PubMed Health⌕ Search

Biomedical subjects

N Noguchi

Publications and source records attributed to N Noguchi.

At least 19 recordsLinked to original sources
PubMed1992

Antioxidant activities of probucol against lipid peroxidations.

The antioxidant activities of probucol were measured in the oxidations of methyl linoleate in homogeneous solution and soybean phosphatidylcholine liposomal membranes and also of low-density lipoproteins. When an excess amount of probucol was reacted with galvinoxyl, the EPR spectrum of galvinoxyl disappeared and a new triplet EPR signal was found: g = 2.0058 and aH(2H) = 0.14 mT. The identical EPR spectrum was observed when probucol was reacted with tert-butoxyl radical generated from di-tert-butylperoxy oxalate. This EPR signal disappeared rapidly when reacted with either alpha-tocopherol or 6-O-palmitoyl-ascorbic acid. Probucol suppressed the free-radical-mediated oxidations of methyl linoleate in hexane and in acetonitrile, in a dose-dependent manner. Its antioxidant activity was 17.5-fold less than that of alpha-tocopherol in hexane. Probucol incorporated into soybean phosphatidylcholine liposomes suppressed its oxidation. The antioxidant activity of probucol was less than that of alpha-tocopherol, but the difference between the two antioxidant activities was smaller in the membranes than in homogeneous solution. Probucol also suppressed the oxidation of low-density lipoprotein. Interestingly, probucol suppressed the oxidation of LDL as efficiently as alpha-tocopherol, implying that physical factors as well as chemical reactivity are important in determining the overall activity of antioxidant in low-density lipoprotein.

Antioxidants↗
PubMed1992

Action of ebselen as an antioxidant against lipid peroxidation.

The action of ebselen (2-phenyl-1,2-benzoisoselenazol-3(2H)-one) as an antioxidant was studied under various conditions to clarify how it prevents oxidative damage. It did not react with diphenylpicrylhydrazyl nor did it suppress the oxidation of methyl linoleate in acetonitrile solution or in aqueous dispersions induced by free radical initiator, suggesting that ebselen does not act as a potent radical scavenging antioxidant. On the other hand, it suppressed the oxidation of methyl linoleate emulsions in aqueous dispersions induced by iron. It also suppressed the spontaneous oxidation of rat brain and liver homogenates, but it did not suppress the oxidation of these homogenates induced by a free radical initiator. It was also found that ebselen reduced the fatty acid hydroperoxides to their corresponding alcohols and this reaction was enhanced by the presence of glutathione. These results suggest that ebselen acts as an antioxidant by reducing hydroperoxides, but that it does not act as a radical-scavenging antioxidant.

Animals↗
PubMed1992

High-level resistance to ethidium bromide and antiseptics in Staphylococcus aureus.

A gene encoding high-level resistance to ethidium bromide (EB) and antiseptics was isolated from a transferable plasmid, pTZ22, in Staphylococcus aureus. DNA sequencing revealed that the plasmid has two copies of the ebr gene that normally mediates low-level resistance to EB and antiseptics. The efflux rate for EB of strains with duplicated ebr genes was twice the rate of strains with a single ebr gene. It was concluded that the duplication of ebr is responsible for the high-level resistance to EB and antiseptics.

Amino Acid Sequence↗
PubMed1992

Suppression of sympathetic nervous system activity by nicorandil during exercise.

1. Treadmill testing was done and plasma epinephrine and norepinephrine were measured during exercise and recovery in 21 patients with coronary artery disease given nicorandil. 2. Epinephrine levels during exercise did not change significantly with nicorandil, but the percent change in epinephrine with nicorandil tended to be lower during exercise. 3. Norepinephrine levels after exercise were suppressed with nicorandil (with, 424 +/- 15 pg/ml; without, 760 +/- 16, P less than 0.05). 4. Also, the percent change in norepinephrine with nicorandil was significantly decreased during exercise and recovery (with, 259 +/- 11%; without, 555 +/- 19, P less than 0.01). 5. Therefore, nicorandil suppressed the sympathetic nervous system hyper-response to exercise.

Adult↗
PubMed1992

Effect of alacepril on blood pressure and neurohumoral factors at rest and during dynamic exercise in patients with essential hypertension.

