Biomedical subjects

M Kinjo

Publications and source records attributed to M Kinjo.

At least 55 records · Page 3Linked to original sources

PubMed1992

[Utricular papillomatosis. A case report].

A case of utricular papillomatosis is reported herein. A 50-year-old male patient consulted our hospital with a complaint of asymptomatic macrohematuria. Endoscopic examination revealed papillomatous tumor tightly growing within the utricle. Transurethral resection of the tumor was performed. Histopathologically, the tumor consisted of numerous villous structures with slender fibrovascular cores and overlying cuboidal cells in 2 to 3 cell layers. Invasive growth or cellular atypia could not be found. Utricular papillomatosis is rare, and only one similar case was reported to my knowledge in the English literature for the last five years. Such rarity and peculiar clinicopathological characteristics prompted us to report this case.

Humans↗

PubMed1991

Changes in phospholipid constituents in mitochondrial membranes after long lasting exercise in rat heart.

Phosphatidylethanolamine, phosphatidylcholine and cholesterol were found to be significantly decreased to 44, 56 and 54% of the control values (p less than 0.001, 0.05 and 0.05, respectively), in cardiac mitochondria from rats which were made to swim bearing a weight representing 3% of body weight for 3 or more hours in water at 35 degrees C. The ratio of cholesterol to phospholipid did not change. Membrane viscosity tended to decrease very slightly. Steady-state anisotropy at infinite time, fluorescence life time and wobbling angle of phospholipids showed no significant change. Electron-microscopy showed no clear morphological damage, swelling or hypertrophy of cardiac mitochondria after long lasting exercise. The number of mitochondria was found to be increased by 19% in the long lasting exercise group compared with the control group. It was noteworthy that the dynamic microstructure and electron-microscopic structure of the cardiac mitochondria remained unaltered despite the remarkable changes in the phospholipid constituents.

Animals↗

PubMed1991

Renal oncocytoma developed in a long-term hemodialysis patient.

A case of renal oncocytoma which developed in a 38-year-old Japanese woman after 7 years of maintenance hemodialysis is reported. An encapsulated round tumor with a diameter of about 5 cm was incidentally discovered by abdominal echography. This is the first case of renal oncocytoma found in a long-term hemodialysis patient. Identification and differentiation of this subgroup from renal carcinomas are very important because of its benign nature. Careful clinicopathological investigation of renal tumors should therefore be required in hemodialysis patients.

Adenoma↗

PubMed1991

Dynamic microstructure of mitochondrial membranes from rabbit heart subjected to reperfusion after ischemia.

The effects of ischemia combined with reperfusion on the dynamic microstructure of mitochondrial membranes were studied in the hearts of anesthetized open-chest rabbits by means of time-resolved fluorometry. The fluorescence of diphenyl hexatriene (DPH) and its anisotropic decay were used to calculate membrane viscosity, wobbling angle of phospholipids and fluorescence life time. The anterior descending branch of the coronary artery was occluded for 15 min and reperfused for 15 min. Mitochondria from the area of the left ventricular wall exposed to ischemia-reperfusion and from an unexposed control area were separately isolated in 8 rabbits. For comparison, mitochondria from ventricular wall exposed to ischemia but not to reperfusion were obtained from 5 rabbits. The membrane viscosity increased from 0.44 to 0.49 poise and the wobbling angle of phospholipids tended to decrease from 59 to 56 degrees at 37 degrees C. The amount of peroxidized lipid rose from 1.5 to 4.3 nmol/mg-protein as expressed with MDA in the mitochondria exposed to ischemia-reperfusion. The fluorescence life time of DPH was slightly longer in the latter than in mitochondria from the control area. None of these parameters was altered in mitochondria exposed only to ischemia. The increase in viscosity observed in mitochondria from the ischemic-reperfused area probably produces a decrease in the diffusion of molecules through mitochondrial membranes. The concurrent tendency of the decrease in wobbling angle of membrane phospholipids suggests a decrease in the size of molecules which can permeate membranes. Limitations in diffusion will affect the metabolic activity of mitochondria and finally, overall cardiac function.

Animals↗

PubMed1991

Protective effects of idebenone against alterations in dynamic microstructure induced by lipid peroxidation in rat cardiac mitochondria.

