is responsible for the induction of bladder tumors, while omega-1 and omega-2 oxidations are considered to be associated with the induction of liver tumors by NDBA. The metabolic fate of the following five NDBA derivatives was investigated in the rat in order to elucidate further the metabolic characteristics of NDBA in relation to its hepatocarcinogenic activity: N-nitroso-N-(3-hydroxybutyl)butylamine (NHBBA-3), N-nitroso-N-(3-oxobutyl)butylamine (NOBBA-3), N-nitroso-N-(2-hydroxybutyl)butylamine (NHBBA-2) and N-nitroso-N-(2-oxobutyl)butylamine (NOBBA-2), which are involved in the omega-1 and omega-2 oxidation pathways of NDBA, and N-nitroso-N-(2-oxopropyl)butylamine (NOPBA), a minor urinary metabolite of NDBA. By characterization of the urinary metabolites, NHBBA-3 and NHBBA-2, primary metabolites of NDBA, were shown to undergo further oxidative metabolic transformation via NOBBA-3 and NOBBA-2, respectively, although conjugation with glucuronic acid to afford the glucuronides was demonstrated to be their principal metabolic pathway. The principal urinary metabolite of NOBBA-2 as well as NOBBA-3 was N-nitroso-N-(carboxymethyl)butylamine, while reduction of the oxo group followed by glucuronidation was found to be a minor metabolic pathway. The glucuronide of N-nitroso-N-(2-hydroxypropyl)butylamine was the principal metabolite of NOPBA, N-nitroso-N-(carboxymethyl)butylamine being a secondary metabolite. The hepatocarcinogenic activity of the three oxo compounds (NOBBA-3, NOBBA-2 and NOPBA) in relation to that of NDBA is discussed from the metabolic point of view.

Animals↗

Alpha-hydroxylation and mutagenicity of unsymmetrical N-nitrosodialkylamines with a butyl group.

In order to compare the extents of metabolic alpha-hydroxylation of the two alkyl groups in unsymmetrical N-nitrosodialkylamines, N-nitroso-N-alkylbutylamines (alkyl = methyl, ethyl, propyl, butyl, and amyl) were incubated with liver microsomes prepared from phenobarbital- or polychlorinated biphenyl (PCB)-treated and untreated rats, and aldehydes produced by the alpha-hydroxylation were determined quantitatively. Although an increased production of aldehydes was observed with the induced microsomes compared with the non-induced microsomes, no marked differences were noted between the two alkyl groups of these unsymmetric nitrosodialkylamines in regard to the extent of alpha-hydroxylation with the exception of N-nitroso-N-methylbutylamine (NMBA). The amount of aldehydes produced from these nitrosamines increased with elongation of the alkyl chain, amounting to 10-30% of the compounds incubated, and the recovery in the incubation (total aldehyde + nitrosamine recovered) was found to be more than 90%, indicating that alpha-hydroxylation is the principal oxidative metabolic pathway of the nitrosamines in vitro. The microsomal alpha-hydroxylation was inhibited by dimethyl sulfoxide and the extent of the hydroxylation was shown to be positively correlated with the mutagenic potency of the nitrosamines. Based on the mutagenic behavior of NMBA tested on Salmonella typhimurium TA1535 and Escherichia coli WP2 hcr- and the extent of the formation of formaldehyde and butyraldehyde from NMBA in the presence of the induced microsomes and S9 mix, it was concluded that NMBA acts as both a methylating and a butylating agent.

Animals↗