Search PubMed⌕ Search

Biomedical subjects

S Imanishi

Publications and source records attributed to S Imanishi.

At least 37 records · Page 2Linked to original sources
PubMed1994

Effects of dietary oat, barley, and guar gums on serum and liver lipid concentrations in diet-induced hypertriglyceridemic rats.

Effects of dietary oat, barley, and guar gums on serum and liver triglyceride or cholesterol concentrations were examined in diet-induced hypertriglyceridemic rats. Male Sprague-Dawley rats were fed a hypertriglyceridemic diet that contained 20% coconut oil, 17.5% fructose, 17.5% sucrose, and 5% cellulose at 4 weeks of age for 14 days. In the gum-supplemented diets, 2% cellulose was replaced by oat gum, barley gum, or guar gum. Hypertriglyceridemia was observed in the control group, whereas serum cholesterol concentration was not increased. All of the gums lowered serum and liver cholesterol concentrations except barley gum which had no significant effect on liver cholesterol. Both oat and barley gums suppressed the elevation of serum and liver triglyceride concentrations but guar gum had no effect.

Animals↗
PubMed1993

Effects of elastase on contractility and morphology of elastic tissue in isolated guinea pig papillary muscles.

Elastase (ELA) is an enzyme catalyzing the digestion of elastin, an essential constituent of elastic fibers. Using isolated guinea pig papillary muscles, we examined the effect of ELA (3 x 10(-7) -3 x 10(-4) g/ml) on resting tension (RT) and twitch tension (TT). The effects of ELA on elastic fibers located in the subendocardium were examined histologically. A relatively high concentration of ELA (3 x 10(-4) g/ml) increased TT transiently, with progressive decreases in RT. In contrast, a relatively low concentration (3 x 10(-5) g/ml) decreased both TT and RT straightforwardly. Much lower concentrations (3 x 10(-6) -3 x 10(-7) g/ml) did not reveal significant effects. The ELA-induced increases in TT were unaffected in the presence of atenolol (10(-5) g/ml), ouabain (10(-7) M) or ryanodine (10(-6)M). ELA did not increase the maximum rate of rise of slow action potentials recorded using standard microelectrodes. ELA (3 x 10(-5) g/ml) decreased the maximum TT obtained at optimal RT or Lmax, and decreased the slope of the ascending and descending limbs of the TT-RT relation curve (Frank-Starling's). Electron-microscopic findings revealed that subendocardial elastin was mostly digested at ELA concentrations of 3 x 10(-5) -3 x 10(-4) g/ml. These findings suggest that the decrease of RT by ELA may be, at least in part, caused by a decomposition of the elastic fibers. On the other hand, the increase of TT by ELA could not be attributed to a release of endogenous catecholamine, an inhibition of Na+, K(+)-pump, a release of Ca2+ from sarcoplasmic reticulum, or an increase of slow inward current.

Animals↗
PubMed1993

Intracellular Na+ activity of "diseased" human atrial muscles and its modifications by dihydro-ouabain.

In quiescent human atrial muscles obtained from patients with various cardiac diseases, the intracellular Na+ activity (aNai) and the resting membrane potential (Vm) were recorded simultaneously, using double-barreled Na(+)-selective microelectrodes. The Vm averaged -44.1 +/- 5.0 mV and the aNai, 6.9 +/- 1.7 mM under normal Tyrode's solution containing 5.4 mM [K]oi,The aiNa value was within the range of aNai reported in various cardiac tissues from intact animals. Dihydro-ouabain (10(-5) M) significantly increased the aNai and depolarized the Vm. The results suggest that even in these depolarized atrial muscles the aNai remains within physiologic levels and that the Na-K pump may not be impaired. This is the first report to measure the aNai in human atrial muscles.

Adolescent↗
PubMed1993

[Electrophysiological changes in the failing myocardium].