The antioxidative effect of idebenone was studied in isolated mitochondria from the rat heart. Variables for dynamic microstructure, membrane viscosity and wobbling angle of phospholipids, were measured by means of a nanosecond time-resolved fluorometer. Exposure of isolated cardiac mitochondria to oxidative conditions in vitro caused significant alterations in lipid peroxidation, wobbling angle of phospholipids and membrane viscosity. Exposure of mitochondria to oxidative conditions after idebenone pretreatment resulted in no significant alterations in membrane viscosity and wobbling angle of phospholipids. Alterations in these variables seemed to be related to the amount of peroxidized lipid. Protection of phospholipids against peroxidation by antioxidative substances is effective in maintaining nearly normal physical properties in the dynamic microstructure of cardiac mitochondrial membranes.

Animals↗

PubMed1991

[Vasitis nodosa: report of two cases].

Two cases of vasitis nodosa are reported hereon. The two patients were 47 and 40 year old males with desire of refertility. They were performed vasectomy 23 and 10 years ago. They were subjected to vaso-vasostomy. During the operations, spindle shaped nodules were found in the vas deferens at the site of the previous vasectomy. Histologically, they showed focal proliferation of epithelial components forming glands, where a plentiful number of sperms were present, and this was also associated with proliferative change of smooth muscle bundles of vas deferens. Some foci of spermatic granulomas were also found. This condition was similar those of salpingitis isthmica nodosa in the fallopian tube. Vasitis nodosa should be differentiated from metastatic adenocarcinoma histologically. This condition may lead to re-canalization.

Adult↗

PubMed1990

Microdynamics of outer and inner membranes of mitochondria from bullfrog myocardium.

Outer and inner mitochondrial membranes were separated from bullfrog myocardium. Membrane viscosity and wobbling angle of phospholipids were measured with a nanosecond time-resolved fluorometer using a fluorophore, DPH, in each membrane. Measurements were also made on liposomes prepared from lipids extracted from each membrane. The anisotropy decay curve for DPH fluorescence was assumed to represent a mean value of decays in several microenvironments in membranes. Phospholipid constituents in membranes were analyzed by HPLC. A high proportion of PE and CL, both of which contain large amounts of unsaturated acyl chain, were found in the inner membrane. The low viscosity and large wobbling angle of phospholipids in the liposome from the inner membrane were consistent with the probable high content of unsaturated acyl chains and the low content of cholesterol in the inner membrane. Measurements of the dynamic microstructure of mitochondrial membranes suggested multifactorial characteristics probably resulting from the lipid-protein interactions. The average viscosity was found to be 0.39 +/- 0.08 P in the outer membrane and 0.58 +/- 0.01 P in the inner membrane. The wobbling angle of phospholipids in the outer and the inner membrane was, respectively, 47 and 49 degrees (non-significant difference). The liposomes prepared from lipid extracts of the membranes showed a lower viscosity and/or higher wobbling angle of phospholipids compared with the membranes themselves. The difference in the viscosity and wobbling angle between the mitochondrial membrane and its respective liposome was large in the inner membrane. These results suggest that the motion of phospholipids is limited by membrane proteins and the limitation of molecular motion of phospholipids results in an increase in the average viscosity. The results also suggest that the microdynamic values obtained in the inner membrane fraction reflect the interaction between phospholipid and protein which is abundant in the inner membrane.

Animals↗

PubMed1990

Dynamic microstructure and hydration of peroxidized membrane of rat cardiac mitochondria and effects of adriamycin.

Nanosecond time-resolved fluorometry of diphenyl hexatriene, DPH, fluorescence was used to study the effects of lipid peroxidation caused by NADH or adriamycin treatment on the dynamic microstructure of mitochondrial membranes from rat myocardium. Isolated mitochondria were incubated with NADH, FeCl3, and ADP, or with adriamycin. Parameters for microdynamics were calculated from the fluorescence intensity and anisotropy decay curves for DPH fluorescence. Peroxidized lipids were measured as malondialdehyde (MDA) resulting from the thiobarbiturate reaction. As peroxidized lipids accumulated, the membrane viscosity increased and the wobbling angle of the phospholipids decreased. The structural changes induced in unsaturated phospholipids by peroxidation probably increased the friction of neighboring phospholipids and restricted the range of their wobbling motion. The fluorescence intensity and fluorescence lifetimes decreased significantly when MDA was higher than 10 nmol/mg protein. These alterations in the behavior of DPH fluorescence strongly suggest that the hydration of the phospholipid layer of the mitochondria is occurring as a consequence of lipid peroxidation, since the fluorophore, DPH, is hydrophobic and its fluorescence is known to be quenched by increasing the dielectric constant of the surrounding media. The present results provide experimental supports to the hypothesis of membrane hydration induced by lipid peroxidation.

