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Biomedical subjects

T Fujimoto

Publications and source records attributed to T Fujimoto.

At least 739 records · Page 41Linked to original sources
PubMed1982

[Laboratory and clinical studies of cefmetazole in serious infection by Staphylococcus (author's transl)].

Cefmetazole (CMZ) is an antibiotic agent belonging to the cephamycin group, which is resistant to beta-lactamase and has a broad antibacterial spectrum covering from Gram-negative to -positive organisms. Although this agent has been proved to have an antibacterial activity against Staphylococcus spp., it has not been used for treatment of the infections caused by the organism. Thus, 62 strains of S. aureus isolated clinically were compared for their sensitivity to CMZ, cefoxitin (CFX), cefuroxime (CXM), cefazolin (CEZ), and ampicillin (ABPC). In addition, 5 children suffering from septicemia due to S. aureus were treated with CMZ 158 mg/kg at a mean daily dose for a mean period of 14 days. The dose was used after dividing into 3 and 4 equal parts in 1 and 4 children, respectively. One old patient with septicemia was given 2,000 mg of CMZ twice daily for 4 days and once daily for subsequent 3 days. Another child with bacterial meningitis was treated with 50 mg/kg of CMZ 4 times daily for 63 days. The drug was given intravenous injection by one-shot or drip infusion in all cases under observation of clinical effects, bacteriological effects and side effects. The MIC of CMZ against S. aureus at inoculum sizes of 10(6) and 10(8) cells/ml was 1.56 mcg/ml in 72.6 and 56.5% of the strains, respectively. When 5 drugs were compared on the basis of the MIC to which the largest number of strains were sensitive, CEZ was most active, and CMZ was ranked in the next place and similar to CXM in activity. However, when the whole range of the MIC was considered, CMZ was more excellent than CXM, its MIC was lower than those of CEZ, CFX and ABPC in a greater number of strains. It was considered from the results that the serum level of CMZ was effective against 100 and 93.5% of strains at an inoculum size of 10(6) cells/ml and against 100 and 83.9% of strains at an inoculum size of 10(8) cells/ml until 4 and 6 hours after a one-shot intravenous injection of 50 mg/kg of Moni-trol I standard, respectively in the children. Thus, CMZ is expected to manifest a sufficient effect on septicemia caused by S. aureus in children who receive a one-shot intravenous injection of 50 mg/kg of it 4 times daily. Treatment with CMZ was clinically evaluated to be excellent in 3, good in 3 and poor in none of 6 patients with septicemia due to S. aureus, and fair in the 1 with Staphylococcal meningitis. The bacteriological result was excellent, since the causal organisms were eradicated in all cases. With regard to side effects, abnormal eosinophilia was found in 2 cases, but it was no ascribable to this drug in 1 of them. GOT showed an abnormal rise in 1 case and both GOT and GPT in 1, although they were considered not to be related to this drug in either case. It is considered from these results that CMZ is a valuable drug in treatment of septicemia due to S. aureus.

Aged↗
PubMed1982

A case report of Henoch-Schoenlein purpura nephritis associated with a postbulbar duodenal ulcer.

We experienced an adult patient with Henoch-Schoenlein purpura (HSP) nephritis associated with a postbulbar duodenal ulcer. Chronic inflammatory changes of the arterioles (i.e. vasculitis) in the kidney and skin were prominently observed by immunofluorescence and light microscopic analysis. It is postulated that a postbulbar duodenal ulcer occurred in this patient and was mediated by vascular deposition of circulating immune complexes. It was suggested that HSP nephritis is a diffuse vascular form of IgA nephropathy.

Duodenal Ulcer↗
PubMed1982

[Experimental study on pharmacokinetics of methotrexate and its metabolite (7-hydroxy-methotrexate) in tissue].

The metabolism of methotrexate was investigated in rabbits with six hours infusion of (3'5'7-3H) methotrexate (50mg/kg). Methotrexate and its metabolites were analyzed by reverse-phase high-pressure liquid chromatography and by counting of radioactivity. 7-Hydroxymethotrexate was found to be the major metabolite in the plasma, urine, bile and tissues of rabbits. Cumulative production of 7-Hydroxymethotrexate during the first six hours was 31.8% of the total dose. The 7-Hydroxymethotrexate concentration in plasma was reached to peak level in six hours after the initiation of the infusion, and was declined slower than that of methotrexate. The highest total radioactivity was found in the kidney after six hours, which was 7.24 times higher than that in plasma. Ratio of 7-Hydroxymethotrexate/methotrexate increased in the liver, small intestine, lung, kidney and testis. This data suggested that conversion of methotrexate to 7-hydroxymethotrexate took place in lung and kidney as well as in liver.

