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Biomedical subjects

H Inoue

Publications and source records attributed to H Inoue.

At least 1,675 records · Page 93Linked to original sources
PubMed1987

Anatomic and clinical studies of the extensor digitorum brevis manus.

The extensor digitorum brevis manus muscle (EDBM) was found in 17 (3.0%) out of 559 dissected hands of 286 cadavers. The anatomy of the EDBM was classified into three types. The EDBM frequently arose on the distal margin of the radius, but without direct attachment to the carpal bones. The insertion of the EDBM was the same as that of the extensor indicis proprius. The EDBM and the extensor indicis proprius were often joined and had the same nerve and arterial supply. The EDBM muscle was considered to be a variant of the extensor indicis proprius muscle. Clinically five of 29 patients with an EDBM were treated.

Adult↗
PubMed1987

Intracoronary ethyl alcohol or phenol injection ablates aconitine-induced ventricular tachycardia in dogs.

The hypothesis whether localized ventricular tachycardia could be ablated by myocardial necrosis induced with chemical agents injected into a coronary artery was tested. In 59 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated either occlusively or nonocclusively. Localized ventricular tachycardia was induced by injecting approximately 0.01 ml of 30 micrograms/ml of aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch in 54 dogs. In eight untreated control dogs, aconitine-induced ventricular tachycardia lasted 10.2 +/- 2.3 minutes or degenerated into ventricular fibrillation after 7.0 +/- 4.0 minutes. In the remaining 46 dogs, 1 ml of saline solution, 25, 50 or 100% ethyl alcohol or 0.94 ml (mean [range 0.4 to 2.0]) of 25% phenol at room temperature was injected into the occluded coronary artery and 1 ml of 100% ethyl alcohol at body temperature was injected into the nonoccluded coronary artery. Ventricular tachycardia was eliminated in 9 (82%) of 11 dogs receiving phenol, 7 (88%) of 8 dogs receiving 100% ethyl alcohol occlusively, 6 (75%) of 8 dogs receiving 100% ethyl alcohol nonocclusively and 6 (67%) of 9 dogs receiving 50% ethyl alcohol for an entire follow-up period of 10 to 60 minutes. However, saline solution and 25% ethyl alcohol suppressed ventricular tachycardia only transiently in 8 (53%) of 15 and 3 (60%) of 5 dogs, respectively. Left ventricular end-diastolic pressure rose from 8.0 to 11.2 mm Hg (p less than 0.05) immediately after injection of 100% ethyl alcohol in seven dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aconitine↗
PubMed1987

In vivo stimulation of granulopoiesis by recombinant human granulocyte colony-stimulating factor.

Osmotic pumps containing Escherichia coli-derived recombinant human granulocyte colony-stimulating factor (rhG-CSF) were attached to indwelling jugular vein catheters and implanted subcutaneously into Golden Syrian hamsters. Within 3 days, peripheral granulocyte counts had increased greater than 10-fold with a concomitant 4-fold increase in total leukocytes. Microscopic examination of Wright-Giemsa-stained blood smears from rhG-CSF hamsters showed that only the neutrophil subpopulation of granulocytes had increased. No significant changes in lymphocyte or monocyte counts were observed during the course of continuous rhG-CSF treatment. After subcutaneous injection at rhG-CSF doses of up to 10 micrograms X kg-1 X day-1 only granulocyte counts were affected. However, at higher dose levels, a transient thrombocytopenia was noted. Erythrocyte had lymphocyte/monocyte counts remained unaffected by rhG-CSF over the entire dose range (0.3-300 micrograms X kg-1 X day-1) studied. Total leukocyte counts increased 3-fold within 12 hr after a single s.c. injection of rhG-CSF. This early effect was associated with an increase in the total number of colony-forming cells and the percent of active cycling cells in the marrow. A sustained elevation of peripheral leukocyte and marrow progenitor counts was observed following seven daily s.c. injections of rhG-CSF. The ability of rhG-CSF to increase the production and release of granulocytes from the marrow may underlie the beneficial effect it produced on the restoration of peripheral leukocyte counts in hamsters made leukopenic by treatment with 5-fluorouracil.

Animals↗
PubMed1987

Observation of fallout in Hiroshima caused by the reactor accident at Chernobyl.

