Search PubMed⌕ Search

Biomedical subjects

I Toda

Publications and source records attributed to I Toda.

At least 91 records · Page 5Linked to original sources
PubMed1994

A quantitative estimation of electric current due to myocardial injury.

Myocardial injury causes electric current at the border of injured muscle and the surrounding intact region. In order to determine the magnitude of the injury current, experiments were performed with the isolated canine heart perfused with Tyrode's solution. The anterior descending branch of the left coronary artery was perfused selectively with high potassium (K+) solution and the resulting injury current was reflected in the ST shift of the orthogonal electrocardiogram, derived from the surface of a cubic container in which the heart was placed. After measurement of the ST vector with different K+ concentrations, the heart has fixed with formalin and the injury zone was delineated with serial sections. The boundaries of the selectively perfused region were reconstructed. The algebraic sum of orthogonal components of boundary surfaces determined the average direction normal to the boundary, which was found to be parallel with the ST vector. With increasing K+ concentrations, the ST shift became more marked. However, it was saturated at about 30 mEq/L K+. The maximum injury current, calculated from the saturated value of the ST magnitude, amounted to 0.10 mA.cm per unit area of the boundary surface. Additional experiments were performed with right ventricular papillary muscle preparations. Injuries were caused by a cotton pad containing high K+ solution placed in two directions to make the border along and across the long axis of the papillary muscle. The results indicate that the injury current in an anisotropic structure was essentially directed along the fiber orientation.

Aged↗
PubMed1993

Ocular fatigue is the major symptom of dry eye.

A total of 524 consecutive new patients (195 male, 329 female, 43.4 +/- 20.8 y.o.) were evaluated for the presence of ocular fatigue and/or dry eye. Dry eye was diagnosed based on our criteria, which included symptoms, vital staining, break-up time (BUT) measurement, and the Schirmer test. Among all the patients, 21.2% (111/524) reported symptoms of ocular fatigue and 15.3% (80/524) were diagnosed as having dry eye with symptoms. Of the 111 patients who complained of ocular fatigue, 51.4% (57/111) had dry eye, which was significantly higher than the 15.3% for the entire group (p < 0.001). Additionally, 71.3% (57/80) of dry eye patients with symptoms complained of ocular fatigue, which was also significantly higher than the 21.2% among all patients (p < 0.001). Dry eye patients had a greater number of complaints (4.3 +/- 2.1 per patient) compared to controls (1.9 +/- 1.3 per patient) (p < 0.001). These findings suggest that there is a strong relation between ocular fatigue and dry eye.

Adult↗
PubMed1993

Estimation of infarct size using serum troponin T concentration in patients with acute myocardial infarction.

To estimate the size of myocardial infarction, serum troponin T concentration was measured in 34 patients with acute myocardial infarction. Left ventriculography, 2-dimensional echocardiography and resting 201thallium myocardial single photon emission computed tomography (SPECT) were performed about 4 weeks after the onset of myocardial infarction and used for correlation with the late serum troponin T peak concentration which occurred on the 3rd to 5th day after onset. Both left ventricular ejection fraction (LVEF) obtained from left ventriculography and wall motion index (WMI) obtained from 2-dimensional echocardiography were inversely related to late troponin T peak value (LVEF: r = 0.68, p < 0.001, WMI: r = 0.70, p < 0.001). Extent score (ES) and severity score (SS), which were estimated from the initial resting 201thallium SPECT image, showed excellent linear correlations with late troponin T peak concentrations (ES: r = 0.77, p < 0.001, SS: r = 0.66, p < 0.001). This correlation was present both in patients with an early troponin T peak on day 1 (group A-16 patients) and in those without an early peak (group B-10 patients). Thus, late troponin T peak concentration can be used to predict infarct size regardless of the kinetics of its appearance in serum.

Adult↗
PubMed1992

Brain natriuretic peptide as a cardiac hormone in essential hypertension.