Animals↗

PubMed1990

Dynamic microstructure of plasma and mitochondrial membranes from bullfrog myocardium--a nanosecond time-resolved fluorometric study.

The viscosity of the phospholipid bilayer and the wobbling angle of the phospholipid molecules of mitochondrial membranes and plasma membranes from bullfrog myocardium were measured with a nanosecond time-resolved fluorometer using pulsed excitation of a hydrophobic fluorescent probe, 1,6-diphenyl-1,3,5-hexatriene (DPH). The mean +/- S.D. in the viscosity of the mitochondrial and plasma membranes was 0.54 +/- 0.9 and 0.37 +/- 0.03 P, respectively, at 30 degrees C. The wobbling angle of phospholipid molecules was 42 +/- 1 and 47 +/- 1 degree, respectively. Cholesterol content was lower in mitochondria (6.4 micrograms/mg protein) than in plasma membranes (43.7 micrograms/mg protein) but phosphatidylethanolamine concentration was higher in mitochondria (31.8%) than in plasma membranes (27.3%). Cardiolipin was contained only in mitochondria. The results of these lipid analyses appear consistent with the measurements of membrane viscosity and phospholipid wobbling angle. When the results are compared with those from a previous study on the erythrocyte membranes from bullfrogs, viscosity is found to increase in the order mitochondrial membranes less than plasma membranes less than erythrocyte membranes. The complex requirements of biomembranes of organelles performing different functions appear to be met by the particular dynamic microstructure of the biomembrane. The effect of membrane viscosity on oxygen diffusion through membranes is discussed.

Adenosine Triphosphatases↗

PubMed1990

[The effect of pressure support ventilation on breathing patterns and the work of breathing].

We assessed breathing patterns during pressure support ventilation (PSV) and its relationship with the work of breathing in 10 postoperative patients. With increasing levels of pressure support, minute ventilation and tidal volume increased with a decrease in respiratory frequency. Increased minute ventilation was achieved by increased mean inspiratory flow. Duty cycle, however, decreased with PSV. This decrease might allow the diaphragm a longer rest period between contractions, which might decrease the risk of diaphragmatic fatigue. Furthermore, PSV reduced the inspiratory work added by a ventilator to near zero. Oxygen consumption was also decreased with PSV. We conclude that PSV improved the breathing patterns and minimized the work of breathing spontaneously via a ventilator.

Adult↗

PubMed1989

Oxygen diffusion through mitochondrial membranes.

The effect of the mitochondrial membrane on the oxygen supply to the interior of mitochondria was analyzed with a cylinder model of diffusion. This estimation is based on the assumption that cytochrome a,a3 is distributed only on the inner surface of the mitochondrial inner membrane. The diffusion coefficient in the mitochondrial membrane was approximated from the fluorescently-determined viscosity of rat mitochondrial membrane. A pico-second time-resolved fluorometer at 37 degrees C gave values of 43.8 cp for intact mitochondria and 51.4 cp after phospholipase A2 treatment. Using the mean oxygen consumption rate of 10 ml O2/100 g tissue/sec in beating heart, oxygen gradients of 3.9 and 4.6 nmol was predicted across the intact and phospholipase-A2 treated mitochondrial membranes, respectively. The increased oxygen consumption during systole will yield oxygen gradients of 11.6 and 13.7 nmol. These gradients were much larger than the values estimated in a hypothetical case using the diffusion coefficient for the mitochondrial membrane of 1.5 x 10(-5) cm2/sec. The predicted oxygen gradient suggests a non-uniform distribution of oxygen in the myocardial cell and may be of importance in understanding the relationship between oxygen supply and myocardial function in hypoxia. Phospholipase A2, which is known to be activated in ischemia, destroys the microstructure of myocardial cells, seems deleterious to oxygen transport to cytochrome a,a3.

Animals↗

PubMed1989

Presynaptic effect of muscle relaxants on the release of 3H-norepinephrine controlled by endogenous acetylcholine in guinea pig atrium.