Fallout from the reactor accident at Chernobyl has been surveyed at Hiroshima. gamma-rays from samples of aerosol, rain water and tap water were measured using low-background gamma-ray spectrometers and concentrations of activities were followed. Almost all of the nuclides detected in Europe were observed in Hiroshima. In addition to dominant volatile fission products of 131I, 132Te-132I and 103Ru, long-lived fission products 137Cs, 106Ru-106Rh, 125Sb and activities produced through the (n, gamma) process in the reactor such as 134Cs, 136Cs and 110mAg were observed in relatively high concentrations.

Accidents↗
PubMed1987

Identification of dimethyl disulfide-forming bacteria isolated from activated sludge.

Twenty-four strains with high dimethyl disulfide (DMDS)-forming ability were isolated from activated sludge and identified to the genus level. These bacteria were classified into four groups (A, B, C, and D) by the API ZYM System (API System S.A., Montalieu, France). Group A (three strains) was identified as genus Lactobacillus by the API 20B System, by the method of Cowan and Steel, and by production of lactic acid as confirmed by gas-liquid chromatography. Group B (eight strains) was identified as genus Corynebacterium by API 20B and the Cowan and Steel method. Group C (one strain) was suggested to belong to genus Corynebacterium by the API 20B System. Group D (12 strains) was identified as genus Pseudomonas or Alcaligenes by the API 20B System, as genus Alcaligenes by the Cowan and Steel method, and as Achromobacter group Vd by the API 20NE System. However, on the basis of guanine-plus-cytosine contents in DNA and form of flagella, these strains were identified as genus Pseudomonas. Formation of DMDS from DL-methionine and S-methyl-L-cysteine was tested. DMDS-forming bacteria isolated from activated sludge formed DMDS from both precursors. In genus Pseudomonas, P. aeruginosa could not form DMDS from either precursor, but P. acidovorans, P. alcaligenes, P. pseudoalcaligenes, and P. testosteroni formed DMDS. In genus Alcaligenes, A. denitrificans subsp. xylosoxydans, A. denitrificans subsp. denitrificans, A. faecalis, and A. odorans formed DMDS from both precursors. Achromobacter group Vd formed DMDS from S-methyl-L-cysteine, but could not from DL-methionine.

Alcaligenes↗
PubMed1987

Effect of digitalis on the diaphragm in anesthetized dogs.

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

Animals↗
PubMed1987

Possible sensory receptor of nonadrenergic inhibitory nervous system.

To determine the sensory receptor of the nonadrenergic inhibitory nervous system (NAIS), 22 cats were anesthetized and serotonin was continuously administered (50-250 micrograms.kg-1.min-1 iv) to increase pulmonary resistance (RL) to 377 +/- 57% (SE) of the control value. We then 1) mechanically irritated the trachea, 2) intravenously administered capsaicin (5 micrograms/kg), or 3) induced hypoxia (arterial PO2 30-40 Torr) to stimulate irritant and bronchial C-fiber receptors, pulmonary C-fiber receptors, or the carotid body (chemoreceptors), respectively. After treatment with atropine (3 mg/kg iv) and propranolol (2 mg/kg iv), the serotonin-induced change in RL was reduced by 58.6 +/- 14.3% by mechanical irritation and 63.3 +/- 12.1% by intravenous capsaicin. However, hypoxia produced no dilatation of the airways. In further experiments, we employed capsaicin inhalation to stimulate bronchial C-fiber receptors. Inhaled capsaicin (0.1%, for 5 breaths) also reduced RL by 79.2 +/- 9.2% of the elevated value, after atropine and propranolol. Treatment with a ganglionic blocking agent, hexamethonium (2 mg/kg iv), abolished bronchodilator responses, implying that a reflex pathway through vagal nerves is involved in this phenomenon. These results suggest that pulmonary and bronchial C-fiber receptors may be involved as sensory receptors in NAIS reflex bronchodilatation.

Airway Resistance↗
PubMed1987

Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.