PURPOSE: A natriuretic peptide, brain natriuretic peptide (BNP), has been isolated from porcine hearts. We performed this study to determine if BNP is secreted from the heart and to identify changes, if any, in the plasma BNP concentration in essential hypertension. PATIENTS AND METHODS: We measured the immunoreactive (ir) BNP concentration at intracardiac sites including the coronary sinus of five patients with heart disease during cardiac catheterization. We examined plasma ir-BNP in 48 hypertensive patients, 15 borderline hypertensive patients, and 25 normotensive subjects. RESULTS: Plasma ir-BNP in the coronary sinus was greater than at other cardiac sites. The concentration was significantly higher in hypertensive subjects than in borderline hypertensive or normotensive subjects. Hypertensive patients with left ventricular hypertrophy (LVH) established by echocardiography had higher plasma ir-BNP levels than those without LVH. In the hypertensive group, plasma ir-BNP was closely correlated with the LV mass index. In these patients, BNP levels were correlated with mean arterial pressure and inversely correlated with the LV ejection fraction, although these correlations were weak. Reverse-phase high-pressure liquid chromatography showed that the major component of circulating ir-BNP in the hypertensive and normotensive subjects corresponded to authentic human BNP-32. CONCLUSIONS: Human BNP-32 was secreted through the coronary sinus from the heart and may act as a cardiac hormone. Plasma BNP was increased in many of the hypertensive subjects with LVH. The increase in BNP seemed to be related to LVH or the cardiac overload associated with LVH.

Adult↗
PubMed1992

Clinical significance of reverse redistribution on thallium-201 single-photon emission computed tomography in patients with acute myocardial infarction.

To determine the clinical significance of reverse redistribution (RR), resting thallium-201 myocardial single-photon emission computed tomography was performed once or twice in 80 patients in subacute phase (1 week to 2 months) of myocardial infarction. Thirty eight patients demonstrated RR on at least one study (group RR) and 32 a fixed defect only (group FD). Group RR had significantly smaller defects than group FD. Standardizing the relation of the severity of wall motion abnormality of left ventricle on echocardiogram with that of perfusion defect, in group RR wall motion abnormality in the acute and subacute phase reflected the defect of delayed image, while that in chronic phase, which was thought to reflect the viability of myocardium in the infarct region, reflected the defect of initial image. In serial thallium-201 studies, only the defect of delayed image of group RR improved on the second study, while the defect of initial image of group RR and defect of group FD did not improve. Wall motion of group RR improved with the disappearance of RR, and when RR remained, wall motion did not improve so much. We concluded that RR was thought to be demonstrated in viable myocardium with severe wall motion abnormality.

Adult↗
PubMed1992

Scanning electron microscopic studies of the oral mucosa and its microvasculature: a review of the palatine mucosa and its microvascular architecture in mammals.

The present paper deals with the microvascular architecture of the palatine mucosa in primates, carnivorae, and rodentia utilizing microvascular corrosion castings and epithelium-separated specimens. The submucous vascular network is under-developed since the hard palatine mucosa was designated the mucoperiosteum, except some areas. The palatine venous plexus appears to show regional differences with animal species differences. The well-developed plexus is observed to be two-layered and may contribute to the process of regurgitation of rough food and assist in mastication with the palatine plicae. Formation and patterns of the arterial network in the lamina propria are in a close relation with connective tissue elements. The subepithelial capillary network constitutes an advanced base for the ascending crus of the capillary loop and its pattern is affected by the properties of the connective tissue papillae and the diverging fashion of the capillary loops. Capillary loops of the transverse palatine plica are arranged parallel to the sagittal axis and at right angles to the top line of each plica. Features of the capillary loops are characteristics in the top, the anterior and posterior slopes of the plica, respectively. High connective tissue papillae in both the anterior slope and plical top may be of a resistant form for mollifying exhaustion, affected by the periodicity and mastication function. Although it is difficult to elucidate the lamination of the palatine mucosa in histological slides, it was resolved by examination on its vascular architectures.

Animals↗
PubMed1991

Plasma levels of platelet-derived growth factor in normal subjects and patients with ischemic heart disease.

Plasma levels of platelet-derived growth factor (PDGF) were measured in 24 normal control subjects, 31 patients with stable angina pectoris, 25 patients with unstable angina pectoris, and 31 patients with acute myocardial infarction (AMI) by a sensitive direct radioimmunoassay. The plasma PDGF level in normal control subjects was 273 +/- 25 pg/ml; there was no significant correlation between the plasma PDGF level and age. Plasma PDGF levels in patients with unstable angina pectoris and acute myocardial infarction were significantly lower than those in normal control subjects and patients with stable angina pectoris (p less than 0.05). In patients with acute myocardial infarction the plasma PDGF level in the chronic phase was significantly higher than that in the acute phase (p less than 0.05). These observations raise the possibility that PDGF is involved in the pathophysiology of ischemic heart disease.

Adult↗
PubMed1991

Circulating immunoreactive endothelin in patients undergoing percutaneous transluminal coronary angioplasty.

