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Biomedical subjects

D Inoue

Publications and source records attributed to D Inoue.

At least 73 records · Page 4Linked to original sources

[Value of exercise echocardiography in evaluating left ventricular systolic function in mitral stenosis].

Exercise echocardiography was performed for 34 patients with mitral stenosis (MS) to evaluate left ventricular (LV) systolic function. The patients were categorized in three groups according to the work loads attained: Group I, 14 patients who attained 25 watts; Group II, 10 patients, 50 watts; and Group III, 10 patients, 75 watts. Among these groups, there were no statistical differences between the resting echocardiographic LV systolic function and their cardiac catheterization data. Resting LV end-diastolic and end-systolic dimensions (EDD and ESD) did not differ by group. During exercise, EDD and ESD decreased significantly in all groups, but ESD at the maximum exercise in Group I was greater than those of the other groups. The percent fractional shortening of the left ventricle (%FS) decreased significantly with exercise in Group I, while it increased significantly in the other groups. The mean velocity of circumferential fiber shortening (mean Vcf) increased significantly in all groups, but the extent was least in Group I. The exercise-induced changes in %FS (delta %FS) and mean Vcf (delta mean Vcf) correlated closely with exercise duration (r = 0.80, r = 0.73), but this was not the case in the mitral valve area. Postoperatively, exercise echocardiography was also performed for 14 patients with mitral stenosis; two of seven patients in Group I, four of five in Group II, and two in Group III showed significant improvement in exercise tolerance after surgery. However, the other six patients showed no change in their exercise tolerance. The former patients had positive values in delta %FS and more than 0.5 circ/sec in delta mean Vcf during pre-operative evaluations, while except one patient, those who did not improve had negative delta %FS values and less than 0.5 circ/sec in delta mean Vcf. It was concluded that the change in LV systolic function during exercise echocardiography reflects LV functional reserve in patients with MS, and provides valuable information for evaluating the severity of, indications for and benefits from surgery for MS.

Blood Pressure

Devices external pulse generator: a reliable temporary pacemaker?

Two cases of malfunctioning APC (American Pacemaker Company) Devices pacemakers are reported. Two patients with sick sinus syndrome were temporarily paced using APC Devices pacemaker models EC 4542 and EV 4543 respectively, which showed transient increase (53% and 83% of the preset rate, respectively) in pacing rate. The sudden increase of the pacing rate might be the pacemaker's design to switch to fixed-rate pacing at nominally 25% higher than the selected rate in the presence of an excessive level of electrical interference. However, the increased rate was much faster than the interference rate. Great caution should be paid when APC Devices pacemaker is to be used.

Female

Disappearance of blocking type thyrotropin binding inhibitor immunoglobulin (TBII) during thyroid and steroid medication in a patient with autoimmune thyroiditis.

A 55 year-old female had suffered from 3 consecutive diseases for a year. The diseases were ulcerative colitis, primary hypothyroidism and idiopathic thrombocytopenic purpura, and had been treated with L-thyroxine (50 micrograms daily) and betamethasone (0.5 to 1.5 mg daily). On examination, the thyroid gland was not palpable at all, thyroid 99 mTc pertechnetate uptake was 0%, and an echogram revealed the existence of an atrophic gland. Thyrotropin binding inhibitor immunoglobulin (TBII) in the serum was elevated to 58.0% and her IgG almost completely inhibited the in vitro cAMP increase due to bTSH. After 5 months TBII turned out to be negative and the inhibitory IgG activity was reduced significantly. The thyroid gland also became visible scintigraphically. Thyroid medication was then stopped. Four months after the cessation of thyroxine, she felt quite well and her thyroid functions remained within the normal ranges. Antibody to Yersinia enterocolitica was positive at a low titer (X20) in the early stages, but elevated reciprocally with the fall in TBII and finally reached X320. In conclusion, evidence of the disappearance of blocking type TBII from the serum was demonstrated for the first time. Steroid might have caused some favorable effects, and this clinical report indicates the possibility that remission of hypothyroidism due to blocking type TBII can be expected.