Contraction-excitation feedback is defined as a change in the mechanical state that precedes or alters the transmembrane electrical potential. The latter could be an important electrophysiologic disorder in patients with cardiac failure since the electrophysiological changes may be induced by alterations in ventricular size, pressure or factors common to all types of congestive heart failure, regardless of aetiology. A stretch of the ventricular myocardium caused (1) a shortening of the action potential duration (APD), (2) a decrease in the resting potential (RP) and (3) the early or delayed after-depolarization that culminated in the triggered activity. Failing myocardium without ventricular hypertrophy also showed (1) a reduction in the RP and the action potential upstroke velocity and (2) APD shortening. In contrast, the majority of investigators have found a significant lengthening of the APD in the hypertrophied myocardium. These electrophysiologic changes shown in the failing myocardium with or without hypertrophy and in the mechanically stretched myocardium may be a possible substrate for the genesis of the reentrant circuit and the early or delayed afterdepolarizations, leading to ventricular arrhythmia.

Action Potentials↗
PubMed1992

High level expression of a frog alpha-amidating enzyme, AE-II, in cultured cells and silkworm larvae using a Bombyx mori nuclear polyhedrosis virus expression vector.

A Xenopus laevis peptidyl C-terminal alpha-amidating enzyme (AE-II) gene, modified by deletion of a region encoding the putative membrane-spanning domain and the putative C-terminal cytosolic tail, was expressed in BoMo-15 AIIc insect cells and silkworm larvae using a Bombyx mori baculovirus expression vector system. The expressed enzyme was identified predominantly in the culture medium and the hemolymph of silkworm larvae, indicating successful secretion of the expressed AE-II. The level of recombinant enzyme in the larval hemolymph at 4 days post-infection (40 micrograms/ml) was more than 100-fold the peak levels found in the culture medium (250 ng/ml). The enzyme activity in the larval hemolymph at 4 days post-infection was 3700 units/ml.

Animals↗
PubMed1990

Electrophysiological effects of AN-132, a new antiarrhythmic compound, in guinea pig papillary muscles.

We used electrophysiological techniques to examine the effects of AN-132, a new antiarrhythmic agent, on transmembrane action potentials of isolated papillary muscles of guinea pigs. AN-132 (1-90 microM) produced a dose-dependent decrease in the maximum upstroke velocity of the action potential (Vmax). The resting potential and the amplitude, overshoot, and the duration of the action potential were not affected, even at the highest concentration of the drug used (90 microM). In the presence of AN-132, trains of stimuli at a rate of 0.5, 1, 2, and 4 Hz led to an exponential decline in the Vmax, reaching a new steady state (use-dependent block, UDB). The UDB was augmented by higher stimulation frequencies or lower membrane potentials. In the presence of the drug (60 microM), the time constant and the rate of onset of UDB of Vmax were 13.4-4.5 s and 0.141-0.053 AP-1 at stimulation frequencies of 0.5-4.0 Hz, respectively. The time constant for the recovery of Vmax from the UDB was 81.2 +/- 17.2 s. AN-132 (60 microM) only slightly depressed the Vmax of the first action potential elicited after an 8-min quiescent period (tonic block, TB). In papillary muscles depolarized with 8.4 and 10.4 mM [K+]0, both UDB and TB were augmented, but the augmentation was greater with the former. None of the parameters of the slow response elicited in the presence of 27 mM [K+]0 and 0.2 mM Ba2+ were affected by the drug (30-90 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1989

Comparative positive inotropic effects of TA-064 (denopamine), a new cardiotonic agent, and isoproterenol and ouabain on guinea pig ventricular muscles.