Circulating immunoreactive endothelin (ir-ET) in the coronary sinus (CS) and the femoral artery (Ao) was measured in patients who underwent percutaneous transluminal coronary angioplasty (PTCA). Plasma ir-ET level in the CS was significantly increased from 1.6 +/- 0.8 pg/mL to 2.0 +/- 1.0 pg/mL after PTCA (P less than .05). Plasma ir-ET level in the Ao tended to increase after PTCA, but it was not significant. Plasma ir-ET level in the CS was not related to the plasma thromboglobulin level, plasma thrombin-antithrombin complex level, mean blood pressure, or heart rate. These results suggest that the increase of plasma ir-ET level in the CS may be associated with the coronary endothelial injury by PTCA.

Adult↗
PubMed1991

Two-dimensional and Doppler echocardiographic findings in a case of subaortic "fibrous sac".

We described a 37-year-old man with a subaortic "fibrous sac", admitted for congestive heart failure. On 2-dimensional echocardiography a saccular structure was seen to extend from the left coronary cusp of the aortic valve to the outflow tract of the left ventricle. By color Doppler imaging, a grade 3 aortic regurgitation was recognized. Aortic regurgitant flow was recorded from the left coronary cusp to the saccular lesion. When congestive heart failure became exacerbated, the repeat examination showed the regurgitant flow passing through the perforated bottom of this lesion and reaching the left ventricular cavity. On microscopic examination of the excised valve, capillary proliferation and inflammatory changes were recognized near the annular region of the left coronary cusp. The edge of the valve leaflet and the other 2 cusps were intact. It is likely that our patient had a mycotic aneurysm near the aortic ring. We speculate that aortic regurgitation followed inflammation. It dilated the left ventricular cavity and contributed to congestive heart failure. Inflammation also weakened the tissue near the annulus, causing it to protrude into the subaortic region thus forming a small aneurysm. It may have grown to become a large saccular structure under high aortic pressure. That is, it became a "giant" endocardial pocket with inflammatory process. Finally, the rupture of this sac caused a massive aortic regurgitation, exacerbating congestive heart failure.

Adult↗
PubMed1991

Microvascular architecture of the palatine mucosa in the common squirrel monkey (Saimiri sciureus).

Detailed observations were made of the structure and microvasculature of the palatine mucous membrane of the common squirrel monkey (Saimiri sciureus) by means of the plastic injection method under a scanning electron microscope. The findings obtained were compared with those of the Japanese monkey and other mammals. The osseous palate was flat horizontally and a pair of incisive foramina were apparently open at the anterior end of the hard palate. At the posterior end of the osseous palate, the pterygopalatine incisurae were found bilaterally. The incisive papilla was not obvious in form and size, and a pair of openings of the incisive canal were always situated on both sides of the papilla. The transverse palatine plicae or ridges numbered 7 or 8 symmetrically. They arched posterolaterally with an anterior protrusion near each median end. Posterior plicae were underdeveloped. Numerous openings of the palatine glands were found in the soft palatine mucosa. The arteries supplying the palate were the major palatine artery passing through the major palatine foramen and the soft palatine artery passing through the pterygopalatine incisura. The major palatine artery extended forwards giving off numerous medial and lateral branches, and its end on the respective side entered a small foramen located lateral to the incisive foramen. Medial and lateral branches formed the submucous arterial network. Arterioles diverging from this network were directed to the epithelial surface and formed an arterial network in the lamina propria. Further, capillaries diverging from the latter network built up the subepithelial capillary network immediately beneath the epithelium. Capillary loops sprouting from the capillary network were found in the form of a simple hair-pin without locational differences in their heights. The microvascular architecture thus displayed some similarity with that of the Japanese monkey. However, the vascular networks in the lamina propria and submucous layer were not distinct in size and scale as compared to those of the Japanese monkey. These differences may be related to the stature, living environment and food habits of this species.

Animals↗
PubMed1990

Circulating immunoreactive endothelin in ischemic heart disease.

Circulating immunoreactive endothelin (ir-ET) was measured in nine patients with acute myocardial infarction (AMI), 10 patients with stable angina pectoris (SAP), and 25 normal control subjects. In patients with AMI, the plasma ir-ET level was elevated in the acute phase and was highest on the day of onset (AMI: 3.8 +/- 1.7 pg/ml, normal control value: 0.5 +/- 0.2 pg/ml). The plasma ir-ET level showed a positive correlation with the wall motion abnormality index (rs = 0.56, p less than 0.01), thrombin-antithrombin III complex (rs = 0.55, p less than 0.01), and beta thromboglobulin (rs = 0.39, p less than 0.05). An especially high plasma ir-ET level was detected in patients in whom the Killip subset was IV. The plasma ir-ET level was not increased in patients with SAP (0.8 +/- 0.3 pg/ml). The plasma ir-ET level is increased in the acute phase of AMI. A pathophysiologic state characterized by cardiac dysfunction, an activated coagulation system, and platelet hyperactivity may be associated with this increase in plasma ir-ET.