We assessed blood pressure and neurohumoral factors at rest and during exercise in 10 patients with essential hypertension before and after treatment with the new angiotensin converting enzyme inhibitor, alacepril (25-50 mg day-1). Alacepril significantly lowered mean blood pressure at rest and at the same exercise load as before treatment without affecting heart rate response. The response of plasma renin activity, plasma aldosterone, and plasma adrenaline were not changed by alacepril, but increase of plasma angiotensin II and plasma noradrenaline during exercise were significantly attenuated after alacepril treatment (ANOVA, P = 0.04, both). The change in mean blood pressure during exercise was positively correlated with the decrease in plasma angiotensin II (r = 0.65, P < 0.05). These results demonstrated that alacepril was effective in essential hypertension both at rest and during exercise, suggesting that the antihypertensive effect during exercise might be related to the decrease in pressor hormones, especially in plasma angiotensin II.

Adult↗
PubMed1992

Plasma catecholamine responses to dynamic exercise in patients with coronary artery disease--the relationship between sympathetic activity and systolic blood pressure and exercise-induced ventricular arrhythmias.

In order to investigate the relationship between sympathetic activity and postexercise systolic blood pressure (SBP) and exercise-induced ventricular arrhythmias in patients with coronary artery disease (CAD), we studied 38 patients and 9 normal subjects who underwent treadmill testing. Peak pressure-rate product was similar in the 2 groups. The plasma concentrations of norepinephrine and epinephrine at rest and immediately after exercise were significantly higher in patients with CAD compared with normal subjects (norepinephrine at rest, p < 0.01; norepinephrine immediately after exercise, p < 0.05; epinephrine at rest, p < 0.05; epinephrine immediately after exercise, p < 0.05). The level of norepinephrine immediately after exercise was significantly higher in 15 patients with a postexercise SBP increase than in 23 patients without that SBP change (p < 0.05), whereas the level of epinephrine was similar in the 2 groups. The level of epinephrine immediately after exercise was significantly higher in 10 patients with exercise-induced premature ventricular contractions than in 28 patients without those arrhythmias (p < 0.05), whereas the level of norepinephrine was similar in the 2 groups. We conclude that a postexercise SBP increase is related to the augmentation of sympathoneural activity and that exercise-induced ventricular arrhythmias are related to the augmentation of sympathoadrenal activity.

Arrhythmias, Cardiac↗
PubMed1991

Effects of aprindine on conduction velocity and Vmax in guinea-pig papillary muscles.

One of the effects of antiarrhythmic drugs is the reduction of conduction velocity. Cable theory predicts that there is a nonlinear relationship between conduction velocity and upstroke velocity (Vmax) of action potential. By using conventional microelectrode techniques, aprindine-induced reduction of Vmax of action potential and conduction velocity in guinea-pig papillary muscles were measured. Aprindine-produced, use-dependent, and concentration-dependent changes in conduction velocity and the decline of square of conduction velocity was well fit by a single exponential. Time constants for square of conduction velocity were comparable to simultaneously measured time constants for effects of Vmax. At a concentration of 1 to 10 microM aprindine, onset changes between Vmax and conduction velocity had a log-linear relationship in a predicted fashion. Whereas, in the recovery process from aprindine-induced depression, slow recovery time course of conduction velocity was observed. In conclusion, in the presence of aprindine, only onset block of conduction velocity can be analyzed quantitatively in the relationship to observation on Vmax in vitro. These results suggested that in the presence of aprindine, the recovery of internal conductance may be slower than that of Vmax.

Action Potentials↗
PubMed1991

Effect of urapidil on the action potentials in the guinea-pig ventricular myocardium.

The electrophysiological effects of urapidil, a new alpha 1-adrenoceptor antagonist, were assessed in the reserpinized guinea-pig ventricular myocardium. Urapidil suppressed the maximal rate of rise (Vmax) of steady-state action potentials elicited by the fast responses at high concentrations independently of blockade of myocardial alpha-adrenoceptors, but not the Vmax of Ca(2+)-dependent slow action potentials of partially depolarized muscles in concentrations tested (up to 1.1 mM). Urapidil at high concentrations prolonged the action potential durations of the fast and slow responses in a manner similar to the quinidine-like antiarrhythmic drugs. These results suggest that the inhibitory effect of urapidil on the slow inward Ca2+ current and the Na+ current is in practice negligible.