Animals↗
PubMed1981

Electrophysiologic and hemodynamic actions of diltiazem: disparate temporal effects shown by experimental dose-response studies.

Diltiazem (DT), a potent slow channel blocker, has been found to be clinically useful for treatment of coronary vasospasm, hypertension, and tachyarrhythmias. Nevertheless, only limited data are available on the hemodynamic and electrophysiologic effects of DT. Atrial, His, right ventricular apex, aortic, and Swan-Ganz thermodilution catheters were used in 10 anesthetized dogs, and recordings were made during control period and after each of four infusions of DT (0.01, 0.02, 0.04, and 0.08 mg/kg/min) each lasting 30 minutes. Results showed that heart rate, pulmonary capillary wedge pressure, stroke volume, and HV interval did not change significantly. However, two dogs had second-degree AV block and a third had escape junctional rhythm during DT 0.08 mg/kg/min. Mean aortic pressure (AP), corrected sinus node (SN) recovery time, and systemic vascular resistance (SVR) were significantly reduced, whereas AH interval, AV functional and effective refractory periods were prolonged by DT. AV nodal refractory periods and AH interval were the only parameters significantly affected at DT 0.02 mg/kg/min. SN recovery time was significantly shortened at DT 0.04 mg/kg/min, whereas AP and SVR tell significantly at DT 0.08 mg/kg/min. DT had significant electrophysiologic effects at low doses, whereas hemodynamics were significantly altered only at high doses. Further, major electrophysiologic effects were on the AV node with lesser effects on SN function. Therefore, at a dose when antiarrhythmic effects are evident, the safety of diltiazem is corroborated by lack of adverse hemodynamic effects.

Animals↗
PubMed1981

Effect of verapamil on conduction delay produced by myocardial ischemia and reperfusion.

Changes in conduction times induced by ischemia (delta CT) have been shown to be quantitatively related to genesis of spontaneous ischemic ventricular fibrillation (VF). We studied conduction delay encountered by premature impulses in epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion in eight control and in eight verapamil treated dogs. Acute myocardial ischemia was produced by single-stage ligation of left anterior descending artery below second diagonal initially, and 30 minutes later below first diagonal branch. In treated dogs, verapamil was given, 0.15 mg/kg intravenous bolus, immediately after first ligation and was followed by an infusion of 7.5 micrograms/kg/min. Thus post-treated segment and pretreated segment were obtained in the same animal. delta CT was compared between control and treated dogs in four myocardial zones: (1) normal, (2) ischemic including pre- and post-treated segments, (3) reperfused, and (4) border of reperfusion or ischemia. Results showed that ischemia-induced conduction delay was significantly less in verapamil treated dogs throughout period of ischemia and reperfusion, both in epicardium and endocardium. In addition, in the border of ischemia retrograded conduction showed significantly less depression during ischemia and reperfusion. The protective effect of verapamil was impressive both in pretreated and post-treated segments of ischemic myocardium. We conclude that verapamil offers significant protective action with regard to ischemia-induced conduction delay. Since delta CT is quantitatively related to ischemic VF, verapamil can be antiventricular fibrillatory in myocardial ischemia.

Animals↗
PubMed1981

Effects of nifedipine on conduction delay during ventricular myocardial ischemia and reperfusion.

Nifedipine has been suggested to have more potent slow channel blocking action than other agents of this type. However, its use in the treatment of cardiac arrhythmias has been limited. Electrophysiologic studies on AV conduction have shown that nifedipine lacks any significant effect. However, the action of the drug on intraventricular conduction has not been investigated with regard to its potential in the treatment of ventricular arrhythmias especially during ischemia. Therefore, the effects of nifedipine on conduction delay during ischemia and reperfusion were assessed in the present study. Sixteen dogs (eight control and eight nifedipine-treated dogs) were used. Transmural electrodes were positioned in normal, ischemic, and reperfused tissue, and at the border of these segments. The left anterior descending artery was initially ligated below the second diagonal branch (first ligation) and 30 minutes later below the first diagonal branch (second ligation); the second ligation was released 30 minutes later. Conduction of electrically induced premature impulses from the midwall of the left ventricle was recorded at epicardial and endocardial sites. Conduction delay was measured from the stimulus artifact to the first high-frequency deflection in each zone in the anterograde (base to apex) and retrograde (apex to base) directions. Intravenous nifedipine 0.1 mg/kg was given over 10 minutes immediately after the first ligation. Nifedipine slightly decreased the magnitude of conduction delay in the ischemic myocardium at 15 minutes of ischemia, which corresponded with the peak plasma nifedipine level. However, conduction delay throughout the remainder of the study was essentially unaltered by nifedipine. In conclusion, though nifedipine may improve ischemic myocardial metabolism, infarct size, and hemodynamics, the effect on the electrophysiologic parameters affecting conduction was insignificant. This lack of any further deterioration in conduction in the ischemic and reperfused tissue by the drug further attests to its safety during acute myocardial ischemia.

