[Anatomical principles of the coronary artery].
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Biomedical subjects
Publications and source records attributed to R Okada.
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The homolog of the dnaA gene, which has been reported to be present in the vicinity of the initiation site of replication in the genome of Mycoplasma capricolum (M.Miyata, L.Wang, and T.Fukumura, J. Bacteriol. 175: 655-660, 1993) was mapped precisely. A 9540-bp region containing the dnaA gene was cloned and the entire region was sequenced with the exception of a previously reported region of 2517 bp (Fujita, M.Q., Yoshikawa, H. and Ogasawara, N. Gene 93: 73-78, 1992). The organization of the 9540-bp region was compared with that of corresponding regions in other bacteria. The arrangement and directions of rnpA, rpmH, dnaA, dnaN were conserved, but no other open reading frames were found that were homologous to those that are commonly found around dnaA genes in other bacteria. The directions of movement of the replication fork around the dnaA gene were analyzed by neutral/alkaline two-dimensional gel electrophoresis. The forks developed in a 1569-bp region that consisted of the dnaA structural gene and its downstream non-coding region, and then they proceeded bidirectionally.
Using the new J-2-N strain of cardiomyopathic hamster obtained by cross-breeding Bio 14.6 and Golden hamsters, we investigated the three-dimensional distribution of ventricular myocardial fibrosis and compared it with electrocardiographic (ECG) changes. Twelve-lead ECG recordings were made by our own method. The hearts were cut into serial sections and subjected to light microscopic examination. The distribution, density, and volume of myocardial interstitial fibrosis and replacement fibrosis due to myocardial degeneration (F%) were visualized three-dimensionally using the TRI system (TRI; Three-Dimensional Reconstruction Image; Ratoc System Engineering, Tokyo, Japan). Thirty-two J-2-N hamsters were divided into two groups; one group comprised 17 animals with normal hearts and normal ECG findings similar to those of Golden hamsters, and the other group of 15 hamsters had dilated hearts and abnormal ECG findings. In the normal hearts, the F% values for the right ventricle, left ventricle, and ventricular septum were 6.4 +/- 0.94, 6.5 +/- 0.95, and 6.5 +/- 0.98 (mean +/- SD), respectively. The dilated hearts showed marked fibrosis, which was distributed mainly in the middle layer of the left ventricle and the ventricular septum. The corresponding F% values for the hamsters with cardiac enlargement were 19 +/- 2.6, 19 +/- 1.8, and 22 +/- 3.2 (mean +/- SD), respectively. Replacement of myocytes by fibrosis seemed to correspond to abnormal Q waves in the anterior chest leads and left axis deviation of the QRS complex.
Biopsy specimens were obtained from the anterior wall of the left ventricle during aortocoronary bypass surgery in 79 patients with critical narrowing or occlusion of the left anterior descending artery. The percent of fibrous replacement on histological analysis was calculated using the point-count method and compared with electrocardiographic findings in the precordial leads. In specimens from 19 patients with abnormal Q waves, the percent of fibrosis ranged between 38% and 100% (mean, 61 +/- 17%). Fifteen patients had small q waves or decreased r waves, and the percent of fibrosis in these patients ranged between 20% and 45% (mean, 38 +/- 10%). Specimens from 45 patients with normal QRS complexes had between 3% and 27% (mean, 11 +/- 5%) fibrosis of the entire thickness of the anterior wall. Thus, small q waves or decreased r wave amplitude in the precordial leads indicates a lesser degree of myocardial loss than the presence of abnormal Q waves.
Kindling stimulation was applied to the basolateral amygdala of adult rats, and the density of dendritic synapses was examined under the electron microscope in the medial amygdaloid nucleus (MAN) contralateral to the site of stimulation, and an unfolding correction of biasedness was made. When generalized motor seizures had been induced for 5 days consecutively, the kindling was considered to be complete. The number of dendritic synapses, but not the number of somatic synapses, was markedly decreased in the MAN of the kindled rats. Reductions in numbers were marked in the case of both dendritic shaft and spine synapses. The reductions in numbers of shaft and spine synapses were similarly evident in the MAN of kindled rats 100 days after stimulation was discontinued. The numbers of dendritic synapses were similarly decreased in the rats that received additional bouts of stimulation subsequent to the completion of kindling. Thus, once the kindling was completed, the newly acquired synaptic connectivity was preserved in the MAN. These findings indicate that the remodeling of synaptic connectivity was a morphological correlate of the kindling in the MAN.