The effects of TA-064 (TA) on "fast" and "slow" response action potentials and contractile tensions were studied in isolated guinea pig papillary muscles, and the findings were compared with those of isoproterenol (ISP) and ouabain. The results are as follows: (a) TA produced a dose-dependent (10(-7)-10(-5) M) increase in developed tension, with no significant changes in the resting membrane potential (RMP), action potential duration (APD), and maximum rate of rise of action potential (Vmax). (b) The concentration required to increase the developed tension by threefold ("equivalent concentration") were 10(-6) M with both TA and ouabain, while that of ISP was 5 x 10(-8) M. (c) TA increased the maximum rate of rise, dP/dtmax, and the maximum rate of fall, dR/dtmax, of the developed tension to the same extent, unlike those of ISP and ouabain. (d) Positive inotropic effects of TA (10(-7)-10(-5) M) were not completely abolished by atenolol (3.8 x 10(-5) M), a specific beta 1 blocker, whereas those of ISP were completely abolished. (e) The increasing effects of "equivalent concentration" of TA (10(-6) M) on the Vmax of the slow response were less than those of ISP (5 x 10(-8) M). These results suggest that the positive inotropic effects of TA are mainly due to stimulation of beta 1 adrenoceptors, but that the mode of action of the drug differs in several respects from that of ISP or ouabain.

Action Potentials↗
PubMed1989

Unaffected electrogenic Na-K pump activity in "diseased" human atrial fibers, as assessed by intracellular K+ activity.

To investigate the role of the electrogenic Na-K pump in the resting membrane of "diseased" or "depolarized" human atrial muscles, intracellular K+ activity (aiK) and resting membrane potential (Vm) were simultaneously measured using double-barreled K(+)-selective microelectrodes. Under perfusion with normal Tyrode's solution (37 degrees C) containing 5.4 mM [K]o, Vm averaged -43.9 +/- 1.4 mV, and aiK was 99.7 +/- 1.3 mM (mean +/- S.E., n = 33). The aiK was comparable to that of atrial muscles obtained from other intact mammalian species. In 5.4 mM [K]o, dihydro-ouabain (DHO) at concentrations of 10(-6) and 10(-5) M significantly decreased aiK and depolarized Vm. Similar decreases in aiK were observed when [K]o was decreased from 5.4 to 0.5 mM or when the temperature of the perfusing solution was decreased from 37 to 22 degrees C. Upon returning [K]o from 0.5 to 5.4 mM at 37 degrees C, aiK increased, Vm hyperpolarized markedly for about 3 min, and this was followed by less marked levels of hyperpolarization in the steady state. The high [K]o-induced increases in aiK were inhibited in the presence of DHO, and at low temperature (22 degrees C). Isoproterenol (10(-7) M) increased aiK and hyperpolarized Vm. Acetylcholine (10(-5) M) hyperpolarized Vm with no change in aiK. The rate of reduction of Na(+)-efflux during application of DHO (10(-5) M) was calculated based on the change in aiK and surface-to-volume ratio of the cell measured electronmicroscopically in the same tissue, and estimated to be 2.6 to 3.8 pmol/(cm2.s), close to the value reported for Purkinje fibers excised from intact animals. We conclude that the Na-K pump functions normally even in "diseased" human atrial muscles, thereby keeping aiK within a physiological range.

Adolescent↗
PubMed1989

Electrophysiologic effects of nicainoprol, a putative class I antiarrhythmic agent, on the guinea pig ventricular papillary muscle.

We examined the effects of nicainoprol (1-50 microM), a new antiarrhythmic agent, on the transmembrane action potentials in isolated papillary muscles of the guinea pig. Nicainoprol (greater than or equal to 5 microM) produced dose-dependent decreases in the maximal upstroke velocity (Vmax) of the action potential. Only the highest concentration (50 microM) decreased the amplitude and the overshoot of the action potential and shortened its duration at 50 or 90% repolarization levels (APD50, APD90). The potential at rest was not affected by any concentration tested (1-50 microM). In the presence of nicainoprol, trains of stimuli at the rate of 0.2, 0.5, 1.0, and 2.0 Hz, introduced after a sufficient period of rest, led to an exponential decay of the Vmax to the steady state levels (use-dependent block, UDB). The UDB was augmented with an increase in the stimulation frequency or with a decrease in the potentials at rest. The time constant for the recovery from the UDB was 51.6 +/- 9.4 s at 50 microM. The Vmax and the amplitude of the slow response elicited in the presence of 27 mM [K+]o and 0.2 mM Ba2+ was significantly decreased by application of nicainoprol (10-100 microM), with a significant shortening of APD50 (100 microM). These findings suggest that nicainoprol has electrophysiologic properties in common with those of other class I antiarrhythmic drugs with slow kinetics (Ic) and has a minor but significant inhibitory effect on slow inward current (class IV effect).