The influence of nondepolarizing muscle relaxants (MR) on the resting and electrically evoked release of tritiated norepinephrine (3H-NE) was investigated, in the absence and presence of 10(-4) mol/l cocaine, in the in vitro right atrium preparation of guinea pigs (g.p.) preloaded with 3H-NE. In the absence of MR both resting and stimulated 3H and 3H-NE release remained relatively constant throughout the experiment and the ratios of the evoked release of 3H during consecutive stimulation periods (i.e. S2/S1, S3/S2) were close to unity. None of the MR had any effect on resting 3H release. Atropine (3 x 10(-7) mol/l), gallamine (7 x 10(-5) mol/l), and pancuronium (2 x 10(-6) mol/l), but not d-tubocurarine (5 x 10(-6) mol/l) significantly increased stimulated release of 3H-NE. The effect of MR on resting or evoked release of 3H-NE was not influenced by 10(-4) mol/l cocaine. In the presence of atropine gallamine and pancuronium did not affect the release of 3H-NE. This finding indicates that the effect of MR was mediated via presynaptic muscarinic receptors. Muscle relaxants and atropine inhibited these receptors and removed the tonic inhibitory effect of acetylcholine (ACh) released from the parasympathetic nerve endings on the release of NE from the sympathetic nerve. This was substantiated by the finding that in the present of cholinesterase inhibition, when the effect of endogenous ACh was amplified and thereby the cholinergic tone was dominant, the total release of 3H-NE evoked by stimulation was much lower and muscle relaxants and atropine were much more effective to enhance 3H-NE release. Gallamine and pancuronium also increased the force of contraction of the electrically stimulated atria. These findings indicate that the acceleration of the heart rate observed with gallamine and pancuronium in anesthetized man is due to increased release from, and not the inhibition of reuptake of NE by the sympathetic nerve endings of the right atrium.

Acetylcholine↗

PubMed1989

Heterogeneity of presynaptic muscarinic receptors involved in modulation of transmitter release.

In order to extend the characterization of muscarinic receptors at presynaptic sites their inhibitory effect on the stimulation-evoked release of [3H]noradrenaline and [3H]acetylcholine from different axon terminals was studied and the dissociation constants and potencies of different antagonists were estimated, in guinea-pig and rat. While oxotremorine reduced the release of [3H]acetylcholine and [3H]-noradrenaline in a concentration-dependent manner from different release sites (Auerbach plexus, noradrenergic neurons in the right atrium, cerebral cortex), McN-A 343, an M1 receptor agonist, enhanced their release evoked by field stimulation. When the inhibitory effect of oxotremorine on transmitter release was studied, pancuronium, pirenzepine and atropine were competitive antagonists of presynaptic muscarinic receptors located on the noradrenergic axon terminals of the atrium. While atropine and pirenzepine inhibited the muscarinic receptors of cholinergic axon terminals in the Auerbach plexus, pancuronium and gallamine had a very low affinity. Significant differences were found in the affinity constants of antagonists for muscarinic receptors located in the cholinergic axon terminals of Auerbach plexus and cerebral cortex, and noradrenergic axon terminals of the atrium. While atropine and pirenzepine exerted similar effects on these presynaptic sites, pancuronium, gallamine and (11-(2-[diethylamino)-methyl)-1-piperidinyl)acetyl)-5, 11-dihydro-6(1-pyrido(2,3-b)(1,4)-benzodiazepin-6-on) were much more effective on muscarinic receptors controlling acetylcholine release from the cerebral cortex and noradrenaline release from the heart. There was more than 100-fold (2.0 pA2 units) difference in affinities of these antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗

PubMed1989

Aneurysm in the sequestrated lung and aortitis associated with the malignant rheumatoid arthritis.

A scar phase of rheumatoid aortitis and aneurysms in the sequestrated lung with a lesion continuous to an aortic lesion was found in autopsy specimens from a 50 year-old-woman, who had suffered from generally disseminated carcinoma of the breast. The aorta revealed a scar phase of granulomatous panaortitis continuously from the ascending to the descending thoracic aorta. The media and adventitia of the aorta were largely replaced by scar tissue, although the aortic valve was spared. The systemic arteries in the sequestrated lung were destroyed completely by the necrotizing angiitis and showed saccular aneurysm filled with organizing fibrin thrombus. The pulmonary artery was intact. These findings suggest that the saccular aneurysm in the sequestrated lung was produced by necrotizing angiitis, in association with rheumatoid aortitis.

Aneurysm↗

PubMed1989

Effect of atracurium and laudanosine on the release of 3H-noradrenaline.