Angina Pectoris↗
PubMed1990

Summation of excitation with a single conditioning stimulus in the canine heart.

A subthreshold stimulus was reported to become effective in producing a propagated ventricular response when preceded by another subthreshold stimulus or stimuli, a phenomenon that is known as summation of excitation but has not been studied systematically. Effect on summation of current intensity and coupling interval of a conditioning stimulus (Sc, protocol #1) and that of stimulation site of Sc (protocol #2) were determined in anesthetized, open-chest dogs. Effective refractory period (ERP) was determined with an extrastimulus (S2) at a ventricular pacing cycle length (S1S1) of 500 msec. Pulse width of S1, S2 and Sc was 2 msec. For pacing protocol #1 (12 dogs), current intensity of S1 and S2 was equal (twice diastolic threshold, 2, 5, or 15 mA), and that of Sc was equal to or lower than that of S1. S1S2 interval was fixed 1 msec shorter than ERP, and Sc was delivered 5 msec prior to S2. The S1Sc interval was shortened in 2 msec steps. Summation was present if Sc plus S2 evoked a propagated response. Prevalence of summation increased along with an increase in current intensity of Sc (P less than 0.01). For pacing protocol #2 (7 dogs), current intensity of S1, S2 and Sc was equal (twice diastolic threshold, 5 or 10 mA). As the distance between site of Sc and that of S2 increased, prevalence of summation decreased (P less than 0.01). Summation did not occur when Sc was delivered at a site only 5 mm away from the site of S2. In conclusion, summation of excitation with a single conditioning stimulus was both time and strength dependent, and limited in development spatially.

Action Potentials↗
PubMed1990

Reappraisal of inhibition and summation with a single conditioning stimulus in man.

A noncapturing conditioning stimulus is known to exert inhibitory effect on a subsequent suprathreshold stimulus, while summation occurs rarely in man. The present study was conducted to revaluate whether conditioning stimulus at a relatively low intensity produced inhibition and summation in man. Thirteen patients with various arrhythmias, 47 +/- 19 years old, were studied. Basic ventricular driving stimuli (S1S1 = 600 msec), a conditioning stimulus (Sc), and extrastimulus (S2) were introduced from a catheter electrode. Sc at an intensity of twice the late diastolic threshold inhibited suprathreshold S2 from evoking a response in all 13 patients. The ScS2 interval producing inhibition was from 11 +/- 4 to 38 +/- 26 msec. When Sc preceded S2 by 5 msec, effective refractory period was shortened by 16 +/- 7 msec in 7 of 13 patients, a phenomenon of summation. The present study demonstrates that inhibition and summation are common phenomena with a single conditioning stimulus at relatively low intensities.

Adolescent↗
PubMed1990

The complement system in ischemic heart disease.

The mechanisms by which tissue injury after acute myocardial infarction (AMI) occurs has not been fully elucidated. Recent evidence in experimental models has suggested involvement of the complement system in microvascular and macrovascular injury subsequent to AMI. With respect to angina pectoris, whether or not the complement system is activated is not clear. The present study assessed the role of complement as a mediator of myocardial inflammation by quantifying products of complement activation, including C3d, C4d, Bb, and SC5b-9 complexes, in 31 patients with AMI, 17 patients with unstable angina pectoris, 19 patients with stable angina pectoris, and 20 normal volunteers. The plasma C3d levels increased in patients with AMI and in those with unstable angina pectoris (p less than 0.01). The plasma levels of C4d, Bb, and SC5b-9 increased only in patients with AMI (p less than 0.01). The plasma SC5b-9 level was related to peak creatine phosphokinase (r = 0.71) and inversely related to the ejection fraction (r = -0.71). The plasma SC5b-9 level of patients with congestive heart failure was higher than that of patients without congestive heart failure in AMI. These results show that activation of complement system occurs after AMI and show an association of myocardial damage with complement activation. With respect to angina pectoris, the complement system is mildly activated in patients with unstable angina pectoris; however, the cardiac function of patients with unstable angina pectoris is not damaged. The complement system of patients with stable angina pectoris is not activated.

Angina Pectoris↗