Animals↗
PubMed1981

Effects of diltiazem on conduction of premature impulses during acute myocardial ischemia and reperfusion.

The effect of diltiazem on conduction of cardiac impulses was studied using premature impulses. Conduction times were measured in the epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion of the left ventricular anterior wall. In 16 dogs (8 control and 8 treated with diltiazem), the left anterior descending artery was occluded initially below the second diagonal branch and 30 minutes later below the first diagonal branch. Infusion of diltiazem (0.02 mg/kg per min) was begun at the time of the first ligation in the treated dogs. Conduction delay in normal, ischemic and reperfused myocardium and at the border of ischemia or reperfusion was compared in the two groups. In addition, treated and nontreated ischemic zones were analyzed in the diltiazem-treated group. Results show significantly less ischemia-induced conduction delay in the diltiazem-treated group in both ischemic myocardium and at the border of ischemia. This beneficial effect was seen in the ischemic segment in the treated dogs whether or not the medication was given before or after coronary ligation. Further, the effect of the drug on epicardial and endocardial conduction did not differ significantly. These data suggest that diltiazem may have potential value in the treatment of ventricular reentrant arrhythmias associated with acute ischemia over and above the well recognized hemodynamic and metabolic effects of calcium channel blocking agents.

Animals↗
PubMed1981

Relation between conduction delay and ventricular fibrillation: characteristics of conduction of premature impulses during acute myocardial ischemia.

Critical conduction delay has been shown to be the important factor in reentrant arrhythmias. To determine the causal relation between conduction delay and spontaneous ischemic ventricular fibrillation, conduction delay of induced premature ventricular impulses in the ischemic and the border zones of ventricular myocardium was investigated in 23 dogs. There were 8 control dogs, 9 dogs that manifested ventricular fibrillation within 30 minutes of ligation of the distal left anterior descending coronary artery (group I), and 6 dogs that manifested ventricular fibrillation between 30 and 60 minutes of ligation of the proximal left anterior descending coronary artery (group II). Conduction delay was measured as the change of conduction time from preligation levels to postligation levels in epicardial and endocardial sites in both base to apex (anterograde) and apex to base (retrograde) directions. Conduction delay in all four directions was compared in the control group and groups I and II (ventricular fibrillation). By means of continuous recordings on tape, the origin of ventricular fibrillation was determined to be in the ischemic zone (13 of 15 dogs) or in the border zone (2 of 15 dogs). Conduction delay in all directions was greater in the group with ventricular fibrillation whether the fibrillation occurred after the first or second ligation. Specifically, epicardial anterograde conduction (in the border zone) and retrograde conduction (in the ischemic zone) were significantly delayed in group I. Conduction in group II was significantly delayed in both the ischemic and the border zones in three of four directions at 35 minutes. The rate of change of conduction time in all four directions was significantly greater in the group with ventricular fibrillation than in the control group. Pending further work, this model may provide a reliable marker for the development of spontaneous ventricular fibrillation during acute myocardial ischemia and may permit assessment of various interventions as specific therapy for acute reentrant ischemic tachyarrhythmias leading to ventricular fibrillation.

Acute Disease↗
PubMed1981

Toxicity of aspartame and its diketopiperazine for Wistar rats by dietary administration for 104 weeks.

Aspartame (APM) or L-aspartyl-L-phenylalanine, and a 3 : 1 combination of APM with its decomposition product, 5-benzyl-3,6-dioxo-2-piperazine acetic acid (DKP), were incorporated at levels of up to 4 g/kg in the diet of male and female Wistar rats from 6 weeks to 104 weeks of age. There was a dose-dependent depression of body weight gain at 2 and 4 g/kg AMP and at 4 g/kg APM + DKP in males, and at all dose levels in females, correlated with decreased food consumption and attributed to liberation of amino acids from hydrolysis of APM. Increases in urinary specific gravity and pH, with increase of relative kidney weight, were attributed to the urinary excretion DKP and acidic metabolites of APM. A dose-related increase in urinary calcium probably reflected increased calcium absorption, as from high protein diets. A slight decrease in serum cholesterol and an increase in relative spleen weight appeared to be without adverse effect. It is concluded that the treatments were without toxic effect.

Animals↗