Latex-induced transmural myocardial infarction or epicardial application of phenol interrupts sympathetic fibers innervating myocardium apical to the infarction or to the phenol-painted area. These denervated regions subsequently show supersensitive shortening of effective refractory period (ERP) in response to the infusion of norepinephrine (denervation supersensitivity). The purpose of this study was to test the hypothesis that such denervation supersensitivity is arrhythmogenic. Ventricular arrhythmias were elicited by programmed ventricular stimulation (PVS) during a control period, during bilateral stimulation of the ansae subclaviae (4 msec pulses, 4 Hz and 3 mA), and during the infusion of norepinephrine (0.5 microgram/kg/min). Study groups consisted of 14 sham-operated dogs, 16 dogs with phenol painted over a diagonal branch, 13 dogs with latex embolization of a diagonal branch that resulted in transmural myocardial infarction, 14 dogs with a one-stage ligation of a diagonal branch producing nontransmural myocardial infarction, and 12 dogs undergoing both phenol painting and one-stage ligation of a diagonal branch. Four to 22 days after the first operation, PVS was performed in anesthetized, open-chest dogs after neural decentralization of the heart. Dogs with phenol painting on the epicardium and dogs in which latex was injected into a diagonal branch showed supersensitive shortening of ERP to infused norepinephrine at apical sites. PVS resulted in ventricular fibrillation more often during stimulation of the ansae subclaviae (p less than .001) and infusion of norepinephrine (p less than .001) than during the control state in dogs treated with phenol alone. The incidence of ventricular fibrillation was highest in dogs with ligation-induced infarction that received phenol compared with all other groups during control (p less than .001), stimulation of the ansae subclaviae (p less than .002), and the infusion of norepinephrine (p less than .01). Propranolol (0.5 mg/kg or 10 mg iv at maximum) attenuated supersensitive shortening of ERP and decreased the incidence of induction of ventricular fibrillation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Denervation supersensitivity of refractoriness in noninfarcted areas apical to transmural myocardial infarction.

Denervation supersensitivity was demonstrated in anesthetized dogs 5 to 10 days after transmural myocardial infarction produced by latex embolization of a diagonal branch of the left anterior descending coronary artery. Sympathetic efferent denervation in noninfarcted myocardium apical to the infarction was demonstrated by a 90% depletion of myocardial norepinephrine content in the apical (45 +/- 15 pg norepinephrine/g tissue) vs basal (437 +/- 76 pg/g tissue) regions and by the lack of effective refractory period (ERP) shortening during bilateral ansae subclaviae stimulation in 34% of sites apical to the infarction. Supersensitivity in the area apical to the infarction was manifested by an exaggerated shortening of the ERP during both norepinephrine and isoproterenol infusions, with an upward and leftward shift in the dose-response curves in the apical vs basal regions (p less than .001). The cellular mechanism for denervation supersensitivity did not involve detectable changes in the beta-adrenergic receptor adenylate cyclase system. There was no difference in the density of beta-adrenergic receptors ([125I]-cyanopindolol) in the apical (268.6 +/- 22.7 fmol/mg protein) vs the basal (253.5 +/- 24.8 fmol/mg protein) regions. Adenylate cyclase activity stimulated by guanosine triphosphate plus isoproterenol was slightly greater in the apical (58.7 +/- 17.4%) than in the basal (49.6 +/- 10.9%) region, but this difference did not reach statistical significance (p = .068). Muscarinic modulation of beta-receptor coupling (oxotremorine attenuation of guanosine triphosphate plus isoproterenol-stimulated adenylate cyclase activity) also was not significantly different at the apical (31.6 +/- 17.5% inhibition) and basal (21.4 +/- 20.9% inhibition) sites. These data show that a transmural myocardial infarction produces denervation supersensitivity in areas apical to the infarction, but in this preparation no differences in the total number or a redistribution of beta-adrenergic receptors or adenylate cyclase activity were detected.

Adenylyl Cyclases↗
PubMed1987

Conduction over an isthmus of atrial myocardium in vivo: a possible model of Wolff-Parkinson-White syndrome.