Antibodies, Bacterial

Electrophysiological effects of bethanidine sulfate on guinea-pig papillary muscle.

Bethanidine, a chemical analog of bretylium, increased the plateau phase of the action potential of guinea-pig papillary muscle in 2.7 mM K+ Tyrode solution without changing other electrophysiological parameters. In 25 mM K+ Tyrode solution, the amplitude, duration and Vmax of the Ca2+-dependent action potential were increased in a dose-dependent manner by bethanidine. It is speculated that the mechanism of antiarrhythmic effect of bethanidine might be due to the prolongation of action potential by an increase of the slow inward current.

Action Potentials

beta-Adrenoceptor agonist accelerates recovery from inactivation of calcium-dependent action potentials.

The voltage-activated Ca2+ channel in cardiac muscle plasma membranes is regulated by beta-adrenoceptor agonist, presumably by cyclic AMP-dependent phosphorylation of membrane proteins associated with this channel. In chick ventricle, we find that isoproterenol accelerates the recovery from inactivation of the maximum rate of rise (Vmax) of Ca2+-dependent action potentials without changing the steady-state inactivation of Vmax. These results confirm and extend those of others who found that beta-adrenoceptor agonists accelerated the repriming kinetics of bullfrog atrial Ca2+ current (iCa) channels. Patch clamp experiments showed that beta-adrenoceptor agonists change the kinetics of iCa channels so as to increase the probability that an iCa channel is available to open, primarily by reducing the intervals between bursts of channel openings. It is concluded that the altered kinetics of iCa channel repriming caused by beta-adrenoceptor agonist in multicellular preparations is consistent with the action of these drugs in increasing the probability of channel opening and the time spent in the open state.

Action Potentials

Block of avian cardiac fast sodium channels by tetrodotoxin is enhanced by repetitive depolarization but not by steady depolarization.

The blockade of Na+ channels by tetrodotoxin (TTX) was studied in the avian heart with the maximum rate of rise (Vmax) of phase 0 of the action potential used as an indicator of Na+ conductance (gNa). Inhibition by TTX of Vmax occurred at lower concentrations (IC50 congruent to 20 nM) than those reported in mammalian hearts (IC50, 1 to 10 microM). The IC50 was not affected by K+-induced membrane depolarization. Inhibition of closed Na+ channels by TTX was demonstrated and the degree of inhibition was increased by repetitive excitation. The time constant for recovery (tau Rec) from inactivation of Vmax was increased by TTX, a result consistent with the ability of the toxin to trap Na+ channels in the inactivated state. Reduction of the external Na+ concentration [( Na+]0 by 50% reduced the IC50 5.3-fold. This shift can largely be accounted for by the non-linear relationship between Vmax and gNa, that is, there need not be an important effect of [Na+]0 on toxin binding to its receptor. The interaction between TTX and its receptor in the avian heart is about as sensitive as that observed in peripheral nerve. However, like its less-sensitive mammalian heart counterpart, the TTX-Na+ channel interaction is frequency-dependent and apparently little influenced by membrane voltage or [Na+]0.

Animals

Tachyarrhythmia provoked by coughing and other stimuli.

A rare case of cough-induced tachyarrhythmia is described. The effectiveness of atropine sulfate, and worsening of the arrhythmia resulting from administration of digitalis, suggests that vagal reflex might be the mechanism responsible for the tachyarrhythmia.

Cough

Development of different electrophysiological mechanisms for muscarinic inhibition of atria and ventricles.

