The increased vulnerability of gastric mucosa against intraluminar acid due to high blood ethanol level in rats.
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Animals↗
Biomedical subjects
T Kamada
Publications and source records attributed to T Kamada.
Sequential protooncogene expression during regeneration in rat stomach.
Cellular protooncogenes such as c-myc and c-Ha-ras may play important roles in the control of regeneration of the stomach. In this study, in situ hybridization histochemistry and immunohistochemistry were used to determine how these protooncogenes and the corresponding oncoproteins are expressed at the cellular level during gastric regeneration after mucosal injuries caused by indomethacin. In addition, cells in the S-phase were immunohistochemically detected by means of 5-bromo-2'-deoxyuridine incorporation. Expression of the c-myc gene was localized to nuclei and reached a maximum at 3 h, and that of the c-Ha-ras gene was localized to cytoplasm with a peak at 6-12 h after treatment on the mucous neck, parietal, chief, and enterochromaffinlike cells around the lesions. The distribution of cells in the S-phase roughly coincided with that of cells in which expression of the protooncogenes was detected. In conclusion, various types of gastric mucosal cells participated in the sequential regulated expression of cellular protooncogenes during regeneration of the rat stomach.
Animals↗
Netilmicin affects Na(+)-dependent D-glucose transport and the membrane fluidity of rabbit renal brush-border membrane vesicles: a comparison with gentamicin.
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Animals↗
Increased intracardiovascular clotting in patients with chronic atrial fibrillation.
To clarify whether the formation of thrombi could be induced by atrial fibrillation itself or by factors predisposing to atrial fibrillation such as mitral stenosis, plasma D-dimer levels (cross-linked fibrin degradation products) were measured in 73 patients without atrial fibrillation (Group 2). In Group 1, 49 of the 73 patients had factors predisposing to atrial fibrillation such as valvular heart disease, and the remaining 24 had lone atrial fibrillation. In Group 2, 16 patients had organic heart disease and the remaining 5 had a chest pain syndrome. The plasma D-dimer level was significantly higher in Group 1 (150 +/- 19 ng/ml) than in Group 2 (61 +/- 3 ng/ml) (p less than 0.01, mean +/- standard error of the mean). In both groups, there were no significant differences in plasma D-dimer level between patients with and without organic heart disease (146 +/- 18 versus 156 +/- 46 ng/ml in Group 1; 61 +/- 4 versus 59 +/- 10 ng/ml in Group 2). These findings indicate that atrial fibrillation itself may be more important than factors predisposing to atrial fibrillation in the development of intracardiovascular clotting.
Atrial Fibrillation↗
Doppler echocardiographic quantitation of cross-sectional area under various hemodynamic conditions: an experimental validation in a canine model of supravalvular aortic stenosis.
The hemodynamic effects on cross-sectional area calculated with the continuity equation were assessed in canine experiments. In 13 open chest dogs, 46 supravalvular aortic stenoses were created by aortic root banding. The cross-sectional area of the stenosis was calculated by Doppler echocardiography with application of the continuity equation before and after the following hemodynamic interventions: protocol 1, atrial pacing at 90, 120, 150 and 180 beats/min after sinus node crush; protocol 2, preload reduction by mild and severe clamping of the inferior vena cava; and protocol 3, afterload augmentation by mild and severe clamping of the descending aorta. In each observation, a dimension of the stenosis was directly measured by two-dimensional echocardiography, and the cross-sectional area was determined as a reference standard. As a result of the hemodynamic interventions, significant changes were observed in stroke volume and pressure gradient (protocol 1), in cardiac output, stroke volume and pressure gradient (protocol 2) and in heart rate, cardiac output and pressure gradient (protocol 3). Despite these changes in hemodynamic variables, the Doppler-derived cross-sectional area showed no significant change for a given stenosis. In addition, areas calculated with the continuity equation (x) agreed well with those determined by two-dimensional echocardiography (y) (r = 0.96, p less than 0.001, y = 0.97x + 0.02, SEE = +/- 0.06 cm2). Thus, it is concluded that Doppler echocardiography with application of the continuity equation accurately predicts the stenotic cross-sectional area over a wide range of hemodynamic conditions in supravalvular aortic stenosis.
