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Biomedical subjects

T Kamada

Publications and source records attributed to T Kamada.

At least 379 records · Page 21Linked to original sources
PubMed1993

Higher levels of erythrocyte membrane fluidity in sprinters and long-distance runners.

Erythrocyte membrane fluidity was measured in male sprinters and long-distance runners by a spin-label method. The membrane fluidity was higher in long-distance runners than in sedentary subjects for both measurements by use of two stearic acid spin labels (SAL), 12- and 16-SAL, which represent the fluidity at two different depths of lipid bilayer. In the 12-SAL measurement, higher levels were also evident in sprinters than in sedentary subjects. Increases in the C20:5, C22:5, and total polyunsaturated acyl chains were evident in membrane phospholipids, whereas the C18 and total saturated acyl chains were decreased in long-distance runners compared with sedentary subjects. Only levels of C22:5 were higher in the sprinters than the sedentary subjects. Membrane cholesterol and phospholipid classes did not differ among the three groups. A higher level of erythrocyte membrane fluidity was observed in the athletes, more obviously in the long-distance runners, which was related to the altered phospholipid acyl chain composition. The change may contribute to the beneficial effects on erythrocyte functions related to microcirculation in athletes.

Adult↗
PubMed1993

Ischemic preconditioning increases adenosine release and 5'-nucleotidase activity during myocardial ischemia and reperfusion in dogs. Implications for myocardial salvage.

BACKGROUND: Adenosine has been reported to mediate the necrosis-limiting effects of ischemic preconditioning; however, it is unclear how this mediation occurs. The present study was undertaken to test the hypothesis that ischemic preconditioning increases 5'-nucleotidase activity and adenosine release during sustained ischemia and subsequent reperfusion. METHODS AND RESULTS: After thoracotomy, the left anterior descending coronary artery was cannulated and perfused with blood redirected from the left carotid artery in 32 dogs. Ischemic preconditioning was produced by four cycles in which the coronary artery was occluded and then reperfused for 5 minutes each. After the last cycle of ischemia and reperfusion, the coronary artery was occluded for 40 minutes. This was followed by 120 minutes of reperfusion. In the control group, the coronary artery was occluded for 40 minutes and reperfused for 120 minutes without ischemic preconditioning. The plasma adenosine concentration was measured and blood gases were analyzed in coronary arterial and venous blood samples taken during 120 minutes of reperfusion. Myocardial 5'-nucleotidase activity was measured before and at 40 minutes of sustained ischemia with and without ischemic preconditioning. The adenosine concentration in coronary venous blood during reperfusion was significantly higher in preconditioned hearts than in the control hearts: 1 minute after the onset of reperfusion, 546 +/- 57 versus 244 +/- 41 pmol/ml; 10 minutes after, 308 +/- 30 versus 114 +/- 14 pmol/ml; 30 minutes after, 175 +/- 24 versus 82 +/- 16 pmol/ml, respectively (p < 0.01). Ectosolic and cytosolic 5'-nucleotidase activities increased in both endocardial and epicardial myocardium in the ischemia-preconditioned hearts. Furthermore, 40 minutes of ischemia increased 5'-nucleotidase activity in ischemia-preconditioned hearts more than in control hearts. CONCLUSIONS: Ischemic preconditioning increases adenosine release and 5'-nucleotidase activity during sustained ischemia and subsequent reperfusion.

5'-Nucleotidase↗
PubMed1993

Superoxide dismutase restores contractile and metabolic dysfunction through augmentation of adenosine release in coronary microembolization.