The negative inotropic effect of acetylcholine (ACh) in atrial muscle can be accounted for by a decrease of a voltage- and time-dependent slow inward current (Isi) carried by Ca2+/Na+ and an increase of outward time-dependent current carried by K+ (IK1) through inwardly rectifying channels. The negative inotropic effect of ACh in ventricular muscle is associated with a reduction of Isi; there is no important effect of ACh on IK1 in ventricular muscle. Because atrial and ventricular muscles display IK1 that is sensitive to Ba2+ and have similar numbers of muscarinic receptor sites, it is concluded that ventricular muscle lacks a metabolic link between the muscarinic receptor and inwardly rectifying K+ channels. Although there is much evidence for cyclic nucleotides as the mediator between muscarinic receptors and Isi channels, cyclic nucleotides do not seem to connect these receptors with inwardly rectifying K+ channels. According to this hypothesis, identification of a metabolic link between muscarinic receptors and IK1 channels should be demonstrable in atrial but not ventricular muscle.

Acetylcholine

L-palmitylcarnitine and calcium ions act similarly on excitatory ionic currents in avian ventricular muscle.

Palmitylcarnitine, an amphiphile that accumulates in and leaks from ischemic heart tissue, affected the fast sodium ion channel and the slow calcium channel in avian ventricular muscle. In the presence of 5.4 mM external potassium ion, palmitylcarnitine reduced the maximum rate of rise of the action potential and increased action potential duration at the plateau level without changing the resting potential. Steady state inactivation of the maximum rate of rise, an index of fast sodium ion current, was shifted by 3-6 mV to more positive potentials by palmitylcarnitine. Elevation of external calcium ion to 5.4 mM (normal = 1.8 mM), like palmitylcarnitine, reduced the maximum rate of rise and shifted the voltage at which the action potential was half maximum by 3 mV to more positive potentials without changing the resting potential. Elevated external calcium ion, unlike palmitylcarnitine, reduced the duration of action potentials initiated from a resting potential of -80 mV. Palmitylcarnitine and elevated external calcium ion increased the amplitude, the maximum rate of rise, and duration of calcium ion dependent action potentials recorded in the presence of 25 mM [K+]0 that completely inactivated the fast sodium ion channel. Steady state inactivation of the maximum rate of rise of calcium-dependent action potentials was consistently shifted to more positive potentials by palmitylcarnitine (3 mV) and by elevated external calcium ion (6 mV) when the initial external calcium ion was 0.9 mM. Palmitylcarnitine, like elevated calcium, evoked a positive inotropic effect in the presence of propranolol. The similarity of the effects of palmitylcarnitine (3 X 10(-5) to 3 X 10(-4)M) with those of elevated external calcium is consistent with the hypothesis that palmitylcarnitine, like elevated external calcium, influences sodium and calcium channel operation by an effect on membrane surface charge.

Action Potentials

Comparative study of two methods of estimating sinoatrial conduction time in patients with abnormal sinus node function.

This study compared a new method to estimate sinoatrial conduction time (SACT) using continuous atrial pacing proposed by Narula et al with the widely used method using premature atrial stimulation originally proposed by Strauss et al. The estimated SACTs by the two methods were obtained in 19 patients with normal sinus node (SN) function (Group A) and 8 patients with abnormal SN function (Group B). Estimate of the SACT by the Narula method was taken as the difference between the first atrial return cycle after pacing and the basic sinus cycle length (BSCL). The Narula method was performed for a train of 8 consecutive beats at three different pacing cycle length (PCL); PCL (1) greater than or equal to BSCL--50, PCL (2) greater than or equal to BSCL--100 and PCL (3) greater than or equal to BSCL--150 msec. In group A, the estimated SACTs by the Strauss method was 185 +/- 49.3 msec, meanwhile the SACTs by the Narula method were 148 +/- 80.7 at PCL (1), 181 +/- 58.7 at PCL (2) and 212 +/- 84.5 msec at PCL (3) (mean +/- SD); the coefficient of correlation between the Strauss method and the Narula method were 0.58, 0.84, and 0.67, respectively. On the other hand, in group B, atrial return cycles by the Narula method were abnormally prolonged (over 215 msec) in 5 of 8 cases (63%) even at PCL (2) and in all of the cases (100%) at PCL (3). By the Strauss method, SACTs in 6 of 8 cases could not be defined; however it was possible to assess the type of SN dysfunction by the pattern of the atrial return cycles. In conclusion, the estimated SACT by the Narula method at PCL (2) corresponded well with the SACT by the Strauss method in patients with normal SN function. However, it was difficult to determine SACT in patients with Sick Sinus Syndrome by both methods.

