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Biomedical subjects

D Inoue

Publications and source records attributed to D Inoue.

120 records · Page 7Linked to original sources
PubMed1984

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↗
PubMed1983

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↗
PubMed1982

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↗
PubMed1980

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↗
PubMed1979

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↗
PubMedDate not supplied

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↗
PubMedDate not supplied

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↗
PubMedDate not supplied

Release kinetics and correlation with hemodynamic dysfunction of cardiac troponin T in coronary effluent from isolated rat hearts during reperfusion.

Previously, we reported that cardiac troponin T (TnT) can be detected and measured in coronary effluent from isolated rat hearts during hypoxia. The present study was designed to evaluate the release kinetics of TnT from post-ischemic rat hearts. Using the Langendorff technique, the hearts were reperfused for 4 h after 20 min or 60 min of global ischemia. Coronary flow was measured by timing the collection of the coronary perfusate that dripped from the hearts, and left ventricular pressure (LVP) was monitored continuously during the experiments. The amount of TnT released in 1 min was compared with the release of creatine kinase (CK) and lactate dehydrogenase (LD). The release kinetics of CK and LD showed a monophasic pattern and the levels at 4 h after reperfusion returned to baseline levels. By contrast, the release kinetics of TnT showed a small peak followed by a larger and more sustained peak. There were good negative correlations between developed pressure of LVP and both sigma TnT and the amount of TnT released within 1 min at 4 h after reperfusion. These results indicate that the release kinetics of TnT is different from that of CK and LD during reperfusion, and further that cardiac TnT is a useful indicator of myocardial cell damage and can be used to evaluate the degree of myocardial cell damage in both the early and late phase of acute myocardial infarction.

Animals↗
PubMedDate not supplied

Swallowing-induced tachycardia; three modalities of autonomic nervous effects.

Three cases are reported who have short runs of atrial premature contractions (APCs) induced by swallowing and cough. The occurrence of the APCs were affected by autonomic nervous system in all cases. The precipitating factor is considered to be the increase of vagal tone in case 1, sympathetic tone in case 2 and both of them in case 3. The autonomic mechanism of swallowing-induced tachycardia could be divided into three categories and the treatment of these arrhythmias might be different in each group. Pharmacological autonomic blockade with atropine and propranolol is useful to reveal the underlying autonomic mechanisms.

Adult↗