Animals↗
Short-term influence of 3,5,3'-triiodothyronine infusion on resting metabolic rate of the young pig.
The influence of 3,5,3'-triiodothyronine (T3) on resting metabolic rate (RMR) has been examined in the young pig. A dose of 10, 20 or 40 nmol T3/kg body weight was infused intravenously for periods of between one and 4 h and oxygen consumption and activity were measured over the following 20 h. There was no change in RMR during the period of T3 infusion. Results 12-20 h after infusion were influenced neither by the time at which the animal was fed nor by the length of infusion. Immediately after infusion there was a marked increase in plasma T3 concentration, followed by a rapid decline. Levels were much higher than those recorded previously after feeding. Only after 40 nmol T3/kg was there a significant 12% increase in RMR during the period 12-20 h after infusion (P less than 0.02). The significance of these results in relation to the source of the postprandial increase in plasma T3 and the action of thyroid hormones at the cellular level is discussed.
Animals↗
Kinetics of hydroperoxide degradation by NADP-glutathione system in mitochondria.
Hydroperoxide decomposition by the NADP-glutathione system in rat liver mitochondria was analyzed. Mitochondria were found to contain high concentrations of the reduced form of glutathione (GSH) (4.32 +/- 0.50 nmol/mg) and NADPH (4.74 +/- 0.64 nmol/mg), and high activities of glutathione peroxidase and reductase. In the initial phase of the reaction, the rate of hydroperoxide decomposition was proportional to both the GSH level and the activity of GSH peroxidase. However, in the later steady state, the step of NADP reduction was rate-limiting, and the overall reaction rate was independent of the initial concentration of GSH, and activities of glutathione peroxidase and reductase. Some GSH was released from mitochondria during incubation, but the rate of the decomposition could be simply expressed as kappa [GSH]/2, where kappa is the first-order rate constant of the peroxidase and [GSH] is the intramitochondrial level of GSH in the steady state. The rate of the reaction in the steady state was also dependent on the NADPH level, its reciprocal being linearly correlated with [NADPH]-1. The rate of decomposition of hydroperoxide was influenced by the respiratory state. During state 3 respiration, the rate was greatly depressed, but was still considered to exceed by far the rate of physiological generation of hydroperoxide.
Animals↗
Mucosal blood flow stasis and hypoxemia as the pathogenesis of acute gastric mucosal injury: role of endogenous leukotrienes and prostaglandins.
To clarify the roles of endogenous leukotrienes and prostaglandins in the ethanol-induced gastric mucosal injury, the effect of AA-861 (a selective 5-lipoxygenase inhibitor) and indomethacin (a cyclooxygenase inhibitor) on the ethanol-induced gastric mucosal lesions was investigated in fasted rats. Furthermore, the effect of these agents on the gastric mucosal microcirculatory disturbance induced by ethanol was also investigated using laser Doppler velocimetry and reflectance spectrophotometry. Forty percent ethanol caused mucosal microcirculatory stasis and mucosal hypoxemia, followed by mucosal injury. The pretreatment with AA-861 reduced the mucosal injury and significantly reduced the mucosal congestion and hypoxia induced by 40% ethanol. The pretreatment with indomethacin did not reduce the gastric mucosal damage or influence the mucosal blood flow stasis and the mucosal hypoxemia induced by ethanol. These results suggested that the increase of endogenous leukotrienes after intragastric administration of ethanol is responsible for the mucosal microcirculatory disturbance and mucosal tissue hypoxemia resulting in the mucosal injury, and that the decrease of prostaglandins alone may not play an important role in ethanol-induced mucosal injury.
Animals↗
Protective effect of PGD2 against ethanol-induced gastric mucosal injury in rats.