Adult

Echocardiographic findings of floating thrombus in left atrium.

We describe the M-mode and two-dimensional echocardiographic findings of a floating thrombus in the left atrium. Though the features resembled those of pedunculated left atrial myxoma, two-dimensional echocardiography was helpful in differentiating between thrombus and myxoma in the left atrium.

Adult

Subxiphoid two-dimensional echocardiographic detection of tricuspid valve prolapse.

A patient with click and late systolic murmur syndrome originating in the right side of the heart is described. Prolapse of the anterior tricuspid leaflet was demonstrated by subxiphoid two-dimensional echocardiography alone. Neither of the mitral leaflets showed any evidence of prolapse on the echocardiogram. The prolapsed anterior tricuspid leaflet and mild regurgitation were confirmed by right heart cineangiogram.

Cineangiography

Release kinetics of cardiac troponin T in coronary effluent from isolated rat hearts during hypoxia and reoxygenation.

A newly developed troponin T (TnT) test for the detection of myocardial cell necrosis has been reported to be very efficient in the detection of acute myocardial infarction. The aim of the present study was to determine whether cardiac TnT in coronary effluent from isolated heart perfused with albumin-free perfusion medium could be detected using the enzyme-linked immuno-sorbent assay developed by Katus et al. Isolated rat hearts were perfused according to the method of Langendorff. Coronary flow rate was measured by timed collection of the coronary perfusate that dripped from the hearts during 5 h of hypoxia (protocol A) or 4 h of hypoxia followed by 1 h of reoxygenation (protocol B). Creatine kinase (CK) and lactate dehydrogenase (LD) levels were compared with that of TnT. Myocardial adenine nucleotides were measured by HPLC. There was a strong correlation between TnT levels in albumin-free coronary effluent and TnT levels in coronary effluent diluted 1:1 with 5% bovine serum albumin (r = 0.996, N = 72). The coefficients of correlation between TnT and CK or LD during hypoxia and reoxygenation were 0.891 (N = 88) and 0.871 (N = 88), respectively. The coefficient of correlation between CK and LD was 0.993 (N = 88). There were no significant differences in either the decrease of coronary flow or the increase of TnT content between the hearts in the two protocols. There was no significant correlation between sigma TnT and energy charge of adenine nucleotides. These results indicate that cardiac TnT levels can be easily measured in albumin-free coronary effluent of isolated heart preparations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Effects of ischemic preconditioning on the release of cardiac troponin T in isolated rat hearts.

The aim of this study was to examine the effect of ischemic preconditioning on the releases of cardiac troponin T (TnT) during reperfusion in isolated rat hearts. Experiments were done on 22 rat hearts, which were perfused according to the method of Langendorff and were divided into the control group (n = 14) and the preconditioning group (n = 8). Double 5 min of ischemia each followed by 5 min reflow were applied as ischemic preconditioning. After 20 min of global ischemia, the releases of TnT, creatine kinase (CK), and lactate dehydrogenase (LD) in coronary effluent and the left ventricular developed pressure (LVP) were measured during 60 min of reperfusion. Ischemic preconditioning significantly suppressed the amounts of TnT released during reperfusion, as with those of CK and LD, and also improved contractile dysfunction (nine hearts in which ventricular fibrillation was sustained were excluded from the evaluation for hemodynamics), though the release kinetics of TnT was different from that of CK and LD. There were good inverse relationships between the LVP and the total amounts of TnT released during reperfusion period (sigma TnT) or TnT levels at 60 min of reperfusion. Cardiac TnT can be used as a useful biochemical marker for hemodynamics and myocardial damage after reperfusion.

Animals