Action Potentials↗
PubMed1988

Two differential mechanisms of automaticity in diseased human atrial fibers.

The ionic mechanisms of automaticity in spontaneously active preparations (n = 38) from "diseased" human atria were investigated. The cycle length (CL) of the automatic action potential (AAP) ranged from 0.6 to 4.5 s (mean +/- S.D.: 2.0 +/- 1.0 s). The AAP from preparations obtained from non-digitalized patients (group 1, n = 29) showed various CLs, in that 16 patients had a CL longer than 2.0 s (slow-type AAP) while in tissues from the other 13 patients, the CL was 2.0 s or less (fast-type AAP). On the other hand, all preparations obtained from the digitalized patients prior to cardiac surgery (group 2, n = 9) had the fast-type AAP (CL less than or equal to 2.0 s). The slow-type AAP was accelerated and changed to the fast one after application of ouabain (1 microM) or by perfusing with 50% [Na+]o Tyrode solution. Ryanodine (1 microM), a specific inhibitor of calcium release from the sarcoplasmic reticulum (SR), markedly lengthened the CL of fast-type AAP, without affecting the slow-type AAP. In contrast, caffeine (15 mM) shortened the CL of the slow-type AAP and remarkably lengthened the CL of the fast-type AAP, as is the case in ryanodine. The rate of slow-type AAP was enhanced with an increase in [Ca2+]o and depressed with a decrease in [Ca2+]o or with application of diltiazem, a Ca2+ channel blocker. The slow-type AAP was changed to the fast-type AAP by stretching the preparation by about 20%. In vitro preparations excised from patients with dilated atria revealed a shorter CL of AAPs. We conclude that in "diseased" human atrial preparations, the ionic mechanism responsible for generation of slow- and fast-type automaticity differs. Slow automaticity (CL greater than 2.0 s) perhaps relates to activation of the slow inward Ca2+ current, while the fast-type automaticity (CL less than or equal to 2.0 s) is linked to cyclic increases in [Ca2+]i.

Action Potentials↗
PubMed1987

Electrophysiologic properties differ in the ventricular endocardium and epicardium of the Japanese monkey.

We measured action potential duration (APD) from the endocardium (Endo) and epicardium (Epi) of the left ventricular free wall in Japanese monkey hearts and found that the APD of Endo is significantly longer than that of Epi at a stimulus cycle length of 1500 msec in normal Tyrode solution (control condition). We then hypothesized that shorter APD of Epi results from greater outward pump current and that the difference in the current may be due to a difference in membrane Na,K-ATPase activity between Endo and Epi. If this were the case, interventions which alter the Na,K-pump activity should alter electrophysiologic characteristics in the endocardium and the epicardium to different degrees. An application of ouabain (10(-6) M), an inhibitor of Na,K-ATPase, produced greater shortening of APD and greater depolarization of the resting potential in Endo as compared with Epi. Shortening of stimulus cycle length shortened the APD more markedly in Endo than Epi, resulting in a significantly longer APD in Epi than Endo at a stimulus cycle length of 200 msec. The hyperpolarization and the APD shortening produced when the tissues were returned to 5.4 mM K+ Tyrode solution from K+-free medium were also more marked in Endo than in Epi. Such findings suggest that endocardial cells are more liable to accumulate Na ions intracellularly and K ions extracellularly when the Na, K-pump is suppressed by ouabain or K+-free perfusion, presumably due to lower activity of Na, K-ATPase in Endo compared to Epi.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Factors related to the low resting membrane potentials of diseased human atrial muscles.