The protective effect of prostaglandin D2 (PGD2) in ethanol-, HCl-, or NaCl-induced gastric mucosal injury was investigated. To clarify the mechanism, the gastric mucosal hemodynamics were also investigated using reflectance spectrophotometry and laser Doppler flowmetry in anesthetized rats. PGD2 administered orally significantly reduced the ethanol-induced mucosal injury. Although it did not reach any significance, PGD2 also reduced 0.6 N HCl-induced mucosal damage, and slightly reduced 25% NaCl-induced mucosal damage. Topical application of PGD2 did not affect gastric mucosal hemodynamics at steady state before the administration of necrotizing agent. However, PGD2 significantly improved the gastric mucosal microcirculatory congestion caused by ethanol, and partly improved 0.6 N HCl-induced ischemia. However, it did not improve the 25% NaCl-induced mucosal congestion. The results indicated that PGD2 had a protective effect in the ethanol-induced gastric mucosal injury through the improvement of gastric mucosal microcirculation. However, further investigations are needed to clarify the precise effect of PGD2 in 0.6 N HCl- or 25% NaCl-induced mucosal damage.
Animals↗
Insulin absorption from conjunctiva studied in normal and diabetic dogs.
The dynamics of insulin absorption from the ocular conjunctiva of anaesthetized normal and pancreatectomized dogs have been examined. A porcine insulin preparation of 1000 units mL-1 (pH 8.0) was administered as either 1 or 10 units kg-1 to the upper conjunctival sacs of recumbent dogs following an overnight fast. Plasma insulin concentrations increased significantly at 5 min after the insulin administration. Plasma glucose concentrations decreased significantly, in both normal (given 10 units kg-1) and diabetic dogs (given 1 unit kg-1 or 10 units kg-1). There was a dose-dependent increase in plasma insulin concentration following conjunctival administration. Estimated absorption was significantly higher in diabetic than in normal dogs.
Absorption↗
Polymorphonuclear leukocytes induced vasoconstriction in isolated canine coronary arteries.
To assess how polymorphonuclear leukocytes (PMNs) act on coronary vasoactivity, we measured the changes in isometric tension of isolated rings of canine coronary arteries upon addition of autologous PMNs to organ chambers in which the rings were suspended. When PMNs isolated by the colloidal polyvinylpyrrolidone-coated silica (Percoll) gradient method were added to the chambers, ring preparations of left circumflex coronary arteries developed isometric tension. The increase in tension was dependent on the amount of PMNs (1 X 10(4) to 5 X 10(6) cells/ml). Maximal tension obtained by an optimal amount of PMNs (5 X 10(5) cells/ml) was almost comparable to that produced by prostaglandin F2 alpha (5 microM). Integrity of endothelial cells was not disrupted after the addition of PMNs because the developed tension could be reversed by the addition of acetylcholine in an endothelium-dependent manner. Mechanical rubbing of endothelium abolished the PMN-induced vasoconstriction, which was regained by placing an endothelium-unrubbed ring inside a rubbed ring ("sandwich preparation"). When PMN suspensions were pretreated with 5-lipoxygenase inhibitors of arachidonate, PMN-induced vasoconstriction was greatly suppressed, although the pretreatment of vascular preparations did not alter the development of isometric tension. These findings indicate that PMNs induce the contraction of coronary arterial rings in the presence of intact endothelial cells. The mechanism by which PMNs induce the contraction is the release of vasoconstrictive substances by metabolic interaction between PMNs and endothelial cells. Vasoconstrictive substances produced by the PMN-endothelial system, such as 5-lipoxygenase metabolites through a "leukotriene A4 steal" mechanism, may contribute to the contraction of vascular smooth muscle.
Animals↗
Detection of oxygen-derived free radical generation in the canine postischemic heart during late phase of reperfusion.