BACKGROUND: This study was undertaken to test the hypothesis that administration of superoxide dismutase (SOD) restores the contractile and metabolic dysfunction in coronary microembolization and that these beneficial effects of SOD are attributable to the restoration of 5'-nucleotidase activity and subsequent augmentation of adenosine release. METHODS AND RESULTS: In 78 dogs before and after an injection of microspheres (15 microns in diameter) into the left anterior descending coronary artery, regional coronary blood flow (CBF), fractional shortening (FS), and lactate extraction ratio (LER) were measured with and without administration of recombinant human SOD (50 micrograms/kg/min i.c.). In the untreated dogs (n = 6), both FS and LER decreased after coronary microembolization (2.0 x 10(5) microspheres per ml CBF [mL/min]). FS and LER decreased from 24.2 +/- 1.3% to 5.1 +/- 1.2% and from 23.0 +/- 1.1% to -10.5 +/- 2.9%, respectively. These ischemic changes were associated with coronary hyperemic flow (141 +/- 8 versus 92 +/- 1 mL/100 g/min) and adenosine release (5.8 +/- 0.5 versus 0.4 +/- 0.1 nmol/100 g/min). Pretreatment with SOD augmented the hyperemic flow to 164 +/- 4 mL/100 g/min and enhanced the release of adenosine (9.6 +/- 0.6 nmol/100 g/min) associated with improvement of functional and metabolic dysfunction (FS, 14.8 +/- 2.3%; LER, 15.1 +/- 3.1%). Administration of SOD at 10 minutes (n = 5) and 30 minutes (n = 5) after coronary embolization restored the contractile function and lactate metabolism (at 10 minutes: FS, 16.7 +/- 2.2% and LER, 16.7 +/- 3.9%; at 30 minutes: FS, 11.1 +/- 1.3% and LER, 7.2 +/- 3.1%). However, administration of SOD 60 minutes after coronary embolization (n = 6) did not restore the contractile and metabolic dysfunction. The restoration of the contractile and metabolic dysfunction by SOD treatment was blunted by adenosine receptor blockade with 8-phenyltheophylline (n = 5). Myocardial 5'-nucleotidase activity at 2 hours after embolization was restored with SOD treatment at 10 minutes (n = 5) and 30 minutes (n = 5) after embolization. However, SOD treatment at 60 minutes after embolization (n = 6) did not restore 5'-nucleotidase activity compared with the SOD pretreatment group. Furthermore, coronary submaximal vasodilation induced by papaverine (n = 5) and adenosine (n = 5) abolished the beneficial effects of SOD. CONCLUSIONS: We conclude that 1) in sustained myocardial ischemia, SOD treatment attenuates ischemic injury caused by coronary microembolization by restoration of 5'-nucleotidase activity and augmentation of adenosine release; 2) this beneficial effect of SOD is observed even after coronary microembolization; and 3) the beneficial effects of SOD are attributable to coronary vasodilation produced by augmented adenosine release.

5'-Nucleotidase↗
PubMed1993

Demonstration of functional border zone with myocardial contrast echocardiography in human hearts. Simultaneous analysis of myocardial perfusion and wall motion abnormalities.

BACKGROUND: Although the presence of a functional border zone (FBZ), defined as the nonischemic but asynergic myocardium adjacent to the ischemic area, has been demonstrated in animal hearts, it is not known whether this zone exists in humans. METHODS AND RESULTS: Myocardial contrast echocardiography (MCE) was performed before and during balloon inflation in the area of coronary stenosis by injecting contrast medium through the guiding catheter in 13 patients with effort angina who underwent successful coronary angioplasty. The area showing MCE defect during balloon inflation was determined with reference to the preangioplasty MCE and was regarded as an ischemic area. The size of the FBZ was assessed by measuring the length of the endocardium that showed asynergy in the echo-enhanced (nonischemic) area. The FBZ measured was 13 +/- 4 mm in the short-axis view (n = 5) and 16 +/- 9 mm in the long-axis view (n = 8). CONCLUSIONS: Nonischemic contractile dysfunction exists even in human hearts. The presence of an FBZ may limit the use of wall motion analysis in assessing the risk or ischemic area in patients with myocardial infarction. MCE appears to be a unique technique for assessing the risk or ischemic area.

Adult↗
PubMed1993

Exercise-induced upward shift of diastolic left ventricular pressure-volume relation in patients with dilated cardiomyopathy. Effects of beta-adrenoceptor blockade.