To demonstrate innervation in human atrioventricular valves, we examined the tricuspid and mitral valves of apparently normal autopsied hearts of four men (ages ranging from 50 to 74 years). Whole valve tissues were stained for acetylcholinesterase by a histochemical method. Acetylcholinesterase-positive nerve fibers with a diameter of 2 to 5 microns were distributed widely in the deep atrialis of the atrioventricular valves and partly in the fibrosa. The nerve fibers formed a network or plexus from the base to the anatomical edge of the valves. Meshes of the nerve fiber network were more dense towards the base and at the commissure than either towards the edge or at the body. Thicker nerve fibers, which were interspersed coarsely in the leaflets, were intercalated by special varicose apparatuses at a few sites in their long running course. On the contrary, thinner nerve fibers which were distributed abundantly, ended, as a rule, in small dotor brush-like formations. Approximately half of the chordae tendineae were innervated by the nerve fibers. The mode of vagal innervation suggests that the nerve system may assist valve movement by moderating myocyte contraction in the valve base and change valve structure by sensing a stress in the valves.
The protective effect of N-acyl amino acids (NAAs) against cephaloridine (CER)-induced nephrotoxicity was studied in rabbits. A large single intravenous dose of CER (more than 100 mg/kg) induced severe proximal tubular necrosis. Simultaneous treatment with several NAAs (at dosages of 100, 200 mg/kg, etc., i.v.), such as N-benzoyl-beta-alanine (NBBA), N-benzoyl-6-aminocaproic acid, and N alpha,epsilon-dibenzoyl-D,L-lysine, remarkably suppressed the histopathological damage in the kidney induced by CER. NAAs have generally low toxicity in laboratory animals (e.g., the LD50 of NBBA was more than 3,000 mg/kg, i.v. in rats), and NAAs were suggested to be good candidates for reducing the nephrotoxicity of CER and other beta-lactam antibiotics.
Vasoreactivity of laser-treated vessels was investigated in two different experimental conditions. The canine left circumflex coronary artery (LCx) was lased under perfusion with Krebs-bicarbonate buffer by means of a thermal laser (hot-tip probe, HT) at 7 W for 6 seconds and an argon laser beam through a 300 microns optical fiber at 3 W (tip power) for 1 second at 12 spots. A nontreated segment of the LCx served as a control. Two 3-mm long segments were obtained from the treated segment: one to measure the results of potassium (K) induced contraction, and another 3, 4 diaminopyridine (DAP; K channel inhibitor) induced contraction. In 11 instances, coronary angiography of the perfused artery showed less than 50% stenosis after laser treatment. The segments were then mounted isometrically with 1 g tension in Krebs-bicarbonate buffer. Contraction was induced either with 30 mM KCI or 10(-2) M DAP and expressed as developed tension (gram; g). KCI induced vasocontraction of 4.15 +/- 0.93 g in the control, 0.33 +/- 0.71 g in laser irradiated segments (P < 0.0001 vs control), and 0.02 +/- 0.06 g in thermally-treated segments (P < 0.0001 vs control). DAP induced vasocontraction of 5.21 +/- 1.32 g in the control, 0.39 +/- 0.83 g in laser irradiated segments (P < 0.0001 vs control), and 0.07 +/- 0.13 g in thermally treated segments (P < 0.001 vs control). In 4 instances, more than 50% stenosis remained and additional balloon dilatation reduced the stenosis to less than 50%. The lesions also showed reduced vasoreactivity. In vivo thermal angioplasty resulted in reduced vasoreactivity compared to control in 4 anesthetized dogs. Thus, laser and thermal angioplasty reduced vasoreactivity induced by either KCI or 3, 4 DAP. Neither acetylcholine at 10(-6) M nor papaverine at 10(-4) M was able to induce relaxation of treated segments. In conclusion, 1) the lased coronary artery loses its vasoreactivity to either a constrictive or relaxing agent, 2) although stenosis may be produced by laser energy, additional balloon dilatation can reduce residual stenosis, and 3) laser thermal or argon laser angioplasty may prevent severe coronary spasm.
We report the case of a 42-year-old male who suffered from ventricular fibrillation (VF) without obvious QT prolongation. His electrocardiogram showed incomplete right bundle branch block (IRBBB) and persistent ST segment elevation in the right precordial leads during sinus rhythm. Cardiac catheterization revealed no overt heart disease except moderate endocardial and subendocardial fibrosis in the left ventricle. Mental stress seemed to trigger VF, and ST elevation became prominent just before VF. Propranolol and mexiletine have been effective in preventing VF for over 3 years.