We studied the ionic mechanism of low resting potential (RP) of quiescent "diseased" human atrial fibers. The RP was -49.7 +/- 0.8 mV (n = 179) in normal Tyrode's solution (5.4 mM [K]o, 36 degrees C). The changes in RP measured at various levels of [K]o appeared to fit the RP-[K]o relationship predicted by the Goldman-Hodgkin-Katz equation, assuming PNa/PK ratio (alpha) to be 0.102 and [K]i to be 131.9 mM. The alpha far exceeded the normal value (about 0.01) by a factor of 10. Acetylcholine (ACh, 10 microM) led to marked increases in the RP. An application of tetrodotoxin (TTX, 6 microM) and perfusion with low [Na]o (10% of the control) media in the presence and absence of ACh produced considerable hyperpolarizations of the RP. These findings indicate that increased alpha value is due to a combination of decreased PK and increased PNa. Applications of ouabain (5 microM) and a cooling procedure (12.3 degrees C) depolarized the membrane, whereas epinephrine (1 microM) hyperpolarized it. Transient hyperpolarization, which exceeded the steady state levels of RP at 5.4 mM [K]o, was observed with perfusing of 5.4 mM [K]o media following perfusion with K-free media. These findings suggest that electrogenic Na pump current plays a significant role in the maintenance of the RP. In conclusion, partial depolarization of "diseased" human atrial fibers was attributed to both decreases in membrane K+ conductance and increases in Na+ conductance. The electrogenic outward pump current seemed to protect the fibers from severe depolarization produced by the conductance abnormality (increased PNa/PK).

Acetylcholine↗
PubMed1986

Na,K-ATPase activity and repolarization of ventricular action potentials in simian hearts.

We measured Na,K-ATPase activity and ATP content of 4 different areas of the left ventricular muscle of Japanese monkeys (Mucaca fuscata): The apex, base, and epicardium (Epi) and endocardium (Endo) of the free wall. We compared those values with electrical parameters such as action potential duration (APD) and the level of resing potentials. APDs of base and Endo were significantly longer than those of apex and Epi, respectively. There was no significant difference in ATP contents among the four tissues while Na,K-ATPase activity in Epi was significantly higher, thereby indicating that the maximum capacity of the Na,K-pump activity is greater in Epi than in Endo. This observation serves to explain the following differences in electrophysiology characteristics found between Epi and Endo: greater shortening of APD in Endo when the cycle length of stimulation was shortened (from 2,000 to 200 ms) or when ouabain (0.5-1 microM) was applied; larger amplitude of post-overdrive hyperpolarization in Epi; and marked ouabain-induced depolarization of the resting potential in Endo, as compared to Epi. We conclude that the difference in Na,K-ATPase activity accounts for the different electrical behavior observed in Epi and Endo of the simian ventricle.

Action Potentials↗
PubMed1985

Isoproterenol inhibits residual fast channel via stimulation of beta-adrenoceptors in guinea-pig ventricular muscle.

