[His bundle electrocardiogram].
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Biomedical subjects
Publications and source records attributed to K Hirao.
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An intracardiac electrophysiologic study was performed in a patient with paroxysmal tachycardia. The patient had two previous episodes of myocardial infarction, but abnormal Q waves were absent in previously obtained electrocardiograms. Electrocardiographic diagnosis of inferior and anterior infarction was made because the electrocardiogram taken on admission temporarily showed abnormal Q waves. Atrioventricular reentry with anterograde conduction over a fasciculoventricular Mahaim fiber and retrograde conduction over a concealed Kent bundle was observed during the tachycardia. It was also demonstrated that electrocardiographic masking of the Q waves was caused by conduction over a fasciculoventricular Mahaim fiber.
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Tissues from 12 patients with gastric ulcers, 50 patients with gastric carcinoma, and 2 normal subjects who died suddenly were examined immunohistochemically with antiserum against the beta-subunit of human chorionic gonadotropin. Human chorionic gonadotropin-beta-immunoreactive cells were present in the neck portion of the pyloric and pseudopyloric glands of normal and inflammatory gastric tissue. Gastric cancers located in the antrum-pylorus and the cardia were frequently associated with human chorionic gonadotropin immunoreactivity. These findings indicate that human chorionic gonadotropin-producing cells normally exist in the gastric mucosa, especially in the pylorus. It is speculated that normal human chorionic gonadotropin-producing cells may give rise to cancer in certain cases.
A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.
The presence or absence of ventriculoatrial (VA) conduction in the human heart is assessed by investigating whether 1:1 retrograde atrial capture is observed during constant cycle length ventricular pacing. In this study, a new pacing protocol for assessing VA conduction was designed in which the ventricular extrastimulus was delivered during basic ventricular and atrial simultaneous pacing (VE-VASP method). The effect of this pacing protocol on VA conduction was investigated in 12 patients who showed no evidence of VA conduction with the constant cycle length ventricular pacing method. In 5 of 12 patients, intact VA conduction was demonstrated with the VE-VASP method, while VA conduction was not observed in the remaining 7 patients. These results suggest that VE-VASP method sometimes demonstrates the presence of intact VA conduction in patients who show no evidence of VA conduction during constant cycle length ventricular pacing.
Injection technique, advantages, disadvantages and main indications of DSA were briefly described and discussed. Advantages of DSA: (1) relatively noninvasive, (2) can be performed on an outpatient basis, therefore "cost-effective", (3) real time observation possible. Disadvantages of DSA: (1) limited spatial resolution, (2) artefacts, (3) small visual field. Main indications of DSA: (1) diagnosis and follow up study of vascular diseases, (2) evaluation of patency of by-pass graft, (3) functional assessment (of cardiac output and blood flow etc.). Aortic aneurysms, occlusive changes of the carotid or renal arteries are particularly well demonstrated by DSA. Because of three drawbacks mentioned above, DSA is not a good technique for the diagnosis of neoplasms. Although it is possible to visualize hypervascular tumors by DSA, informations obtained by DSA in cases of neoplasms are limited.
Clinicopathological, radiological, and histological studies were performed on urinary bladder neoplasia induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in five adult beagle dogs and in ten adult mongrel dogs. Tumors of the urinary bladder developed in dogs given various daily doses of BBN p.o. for different periods. The latent period of tumor induction was 4 years in dogs receiving a daily dose of 80 mg of BBN, 2 to 2.5 years in dogs receiving a daily dose of 160 mg of BBN, and 1.5 years in dogs receiving a daily dose of 240 mg of BBN. The total dose of BBN ingested by the dogs until the first tumors were observed by urological examinations was nearly the same in all groups, 100 to 140 g. These results suggest that there is a correlation between dose and induction time, but further dose-response studies are required. Histologically, tumors of the urinary bladder were transitional cell papillomas or transitional cell carcinomas resembling morphologically those found in human cases. It is possible to observe the process of development of urinary bladder tumors from initial lesions to invasive tumors using routine urological examinations. We believe that this experimental model is valuable for clinicopathological studies of urinary bladder tumors.
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Six groups of female outbred Wistar rats were subjected to the following treatments: 2,500 ppm 3-amino-1H-1,2,4-triazole (amitrole) administered in the drinking water (group I); partial thyroidectomy and administration of amitrole in the drinking water (group II); partial thyroidectomy plus autoimplantation of resected thyroid tissue plus administration of amitrole in the drinking water (group III); no treatment (control of group I) (group IV); partial thyroidectomy without amitrole administration (control of group II) (group V); or partial thyroidectomy plus autoimplantation of resected thyroid tissue without amitrole administration (control of group III) (group VI). Goiters developed in all rats given amitrole (groups I-III). Invasive growth of the proliferating follicular tissue through the capsule into adjacent fatty tissue and of pericapsular blood vessels was frequent in these groups (P less than 0.001); invasive lesions were more frequent in the lobectomized thyroid glands of rats (groups II and III). Seven papillary adenomas composed of atypical cells with hyperchromatic nuclei and many mitoses were found in the thyroid glands and grafts in amitrole-treated groups I-II. No invasive growth or adenomas appeared in the control rats of groups IV-VI. Cholangiofibrosis developed in 5 of 100 rats in groups I-III.