Action Potentials↗
PubMed1991

Effects of midaglizole, a new hypoglycaemic drug on the electrophysiological properties of guinea-pig papillary muscle.

1. The electrophysiological effects of midaglizole, a new oral hypoglycaemic agent which is an alpha 2-adrenoceptor antagonist, were assessed in the reserpinized ventricular myocardium of the guinea-pig. 2. Midaglizole suppressed the maximal rate of rise (Vmax) and the amplitude of action potentials (APA) of the fast and the slow responses in a concentration-dependent manner without influencing the resting potentials. 3. Voltage-dependency of the Vmax block of the action potentials by midaglizole (10 microM) did not appear in solutions containing various concentrations of KCl. 4. It is concluded that midaglizole has inhibitory effects on the fast Na+ and slow Ca2+ currents of the membrane independent of the blockade of myocardial alpha-adrenoceptors, and that these effects may be significant in some clinical uses of the drug.

Action Potentials↗
PubMed1991

UGA can be decoded as tryptophan at low efficiency in Bacillus subtilis.

Replacement of cat-86 codon 7 or 144 with the UGA codon permitted the gene to confer chloramphenicol resistance in wild-type Bacillus subtilis. UAA replacements of the same codons resulted in a chloramphenicol-sensitive phenotype in wild-type B. subtilis and a chloramphenicol-resistant phenotype in suppressor-positive strains. N-terminal sequencing showed that UGA at codon 7 was decoded as tryptophan in wild-type cells, at an efficiency of about 6%.

Bacillus subtilis↗
PubMed1991

Delayed cardiac tamponade and hemothorax induced by an acupuncture needle.

We report a 52-year-old man who presented with cardiac tamponade a few years after accidental breakage of an acupuncture needle that had not been removed. Thoracotomy showed a hemopericardium with penetration of the pulmonary artery by the very fine needle which was barely detected on the chest roentgenogram. This lesion was not suspected on the basis of roentgenography, two-dimensional echocardiography, or computed tomography, but was detected by the presence of other thick needles in the neck, chest and abdomen. This case showed a possible threat of 'stealthy' and migrating foreign bodies, such as very fine acupuncture needles.

Acupuncture Therapy↗
PubMed1991

Cooperative enhancement of hyaluronic acid synthesis by combined use of IGF-I and EGF, and inhibition by tyrosine kinase inhibitor genistein, in cultured mesothelial cells from rabbit pericardial cavity.

We examined the combined effects of IGF-I and EGF on hyaluronic acid synthesis using cultured pericardial mesothelial cells from rabbit pericardial cavity. Combined exposure of pericardial cells to IGF-I and EGF cooperatively increased hyaluronic acid synthesis and the level of hyaluronic acid synthase activity over that seen with or without IGF-I or EGF alone, but did not significantly stimulate the sulfated glycosaminoglycan synthesis. Increase in the level of hyaluronic acid synthesis and hyaluronic acid synthase activity induced by these growth factors was blocked after pretreatment with a tyrosine-specific protein kinase inhibitor, genistein. Genistein had no direct inhibitory effect on hyaluronic acid synthase activity. These results suggest that cooperative enhancement of hyaluronic acid synthesis induced by combined use of IGF-I and EGF could be mediated by a receptor tyrosine kinase-involved transmembrane signaling process that is responsive to IGF-I and EGF.

Animals↗
PubMed1991

Bunazosin, an alpha-adrenoceptor antagonist, blocks calcium current in guinea-pig ventricular myocytes.

1. Effect of bunazosin, an alpha 1-adrenoceptor antagonist, upon the slow inward Ca2+ current (ICa) was studied in single ventricular myocytes of the guinea-pig using a whole-cell patch-clamp technique. 2. Bunazosin (10-100 microM) decreased ICa in a concentration-dependent manner with an IC50 of 60 microM during depolarization to + 10 mV from the holding potential of -40 mV. 3. As for the inactivation process of ICa, the steady-state inactivation (f infinity) curve was shifted toward more negative potentials from -12 mV to -17 mV and -21 mV at f infinity = 0.5, by 30 microM and 70 microM bunazosin. 4. Inhibition of ICa by the compound (10 microM) was also dependent on stimulation frequency, with greater block induced at 2 Hz (50%) than at 0.33 Hz (13%). 5. It is concluded that bunazosin possesses a direct Ca2+ channel-blocking (class 4) action in a rate-dependent fashion.