To define the relation between oxygen-derived free radical (oxy-radical) generation in the reperfused ischemic myocardium and the progression of myocardial damage, we measured oxy-radical generation in the ischemic myocardium and the propagating infarct size in a model of canine coronary occlusion (90 minutes) and reperfusion. We used electron paramagnetic resonance spin-trapping techniques (5,5-dimethyl-1-pyrroline N-oxide [DMPO]) to detect oxy-radicals in the rapidly frozen myocardial samples taken by needle biopsy. There was no detectable generation of DMPO adducts in the normal myocardium before or after reperfusion. In the reperfused ischemic myocardium, electron paramagnetic resonance signals of DMPO-OOH (superoxide anion) and DMPO-OH (hydroxyl radical) were detected, with peak concentrations at 1 hour after reperfusion for DMPO-OOH and at 3 hours after reperfusion for DMPO-OH, respectively. These DMPO adducts were also detected during the early phase (15 seconds) of reperfusion, but the concentrations of these signals were much less than those during the late phase of reperfusion. Treatment with human recombinant superoxide dismutase (2.5 mg/kg/hr) and catalase (2.5 mg/kg/hr) during the course of experiments abolished DMPO-OOH formation but had little effect on DMPO-OH formation. Infarct size (percent of risk area infarcted), quantified by a dual staining method with Evans blue dye and triphenyltetrazolium chloride, was 18.3 +/- 4.8% (mean +/- SEM) at 90 minutes of occlusion. After 5 hours of reperfusion, infarct size increased to 43.6 +/- 7.2%. These results indicate that a greater magnitude of oxy-radical generation was sustained in the ischemic myocardial tissue during the late phase (1-3 hours) of reperfusion, associated with the progression of myocardial infarction. The concurrent appearance of oxy-radicals and progressive infarction may support the view that a chain reaction of oxy-radicals contributes to the propagation of myocardial cell damage in the postischemic heart.
Animals↗
Disruption of microtubules as an early sign of irreversible ischemic injury. Immunohistochemical study of in situ canine hearts.
Structural disruption of the cytoskeleton may be involved in irreversible ischemic injury. In the present study, ischemic changes in microtubules during various periods of myocardial ischemia were studied with an immunohistochemical technique in open-chest dogs. In intact myocardium, microtubules were stained as a filamentous network throughout cytoplasm and a circular network around the nucleus, which disappeared with colchicine treatment. In brief ischemia of less than 15 minutes, microtubule patterns were unaltered. After 20 minutes, however, characteristic microtubule stains were partly lost in patchy lesions. As an increase in ischemic period, lesions of loss of microtubule stains were increased in number and size. After 120 minutes of reperfusion following 60 minutes of ischemia, the lesions with intact actin filaments but with disrupted microtubules were replaced by the severely injured cells in which the regular myofibrillar registrations were distinctly disrupted. After 24 hours of reperfusion following 40 minutes of occlusion of the left circumflex artery, the percent area of disrupted microtubules at 40 minutes of ischemia was replaced by that of irreversibly injured lesions in the posterior papillary muscle. These results indicate that disruption of microtubules during ischemia heralds irreversible ischemic injury. However, in in vitro study, the myocardium incubated in hypoxic solution for 60-120 minutes demonstrated earlier disruption of the microtubules than the vinculin. Electron microscopic study also showed minimal irreversible changes in the lesions with disrupted microtubules. Thus, taken together, we conclude that microtubules that support the structural integration of myofibrils and other organelles are disrupted in severe myocardial ischemia before the irreversible injury, promoting the irreversible change after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Ultrasonic evaluation of early carotid atherosclerosis.
We investigated the prevalence of carotid atherosclerosis, including mild early lesions, and its association with cervical bruits and various risk factors (age, male sex, hypertension, hyperlipidemia, diabetes mellitus, obesity, and cigarette smoking) in 232 consecutive Japanese patients. High-resolution real-time B-mode ultrasonography was performed to determine the extent of atherosclerosis, and it was quantified by using a scoring system. The prevalence of carotid atherosclerosis was 49%, 59%, and 41% in all 232 patients, the 100 symptomatic patients, and the 132 asymptomatic patients, respectively. Although carotid lesions were detected frequently (87%) in the 30 patients with cervical bruits, bruits were noted in only 30% of the 88 examined patients with carotid atherosclerosis. Independent risk factors for carotid atherosclerosis in these patients were found to be age, male sex, and hyperlipidemia; diabetes mellitus was a possible risk factor for carotid atherosclerosis. Our study did not show a close association between hypertension and carotid atherosclerosis, and this might be caused by the high prevalence of hypertension in our patients. Our findings suggest an increasing prevalence of carotid atherosclerosis in the Japanese, though this should be confirmed in a population-based study. Our study demonstrates the clinical usefulness of high-resolution B-mode ultrasonography for the evaluation of early carotid atherosclerosis.
Adult↗
Quantitative color flow imaging to measure the two-dimensional distribution of blood flow velocity and the flow rate.