BACKGROUND: The effectiveness of beta-blocker therapy for dilated cardiomyopathy (DCM) may be attributed to the inhibition of detrimental effects on the failing heart of sympathetic stimulation during exertion. However, the harmful effects of activity as well as the protective effects of beta-blockers have not been demonstrated. Diastolic ventricular function is known to be sensitive to transient myocardial metabolic insult. In this study, we investigated the effect of modest exercise with or without beta-blockade on the diastolic left ventricular pressure-volume (P-V) relation in patients with DCM. METHODS AND RESULTS: The diastolic left ventricular P-V relation was obtained by high-fidelity pressure measurements and digital subtraction left ventriculography at rest and immediately after modest supine bicycle exercise in 12 patients with DCM. The effects of intravenous administration of 0.1 mg/kg propranolol on resting and exercise P-V relations were studied. The end-diastolic and lowest left ventricular pressures were significantly elevated by exercise (20 +/- 9 to 32 +/- 13 mm Hg, P < .01, and 12 +/- 6 to 21 +/- 11 mm Hg, P < .01, respectively) despite insignificant changes in left ventricular volumes. The administration of propranolol did not alter the resting diastolic P-V relation. However, propranolol significantly attenuated the exercise-induced upward shift of the diastolic P-V relation despite a significant increase in end-diastolic volume. The significant upward shift and attenuation by propranolol were also observed even when the left ventricular pressure was corrected by the subtraction of right atrial pressure. CONCLUSIONS: These results indicate that even modest exercise exerts detrimental effects on diastolic left ventricular function of the failing heart through beta-adrenergic stimulation. The clinical effectiveness of beta-blocker therapy in patients with DCM can be attributed in part to the inhibition of detrimental myocardial effects of sympathetic stimulation during daily activity.

Adrenergic beta-Antagonists↗
PubMed1993

Reperfusion after brief ischemia disrupts the microtubule network in canine hearts.

Histological changes in the stunned myocardium are believed to be minimal. This study examined whether cytoskeletal structures of microtubules are disrupted in the stunned myocardium. In 38 dogs, the left anterior descending coronary artery was occluded for 15 minutes and reperfused to produce the stunned myocardium. Microtubules were stained immunohistochemically. In intact myocardium, microtubules appeared as a filamentous network throughout the cytoplasm and encircled the nucleus. This pattern was not affected by 15 minutes of ischemia. One hour of reperfusion, however, disrupted microtubular structure substantially (disruption score in the endocardium, 53.4 +/- 6.0%) although actin filaments remained intact. Microtubular structures were reconstituted 1-3 days after reperfusion, showing supernormal immunoreactivity. Five days after reperfusion, the pattern of microtubular staining was normal. In another protocol, the role of Ca2+ during reperfusion in microtubular disruption was examined. When intracoronary infusion of EDTA (1.67 mumol/kg body wt per minute) was performed during the initial 10 minutes of reperfusion, myocardial stunning was attenuated. The fractional shortening in the perfused area after 1 hour of reperfusion was 20.1 +/- 1.2% versus 11.5 +/- 0.5% in the control condition (p < 0.05), and the microtubular disruption score was lower (12.6 +/- 1.4%). Although intracoronary infusion of calcium chloride (9 mumol/kg body wt per minute) for 10 minutes in nonischemic hearts increased contractile function (fractional shortening, 25.3 +/- 2.0%), it severely disrupted microtubular networks (microtubular disruption score, 64.0 +/- 10.6%). We conclude that microtubules supporting the structural integrity of myofibrils and other organelles are reversibly disrupted by reperfusion after brief ischemia probably through calcium overload.

Animals↗
PubMed1993

Delayed effects of sublethal ischemia on the acquisition of tolerance to ischemia.