Antiarrhythmic drugs appear preferentially to prolong refractoriness of accessory pathways compared with atrial or ventricular muscle in patients with the Wolff-Parkinson-White syndrome. This response may be due to intrinsic properties of accessory pathways or to depressed conduction associated with a narrow strip, or isthmus, of tissue. To test the latter possibility, in 16 anesthetized dogs we surgically isolated a portion of the right atrial myocardium in the form of an ellipse (10 to 25 X 8 to 15 mm). The ellipse was connected to the body of the right atrium by a narrow isthmus (cross-sectional area [CSA] 1 to 13.5 mm2) and was perfused by the sinus node artery or its branch. Diastolic threshold (mean +/- SE 0.16 +/- 0.05 vs 0.13 +/- 0.02 mA) and effective refractory period (ERP; 144 +/- 4 vs 139 +/- 5 msec) were the same proximal and distal to the isthmus. In eight dogs, determination of the ERP of the isthmus was limited by the ERP of the atrial tissue proximal and distal to the isthmus, and the CSA of the isthmus in these dogs was significantly larger than that in the remaining seven dogs in which the ERP of the isthmus could be determined (7.4 +/- 1.4 vs 3.2 +/- 0.6 mm2, p less than .05). The shortest pacing cycle length (PCL) with 1:1 conduction from the proximal to the distal segments did not differ from that in the opposite direction in 16 dogs (154 +/- 9 vs 153 +/- 7 msec). The CSA of the isthmus correlated inversely with the shortest PCL with 1:1 conduction in both directions via the isthmus (r = -.84, p less than .01). Vagal stimulation shortened the shortest PCL with 1:1 conduction from the distal to the proximal segment (153 +/- 14 vs 143 +/- 12 msec, p less than .02), but not in the opposite direction. Procainamide (10 to 20 mg/kg iv, serum concentration 8.6 +/- 0.8 micrograms/ml) prolonged the ERP of the proximal site from 145 +/- 5 to 170 +/- 5 msec (p less than .001), the ERP of the distal site from 143 +/- 6 to 168 +/- 6 msec (p less than .001) in 12 dogs, and the shortest PCL with 1:1 conduction (proximal to distal from 149 +/- 8 to 204 +/- 17 msec, p less than .001; distal to proximal from 149 +/- 7 to 197 +/- 12 msec, p less than .001) in 14 dogs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Changes in atrial and ventricular refractoriness and in atrioventricular nodal conduction produced by combinations of vagal and sympathetic stimulation that result in a constant spontaneous sinus cycle length.

The vagal nerves modulate adrenergic effects on sinus cycle length, atrioventricular (AV) nodal conduction, and refractoriness of atria and ventricles. We tested whether varying levels of vagal-sympathetic input could yield the same spontaneous sinus cycle length but also alter effective refractory periods of the right atrium, right ventricle, and left ventricle and AV nodal conduction times. Dogs anesthetized by alpha-chloralose were studied in the open-chest, neurally decentralized state. In 10 dogs, sinus cycle length was maintained constant during 3 levels of bilateral ansae subclaviae stimulation (4 msec, 3 mA at 1, 2, and 4 Hz) by titrating simultaneous bilateral vagal stimulation (varying pulse width and frequency). Each combination of ansae subclaviae-vagal stimulation yielded the same sinus cycle length as the control value, but refractory periods of right atrium and right and left ventricles shortened progressively as the frequency of ansae subclaviae stimulation increased. Atrioventricular nodal conduction time (AH interval) shortened in 2 dogs and lengthened in 3 dogs. His-Purkinje conduction time (HV interval) was unchanged. In 9 dogs, the effect of simultaneous unilateral ansae subclaviae stimulation at 2 Hz and ipsilateral vagal stimulation that yielded the same sinus cycle length were determined. Right-sided ansae subclaviae-vagal stimulation shortened refractoriness of right atrium and anterior left ventricle significantly. The AH interval lengthened in 1 dog. Left ansae subclaviae-vagal stimulation shortened the refractory periods of anterior and posterior left ventricle significantly and reduced the AH interval in 3 dogs. In 8 dogs, the effects of bilateral ansae subclaviae stimulation alone at 2 Hz, vagal stimulation alone at an intensity required to keep the sinus cycle length constant during ansae subclaviae stimulation, and simultaneous bilateral ansae subclaviae and vagal stimulation were tested. The right atrial refractory period was shortened significantly by ansae subclaviae stimulation alone and by vagal stimulation alone and was shortened further by simultaneous stimulation of both autonomic limbs. The right and left ventricular refractory periods were shortened by ansae subclaviae stimulation alone and by simultaneous stimulation of both limbs but tended to be prolonged by vagal stimulation alone and when added to ansae subclaviae stimulation. In 7 dogs, the effects of simultaneous stimulation of bilateral ansae subclaviae at 2 Hz and vagi at intensities that maintained the AH interval constant at an atrial pacing cycle length of 300 msec were determined.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