We examined the effects of atracurium and its breakdown product, laudanosine, on resting and stimulation-evoked release of 3H-noradrenaline (3H-NA) from sympathetic axon terminals of isolated right atria of guinea pigs. Both atracurium 1-100 mumol litre-1 and laudanosine 1-50 mumol litre-1 enhanced the release of 3H-NA evoked by field stimulation (2 Hz, 24 stimuli), but did not affect resting release. When the production of laudanosine from atracurium was inhibited by maintaining the atracurium solution at 4 degrees C, atracurium did not enhance the release of 3H-NA as occurred when it was kept at 37 degrees C. However, atracurium antagonized the inhibitory effect of oxotremorine on release of 3H-NA, whereas laudanosine did not. These data suggest that atracurium possesses an antimuscarinic effect. Its metabolite, laudanosine, in concentrations which would be expected following prolonged administration of atracurium, produced a marked increase in release of 3H-NA. This effect of laudanosine may explain some of the unwanted effects seen following administration of atracurium.

Animals↗

PubMed1989

Thrombosis-inducing activity found in plasma from two patients with advanced lung cancer.

In 2 patients with lung cancer, the coagulation system was supposed to be activated by the findings of elevation of plasma fibrinogen, fibrinogen degradation product (FDP) and/or peripheral platelet counts. The plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha levels in 1 patient were measured and proved to be 160 and 20 times higher than the control level, respectively. When 0.5 ml of plasma from each patient was given intravenously into Balb/c mice, the mice died within 5 min. The multiple thrombosis mainly composed of aggregated platelets and present in the lungs of these mice probably led to death of these animals. On the contrary, no such activity was found in plasma from healthy subjects or other patients with lung cancer who showed no manifestations of enhancement in the coagulation system.

Adenocarcinoma↗

PubMed1989

Presence of thrombosis-inducing activity in plasma from patients with lung cancer.

Thrombosis-inducing activity (TIA) was detected in the peripheral blood of some patients with advanced lung cancer. When plasma from the patients was given intravenously to mice or to guinea pigs, the animals became immobile within 2 min and died at 3 to 30 min after the injection. Multiple thrombosis was found in the lungs and was considered to be the cause of the death. Thrombosis was not formed and the mice survived when heparin was given intravenously 5 min before the injection of the plasma. This TIA was present in plasma from 13 of 42 patients with lung cancer. On the contrary, only two of 32 with chronic lung diseases and two of 31 healthy control subjects had this activity in the plasma. The coagulation system in the 13 patients was considered to be chronically activated, as revealed by elevation of plasma fibrinogen levels, fibrin degradation product levels, and/or peripheral platelet counts. The TIA shared characteristics with tissue factor in that it was heat labile, nondialyzable through a dialysis membrane with a 10,000 molecular weight exclusion limit, sensitive to phospholipase C treatment, precipitated by 50% ammonium sulfate, and bound to concanavalin-A Sepharose.

Adenocarcinoma↗

PubMed1989

Inhibition of mobilization of acetylcholine: the weak link in neuromuscular transmission during partial neuromuscular block with d-tubocurarine.

The authors have demonstrated earlier, by direct measurement of acetylcholine (ACh), that d-tubocurarine (d-Tc) and other nondepolarizing muscle relaxants decrease the release of ACh from the indirectly stimulated mouse hemidiaphragm preparation. It was the purpose of the present study to determine whether the decrease of the stimulated release of ACh and the increase in the intensity of the partial neuromuscular block observed at higher stimulation rates is caused by the inhibition of mobilization of ACh from reserve depots to release sites or by inhibition of the release process itself. To attain our objective, the authors have investigated the influence of the progressive increase of the rate of stimulation from 0.1 to 1, 2, 3, and 5 Hz on the force of contraction on the in vitro phrenic nerve-hemidiaphragm and in vivo sciatic nerve-tibialis anterior preparation in the absence of drugs and after about 20% neuromuscular block produced by d-Tc or by Mg2+. The latter is known to inhibit the Ca2+ dependent release of ACh. In the absence of drugs increasing the stimulation rate increased the force of contraction, in vivo and in vitro, during both indirect and direct stimulation. In the phrenic nerve-hemidiaphragm preparation the increase was significant at 1, 2, 3, and 5 Hz (P less than 0.001) with both types of stimulation. In the sciatic nerve-tibialis anterior preparation the force of contraction was only higher at 3 and 5 Hz (P less than 0.01). The similar magnitude of the increase of the force of contraction during direct and indirect stimulation indicates that it is caused by facilitation of the contraction of the muscle fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