The infarct-limiting effect of ischemic preconditioning is believed to be a transient phenomenon. We examined the delayed effects of repetitive brief ischemia on limiting infarct size in an open-chest dog model by an occlusion (90 minutes) of the left anterior descending coronary artery (LAD) followed by reperfusion (5 hours). The dogs were preconditioned with four brief repeated ischemic episodes induced by 5-minute LAD occlusions with subsequent reperfusion. The size of infarcts initiated by a sustained occlusion immediately or 24 hours after preconditioning was significantly smaller when compared with infarcts in sham-operated dogs (for the immediate occlusion, 14.4 +/- 2.0% versus 39.0 +/- 3.7%, respectively [p < 0.01]; and for the delayed occlusion, 18.8 +/- 3.4% versus 35.1 +/- 4.6%, respectively [p < 0.05]); however, when the infarction was induced 3 hours (31.2 +/- 3.7% versus 37.5 +/- 4.2%, respectively) or 12 hours (25.4 +/- 4.8% versus 35.0 +/- 5.3%, respectively) after repetitive ischemia, the infarct size did not differ. No differences were seen in regional myocardial blood flow or rate-pressure products between the two groups. These results indicate that an infarct-limiting effect of brief repeated ischemia can be observed 24 hours after sublethal preconditioning.

Animals↗
PubMed1993

Attenuation of ecto-5'-nucleotidase activity and adenosine release in activated human polymorphonuclear leukocytes.

To examine whether activation of polymorphonuclear leukocytes attenuates release of adenosine through attenuation of their own ecto-5'-nucleotidase activity, human polymorphonuclear leukocytes were incubated with and without exposure to either N-formyl-methionyl-leucyl-phenylalanine (FMLP) or complement C5a. Ecto-5'-nucleotidase activity of polymorphonuclear leukocytes was attenuated by both FMLP and complement C5a (22.7 +/- 3.6 vs 9.7 +/- 2.6 nmol/min per 10(7) cells at 10(-6) M FMLP, P < .05; 21.5 +/- 2.2 vs 10.2 +/- 1.2 nmol/min per 10(7) cells at 5 x 10(-7) g/mL complement C5a, P < .001), whereas cytosolic 5'-nucleotidase activity was not affected by either FMLP or complement C5a. These reductions of ecto-5'-nucleotidase activity that were caused by both FMLP and complement C5a were dose and time dependent and were inhibited by superoxide dismutase. Desferrioxamine did not inhibit the decreases in ecto-5'-nucleotidase. In accordance with the decreases in ecto-5'-nucleotidase activity, release of adenosine was attenuated in the FMLP-pretreated and complement C5a-pretreated polymorphonuclear leukocytes, which were restored by concomitant administration of superoxide dismutase. The viability of FMLP-pretreated and complement C5a-pretreated polymorphonuclear leukocytes was markedly decreased compared with the untreated group after 60 minutes of hypoxia followed by 60 minutes of reoxygenation. Thus, we conclude that: (1) activation of polymorphonuclear leukocytes attenuates their own ecto-5'-nucleotidase activity and thereby reduces adenosine release, (2) reduction of ecto-5'-nucleotidase activity is attributable to generated superoxide anion in polymorphonuclear leukocytes, and (3) viability of polymorphonuclear leukocytes after hypoxia and reoxygenation largely depends on the extents of decreases in ecto-5'-nucleotidase activity.

5'-Nucleotidase↗
PubMed1993

Reactivity of cerebral blood flow to carbon dioxide in various types of ischemic cerebrovascular disease: evaluation by the transcranial Doppler method.