A quantitative Doppler color flow imaging was employed to measure the two-dimensional distribution of blood flow velocity and flow rate in a large vessel. Regional blood flow velocity was determined by converting the color intensity at the respective pixel into corresponding flow velocity and correcting the flow velocity for spatial ultrasound beam incident angle. Instantaneous flow rate was determined precisely from the image of velocity distribution on the cross-section of the flow tract in a steady flow model circuit. In clinical application, the differences in phasic changes in two-dimensional velocity distribution in the ascending aorta, between normal subjects and the patient with aortic regurgitation, were clearly depicted. The quantitative color flow imaging may have great potential to determine noninvasively and real-timely the two-dimensional distribution of flow velocity as well as flow rate in a large vessel.
Aortic Valve Insufficiency↗
The role of Na+/H+ exchange in norepinephrine-induced protein synthesis in neonatal cultured rat cardiomyocytes.
It is reported that Na+ influx contributes to stretch-induced cardiac hypertrophy. Na+ influx may also be involved in cardiac hypertrophy induced by catecholamine. In the present study, to test whether Na+/H+ exchange plays an important role in norepinephrine-induced cardiac hypertrophy, the effect of Na+/H+ exchange inhibitor, amiloride on protein synthesis was studied in cultured neonatal rat cardiomyocytes in serum free medium. [3H]Phenylalanine uptake was determined 24 and 48 hours after administration of norepinephrine with and without amiloride. In the control, norepinephrine increased [3H]phenylalanine uptake in a dose dependent manner (10(-5)-10(-7) M). Prazosin (10(-7) M) and amiloride (10(-5)-10(-4) M) significantly attenuated the norepinephrine mediated protein synthesis. These results indicate that alpha 1-adrenergic stimulation enhances the protein synthesis through activation of Na+/H+ exchange. Therefore, Na+ influx and/or PH increase may play a key role in cardiac hypertrophy.
Amiloride↗
Pathologic involvement of the left ventricle in chronic cor pulmonale.
To determine whether or not the left ventricle is pathologically involved in patients with chronic cor pulmonale, right and left ventricular weights, wall thickness, myocyte diameters, and percentage of fibrosis in 18 autopsied hearts were examined in patients with chronic pulmonary disease (CPD); ten had right ventricular hypertrophy on their electrocardiograms, and eight were without right ventricular hypertrophy. Five with extracardiopulmonary disease were used as controls. The weight of the right ventricle was significantly increased in CPD when compared to control subjects. Walls of both ventricles were significantly thicker in CPD. Myocyte diameters of both ventricles were significantly greater in CPD. The percentage of fibrosis in the right ventricle was significantly greater in CPD. The percentage of fibrosis in the left ventricle was significantly greater only in patients with right ventricular hypertrophy. We concluded that the left ventricle was also involved pathologically in patients with chronic cor pulmonale in the end stage of the disease.
Adult↗
[Analyses of neurotic symptoms and subjective symptoms of fatigue in seamen during a long voyage].
The variations of neurotic symptoms and subjective symptoms of fatigue were studied in relation to circumstances aboard ship in subsamples of the crew (N = 24) and students and researchers (N = 24) of a training ship belonging to a university during a summer voyage of the North Pacific route in 1987. The data were obtained by a self-administered questionnaire administered seven times before and during the voyage. The present study analysed the data collected during the 40 d voyage (the first four questionnaires including that before departure). Complaints of neurotic symptoms and fatigue were reported to be much greater in the present sample than those in a general occupational setting. Although the complaints reported by students and researchers decreased at landing, complaints of physical fatigue reported by the crew increased at landing but those of mental fatigue hardly changed. With regard to correlation between the values of the responses to circumstances aboard ship and the values of neurotic symptoms and fatigue, "quality of sleep" was significantly correlated with these symptoms for the crew. For the students and researchers, significant correlations were demonstrated between such items as "boredom toward work" and "quality of sleep", and physical fatigue, between the "anxiety over disease" and mental fatigue and "anxiety over disease", "risk of injury" and "fear of death" and neurotic symptoms in the first survey after departure (13th day).
Adult↗