An 81-year-old female patient with an 8-year history of Parkinson's disease was hospitalized because of aspiration pneumonia. The clinical course of her pneumonia was prolonged because of dysphagia with a short period of remission, and she required a long period of bed rest. She received supportive nutrition via a nasogastric tube and many peroral medications that consisted of 3 anti-Parkinsonian drugs and 5 anti-bacterial or anti-tussive agents. Six months after admission, she vomited fresh blood through the nasogastric tube, then went into hypovolemic shock. Hemodynamic stability was temporarily achieved by blood transfusion. Gastroduodenal endoscopic examination could not reveal the exact bleeding site because of massive blood clots. Five days later, the patient died of a massive hematemesis. Autopsy revealed 2 chronic longitudinal ulcers, each 1.7 x 0.4 cm in size, in the upper portion of the esophagus. One of them had developed a fistula to the aorta. Neither esophageal carcinoma nor a foreign body was detected around the fistula. Atherosclerosis of the aorta was mild and the perforation channel was covered with the esophageal epithelium. The fistula was assumed to be a product of local esophageal injury due to drug retention.
Chronological changes in the incidence of valvular heart disease (VHD) in Japan were studied. The VHD data were obtained from the 1969 and 1986 editions of the Annual of Pathological Autopsy Cases in Japan and were categorized in 5 groups: rheumatic (RVD), sclerotic (SVD), inflammatory including infection (IE), congenital (CVD), and other valvular diseases (OVDs). Comparison of actual autopsy data for 1968 and 1985 revealed that total numbers of VHD were 697 in 1968 and 987 in 1985. The percentage incidences of VHD for all autopsy cases were 2.8% and 2.5%, respectively. Changes in VHD incidence were as follows: RVD 0.96% in 1968/0.92% in 1985; CVD 0.36%/0.21%; SVD 0.15%/0.27%; IE 0.16%/0.27%; mitral valve prolapse (MVP) 0.004%/0.045%. The total numbers of VHD, and the incidence of RVD and CVD decreased, while the incidence of SVD, IE, and MVP increased. The RVD decrease is compatible with previous reports. In contrast, the increase in the incidence of IE is paradoxical since there was an increase in the variety of antibiotics available in 1985. The higher incidence might be due partially to immune compromised host, artificial heart valves, and other similar factors. The increase in SVD may be due to the steady increase in the elderly population.
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1. Single comb white leghorn laying hens were given diets with additional mould, Mucus circineloides, containing gamma-linolenic acid (GLA) at levels of 0, 2.59 and 5.06 g GLA/kg diet ad lib. for 2 weeks and serum lipid contents were determined in experiment 1. 2. Serum low density lipoprotein and chylomicron levels were significantly reduced with the increase of dietary GLA levels. Serum triglyceride and cholesterol tended to be lowered by dietary GLA, but not significantly different. 3. Effects of mould GLA and extracted oil GLA on the egg yolk cholesterol concentration and fatty acid composition were compared in experiment 2. Both mould GLA and extracted oil GLA diets containing 5.32 and 4.71 g GLA/kg diet were given ad lib. for 2 weeks. 4. Yolk cholesterol content was not affected by dietary GLA sources. Content of GLA in the yolk was not altered, although that of arachidonic acid was enhanced by dietary GLA supplementation, particularly by the extracted oil GLA. 5. It is suggested that GLA is rapidly metabolized to arachidonic acid in the body and incorporated into the yolk.
We report a case of a degenerative approach lesion in an 83-year-old male with diabetes mellitus, hypertension, and ischemic heart disease. His ECGs changed from first-degree atrioventricular (AV) block 14 years ago, to third-degree AV (A-H) block. A pacemaker was implanted for bradycardia. He died 4 years later from heart and renal failure. Serial sections through the conduction system revealed total depletion and fatty replacement of the atrial muscle at the approaches to the AV node.
We report the case of a neonate with a rare association of tetralogy of Fallot and aortic valve stenosis, who died following percutaneous balloon valvuloplasty. Postmortem examination confirmed a tetralogy of Fallot morphology with a markedly hypoplastic pulmonary tree, hypertrophy of both ventricles, and a thickened and dysplastic aortic valve. Valvuloplasty was not effective despite the presence of a fissure in the cusp. The findings suggest that the left ventricular impairment and associated anomalies, with or without a dysplastic valve may contribute to the failure of balloon valvuloplasty in neonates with critical aortic valve stenosis.
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