BACKGROUND AND PURPOSE: The response of cerebral blood flow to changes in the arterial carbon dioxide partial pressure (i.e., carbon dioxide reactivity) has been evaluated as a parameter of cerebral perfusion reserve in patients with cerebrovascular disease. In this study, variations in this reactivity in various ischemic cerebrovascular diseases were evaluated by a newly established method, a transcranial Doppler technique. METHODS: Thirty-three patients with symptomatic cerebrovascular disease, 13 patients with asymptomatic cerebral infarction, and 25 age-matched normal control subjects were investigated. The symptomatic patients were divided into three groups; those with unilateral carotid artery obstruction, those with cortical infarction, and those with lacunar infarction. The carbon dioxide reactivity of each subject was determined by simultaneously measuring the mean spatial Doppler frequency in the middle cerebral artery and the end-tidal carbon dioxide partial pressure under normocapnic, hypercapnic, and hypocapnic conditions. RESULTS: In the patients with carotid obstruction, the carbon dioxide reactivity of the hemisphere ipsilateral to the obstruction was more impaired than the reactivity of the symptomatic hemispheres in any other group, and was significantly less than in the contralateral asymptomatic hemisphere (p < 0.01). In patients with cortical infarction, the carbon dioxide reactivity of the symptomatic hemisphere was significantly less than in normal control subjects (p < 0.05) and was also less than that of the contralateral asymptomatic hemisphere (p < 0.05). In patients with lacunar infarction, the carbon dioxide reactivity of both hemispheres was significantly less than that in normal controls (p < 0.01), although there was no difference between the symptomatic and asymptomatic hemispheres. In patients with asymptomatic infarction, the carbon dioxide reactivity was also less than that in normal controls (p < 0.01). CONCLUSIONS: The carbon dioxide reactivity of cerebral blood flow measured by this transcranial Doppler technique may be useful for characterizing the hemodynamic changes that occur in various types of ischemic cerebrovascular disease.

Brain Ischemia↗
PubMed1993

Rate of successful recording of blood flow signals in the middle cerebral artery using transcranial Doppler sonography.

BACKGROUND AND PURPOSE: To assess the usefulness of transcranial Doppler sonography, we investigated the rate of blood flow signal recording failure in the middle cerebral artery in Japanese subjects. Furthermore, we studied the effect of increased emitted power on the rate of successful recording in some of the patients in whom recording failure had been detected at the standard transducer power of 100 mW/cm2. METHODS: To evaluate the rate of successful recording, we measured blood flow signals in 597 patients (age range, 16 to 89 years) for screening of cerebrovascular disease by using a 2-MHz range-gated, pulsed-wave Doppler instrument at the standard transducer power. In 18 elderly patients with recording failure at the standard power, we assessed the effect of increased emitted power of 400 mW/cm2 on flow signal recording. RESULTS: Blood flow signals were recorded in 920 (77.1%) of the 1194 middle cerebral arteries of the 597 patients studied. The rate of successful recording of bilateral middle cerebral artery flow signals (70.9%; 423 of 597 patients) decreased with age, especially in females (17.0% in women aged 70 years or older). In 12 of 18 elderly patients with recording failure at the standard power, blood flow signals could be detected at the increased emitted power of 400 mW/cm2. CONCLUSIONS: The rate of successful recording of blood flow signals in Japanese subjects decreases with advancing age, especially in females. Increasing the emitted power markedly improves the successful recording rate.

Adolescent↗
PubMed1993

Glomerulosclerosis induced by in vivo transfection of transforming growth factor-beta or platelet-derived growth factor gene into the rat kidney.

Glomerulosclerosis, a final common lesion of various glomerular diseases, is characterized by mesangial cell proliferation and extracellular matrix (ECM) expansion. TGF-beta and PDGF are known to play a critical role in the regulation of ECM metabolism and mesenchymal cell proliferation, respectively. However, there is little evidence to demonstrate the direct role of each of these growth factors in the pathogenesis of glomerulosclerosis. Using an in vivo transfection technique, we could realize the selective overexpression of single growth factor in the kidney. The introduction of either TGF-beta or PDGF-B gene alone into the kidney induced glomerulosclerosis, although the patterns of action of these growth factors were different; TGF-beta affected ECM accumulation rather than cell proliferation and PDGF affected the latter rather than the former.

Animals↗
PubMed1993

Risk factors for carotid atherosclerosis and silent cerebral infarction in patients with coronary heart disease.