When perfused with high K+ (8.1 to 14.9 mM)-Tyrode's solution, the upstroke of action potentials in the isolated guinea-pig ventricular muscle is composed of two components and there are two separable peaks in the first derivative, i.e., Vmax, fast and Vmax, slow. The Vmax, fast was a measure of activation of the residual fast channel, while the Vmax, slow was that of the slow channel. Isoproterenol depressed Vmax, fast with increase in Vmax, slow, in a concentration-dependent manner (10(-8) to 10(-6) M). This depression of Vmax, fast was greater at more depolarized levels of membrane potential. Therefore, the isoproterenol-induced depression of Vmax, fast may be due to a negative shift of the curve relating Vmax, fast to the take-off potential (Em) (Vmax--Em relationship), along the voltage axis. The negative shift of Vmax--Em relationship by isoproterenol was also recognized in small preparations the size of which is well within the space constant. The negative shift was inhibited in the presence of beta-blockers (pindolol 1 microgram/ml or atenolol 10 micrograms/ml) but not by a calcium antagonist, 1-verapamil (1 microgram/ml). These results suggest that isoproterenol blocks sodium channels in the depolarized ventricular muscle via stimulation of the beta-adrenoceptors and that the depression of Vmax, fast is not mediated by the well-known effects of isoproterenol on Vmax, slow, i.e., increased influx of Ca2+ ions.

Action Potentials↗
PubMed1983

Nature of "residual fast channel" dependent action potentials and slow conduction in guinea pig ventricular muscle and its modification by isoproterenol.

The nature of "residual fast channel" dependent action potentials and conduction was studied in guinea pig ventricular papillary muscle in which the resting potential was reduced to 58 +/- 1 mV in high K+ (16.7 mM) Tyrode's solution, with or without isoproterenol (0.1 microM). In the absence of isoproterenol, the action potential had a slur on the upstroke and the maximum rate of rise (Vmax) was composed of 2 separable peaks: the early large (32 +/- 7 V/s, Vmax,fast) and the late small (10 +/- 2 V/s, Vmax,slow) ones. The conduction velocity ranged from 30 to 35 cm/s. The Vmax,fast was selectively depressed by l-verapamil (1 microgram/ml), indicating that the impulses were transmitted through incompletely inactivated ("residual") fast channels. Lidocaine (2 micrograms/ml) depressed Vmax,fast with reduction of conduction velocity to about 20 cm/s just before the conduction block. Isoproterenol quadrupled the Vmax,slow but decreased Vmax,fast. As a result, the Vmax,slow overrode the Vmax,fast without change in the conduction velocity. In the absence of isoproterenol, there was no rate-dependent change in the action potential duration and the effective refractory period among the rates of 0.1, 0.5, and 0.9 Hz. Isoproterenol produced rate-dependent shortening in action potential duration with rate-independent shortening of postexcitation refractoriness, thereby resulting in a significant shortening in the effective refractory period at faster rates (0.5 and 0.9 Hz). Results suggest that the "residual fast channel" could produce "slow conduction" and that the ionic channels (fast or slow) responsible for the slow conduction may alternate according to local concentrations of tissue catecholamines.

Action Potentials↗
PubMed1983

Electrocardiogram and His bundle electrogram of Japanese monkeys (Macaca fuscata).

Electrocardiogram (ECG) was taken from Macaca fuscata in the supine position under secobarbital anesthesia. The ECGs were recorded in the leads of standard (I, II, III), augmented unipolar limb (aVR, aVL, aVF) and unipolar chest (V4R, V1, V2, V3, V4, V5, V6,). The ECG was similar to that of humans as well as the monkeys of other species in their general patterns and the voltage of each wave (P, Q, R, S, T), though the heart rate was considerably different. The direction of T wave was consistent with that of human ECG. The PR, QRS and QT intervals and the duration of P wave were in good agreement with those of monkeys of other species, and amounted to about 50% of those of human ECG. His bundle electrogram (HBE) was recorded with a tripolar electrode catheter inserted into the right ventricle via the femoral vein, and PA, AH, HV and PV intervals were measured. All of the values were also approximately 50% and PV intervals were measured. All of the values were also approximately 50% of those reported in human HBE. Such short time intervals observed in Macaca fuscata may be due to a smaller heart size of the monkey as compared to the human's. The measurements of ECG and HBE reported in the present study may be used as a normal reference in ECG and HBE of Macaca fuscata under anesthesia. The study suggests that the Macaca fuscata is useful as an animal model to investigate the repolarization process of human ECG.

Animals↗