Histological types and grades of 613 urinary bladder cancers induced in rats by N-butyl-N-(4-hydroxybutyl) nitrosamine(BBN) were analyzed. Most of them (95.1%) were transitional cell carcinomas, the remainder being squamous cell carcinomas (3.3%), undifferentiated carcinomas (2.5%), and carcinosarcomas (0.3%). Among the transitional cell carcinomas, 23.3% were Grade I anaplasia, 55.2% Grade II, and 21.5% Grade III. Among the squamous cell carcinomas, 20% each were Grade I and II, and 60% Grade III. Most of the undifferentiated carcinomas were Grade III. Some of the cases of transitional cell carcinoma had areas of squamous metaplasia and/or glandular metaplasia, and the incidence of metaplasia increased with the grade of anaplasia. Approximately 36% of the cases of transitional cell carcinoma were of the invasive type. Invasive types were twice as numerous among cases of squamous cell carcinoma as among those of transitional cell carcinoma and all of undifferentiated carcinomas were invasive. The incidence of invasive type was closely related to the grade of anaplasia. These results show that the morphological characteristics of urinary bladder carcinomas induced by BBN in rats are similar to those seen clinically in humans.
The effects of prolonged p.o. administration of quinoline or 2-chloroquinoline on rat liver were examined histologically. Hepatocellular carcinomas and hemangioendotheliomas were observed in the livers of rats fed a basal diet containing 0.05, 0.10, or 0.25% quinoline for about 16 to 40 weeks. However, no neoplastic changes were seen in the livers of rats fed a basal diet containing 0.05, 0.10, or 0.25% 2-chloroquinoline for 40 weeks. In groups that received low concentrations of quinoline, the incidences of hepatocellular carcinomas were higher and the incidences of hemangioendotheliomas were lower than in the group that received a high concentretion of quinoline. The liver tumors induced by quinoline were classified histologically as hemangioendotheliomas or hemangiosarcomas and trabecular hepatocellular carcinomas. Typical nodular hyperplasias were occasionally seen in the livers of rats treated with quinoline. 2-Chloroquinoline did not induce any nodular hyperplasia or other neoplastic changes, but it caused diffuse fatty changes of parenchymal cells. Oval cell infiltration and bile duct proliferation were slight or moderate. Cirrhotic changes were rare in the livers of rats treated with either quinoline or 2-chloroquinoline. The serum levels of glutamic oxaloacetic transaminase and alkaline phosphatase were slightly changed in groups treated with quinoline, but no other remarkable changes were detected.
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Histological studies were made on the nephrotoxic effect of citrinin on the kidneys of rats, with or without previous treatment with the nephrotoxic chemicals, N-(3,5-dichlorophenyl)succinimide (NDPS) and N-nitrosodimethylamine (DMN). Oral administration of 0.02% or 0.05% citrinin alone caused signs of kidney injury but did not induce kidney tumors. On treatment with DMN alone, 8 of 14 rats (57.1%) developed kidney tumors; two (14.3%) were renal cell tumors, eight (57.1%) embryonal cell tumors, and one (7.1%) hemangioendothelioma. On the other hand, kidney tumors developed in 18 of 19 rats (94.7%) and 13 of 15 rats (86.7%) by the administration of 0.02% and 0.05% citrinin, respectively, after DMN. The tumors in these two groups were diagnosed histologically as renal cell tumors in 18 (94.7%) in group IV and 13 (86.7%) in group III, and as embryonal cell tumors in 14 (73.7%) in group IV and 9 (60.0%) in group III. Thus, in groups treated with citrinin after DMN the incidence of renal cell tumors was much greater and the incidence of embryonal cell tumors slightly greater than in the group treated with DMN alone. Kidney tumors developed in 4 of 18 rats (22.2%) treated with 0.02% citrinin after NDPS, but treatment with NDPS alone did not induce kidney tumors. Thus, treatment with citrinin changes the histological type and incidence of kidney tumors in rats induced by DMN. Moreover, this study confirms that citrinin in combination with NDPS can induce kidney tumor in rats, which was renal cell tumor (adenoma) histologically.
The tumorigenic effect of a diet containing the alpha-isomer of benzene hexachloride (alpha-BHC) on the liver of various animals was examined. It was found that alpha-BHC induced liver tumors in male and female mice but not in rats or hamsters in the present observations. Histological changes in the liver of mice induced by alpha-BHC were also much greater than those induced in rats or hamsters. Male animals were more susceptible to the tumorigenic action of alpha-BHC than females. Among different strains of mice, the DDY showed greatest susceptibility and the C57BL/6 showed the least. Induction oflpha-BHC was not inhibited by concomitant feeding of 1-naphthyl isothiocyanate or p- hydroxypropiophenone. However, 3-methylcholanthrene slightly inhibited their induction by alpha-BHC.