In this study, the authors examined relations between coronary and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction. They ascertained the risk factors for carotid atherosclerosis and silent cerebral infarction complicating coronary heart disease (CHD) in 77 Japanese subjects. As coronary atherosclerosis progressed, the carotid ultrasonographic score and the brain computed tomographic score increased. Multivariate analyses showed that the significant and independent risk factors for carotid atherosclerosis in patients with CHD were age (p < 0.01) and apolipoprotein (apo) B (p < 0.05) and the factors for silent cerebral infarction were age (p < 0.05) and hypertension (p < 0.05). Their study confirms a positive relation between coronary atherosclerosis and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction in patients with CHD. Their data suggest that carotid atherosclerosis should be looked for in patients with CHD who are old and have a high value of apo B, and silent cerebral infarction should be looked for in those who are old and have hypertension, to prevent complicating symptomatic cerebral vascular disease (CVD). If severe carotid atherosclerosis or silent cerebral infarction are detected, antithrombotic medication should be given.

Age Factors↗
PubMed1993

Effects of vasodilators on pulmonary venous and mitral flow velocity patterns in patients with congestive heart failure.

To characterize abnormalities in pulmonary venous flow velocity patterns and to explore the changes in these patterns following short-term (3 to 14 days) administration of vasodilators, pulmonary venous and mitral flow velocity patterns were serially studied at congestive heart failure and after vasodilator administration in 18 patients. Peak mitral early diastolic filling velocity (E) and the ratio of E to peak filling velocity at atrial contraction (E/A) consistently decreased after vasodilator administration by 30 +/- 4 cm/s and 0.74 +/- 0.13 (mean +/- SD), respectively. Peak pulmonary venous diastolic forward flow velocity also decreased by 29 +/- 4 cm/s. However, changes in peak pulmonary venous systolic forward flow velocity (S, cm/s) did not correlate with changes in E, the E/A ratio, or D (peak pulmonary venous diastolic forward flow velocity). Thus, when patients were divided into two groups on the basis of changes in S, indices of left ventricular systolic performance, such as end-systolic dimension and fractional shortening, improved more in the group which showed an increase in S after vasodilator administration than in the group which showed a decrease in S (-7 +/- 6 vs -1 +/- 4 mm, p < 0.05; 8 +/- 6 vs -1 +/- 4%, p < 0.05). Although the mitral flow velocity pattern changed uniformly with vasodilator administration in patients with mild to moderate congestive heart failure, the changes in pulmonary venous flow velocity patterns were not uniform among patients. Pulmonary venous flow velocity patterns appear to reflect changes in left ventricular systolic performance in addition to those in left ventricular diastolic performance.

Adult↗
PubMed1993

Esophageal squamous cell papilloma, suspected of squamous cell carcinoma.

A 46-year-old male without any subjective complaints was diagnosed by radiography as having one polypoid lesion at the distal esophagus. Endoscopy indicated a semipedunculated polyp about 1 cm in size, the specimens of which included atypical cells with a high N/C ratio in the submucosa. Squamous cell carcinoma of the esophagus was suspected. Cytological studies of PAS, CEA and keratin staining to atypical cells were all negative, with Lugol solution staining of the tumor. After polypectomy the lesion was diagnosed as a squamous cell papilloma of the esophagus; and the atypical cells were determined to be immature fibroblasts and/or endothelium.

Carcinoma, Squamous Cell↗
PubMed1993

[Serodiagnosis of hepatitis C by a recombinant hepatitis C virus protein].

Anti-HCV prevalence was high in chronic non-A, non-B liver disease. Anti-C100-3 was detected frequently in each category of chronic non-A, non-B liver disease. Antibody to HCV core protein was detected more frequently in 95% with high titers. A significant correlation was observed between the occurrence of high titers of antibody to HCV core and serum HCV RNA positivity. In patients negative by the anti-C100-3 assay, 69% were anti-HCV-positive by the second-generation enzyme-linked immunosorbent assay and also positive by the reverse transcription-polymerase chain reaction. Thus, HCV is a major causative agent of chronic non-A, non-B hepatitis in Japan.

Antigens, Viral↗