Adrenergic alpha-Antagonists↗
PubMed1990

Bunazosin induces use-dependent slowing of conduction in guinea-pig ventricular myocardium.

The use-dependent effects of bunazosin on the maximal rate of rise (Vmax) of the action potential and conduction velocity were studied in isolated papillary muscles of guinea-pig. Standard microelectrode techniques were used to monitor the conduction and action potential of the muscles. In the presence of 30 microM bunazosin, the time constants for the start of the use-dependent inhibition of Vmax during a 0.2, 1, 2 and 3 Hz stimulation were (means +/- S.E.M. in s) 30.9 +/- 8.0, 15.0 +/- 1.6, 7.4 +/- 0.9 and 3.9 +/- 0.7 (n = 4) and those for conduction velocity were 17.3 +/- 2.3, 17.3 +/- 5.2, 6.5 +/- 0.9 and 3.4 +/- 0.2, respectively. These results showed that in the cardiac ventricular muscle of the guinea-pigs, bunazosin produces use-dependent changes in conduction velocity with onset kinetics comparable to those measured simultaneously using Vmax. The characteristics of the use-dependent inhibition of conduction velocity induced by bunazosin are similar to those found with slow kinetic drugs such as disopyramide rather than with fast ones.

Action Potentials↗
PubMed1990

An electrophysiological study of 9-amino-1,2,3,4-tetrahydroacridine (THA) on sino-atrial node preparations of rabbits.

1. The electrophysiological effect of 9-amino-1,2,3,4-tetrahydroacridine (THA) on the rabbit sino-atrial node was studied using double-microelectrode voltage clamp methods. 2. THA (above 10 microM) caused statistically significant decreases in the maximum rate of rise, the action potential amplitude, the rate of diastolic depolarization, and increases in the spontaneous cycle length, the action potential duration at 50% repolarization. 3. On the current systems, THA obviously depressed the time-dependent outward K+ current. The compound also decreased the slow inward Ca2+ current and the hyperpolarization-activated inward current. 4. These findings indicate that THA exerts an inhibitory action on the automaticity of sino-atrial node via effects on both outward and inward current systems.

Action Potentials↗
PubMed1990

Use-dependent effects of pirmenol on Vmax and conduction in guinea-pig ventricular myocardium.

1. The use-dependent effects of pirmenol, a new antiarrhythmic drug, on the maximal rate of rise (Vmax) of the action potential, conduction velocity, and their corresponding recovery kinetics were studied in isolated papillary muscles of guinea-pig. Standard microelectrode techniques were used to monitor the conduction and action potential characteristics of the muscles. 2. Pirmenol decreased Vmax and the overshoot of action potentials in a dose-dependent fashion. Also, doses of pirmenol greater than 1 mM abolished the generation of action potentials. Low concentrations of pirmenol (3 and 10 microM) prolonged the action potential duration, while concentrations greater than 0.1 mM shortened it markedly. 3. The resting block of Vmax in the presence of 10 and 30 microM pirmenol was 9.48 +/- 3.12 and 20.36 +/- 3.61%, and that of conduction velocity 2.87 +/- 1.52 and 6.58 +/- 2.09%, respectively. 4. The degree of use-dependent block induced by 10 and 30 microM pirmenol during 0.2, 1, 2 and 3 Hz stimulations was dose- and rate-dependent. 5. In the presence of 30 microM pirmenol, mean values of time constants for the onset of the use-dependent inhibition of Vmax and conduction velocity during a 2 Hz stimulation were 1.32 +/- 0.15 and 1.28 +/- 0.09 s, respectively. The recovery time constants averaged 15.83 +/- 2.14 (for Vmax) and 27.80 +/- 8.74 (for conduction velocity) s in the presence of 30 microM pirmenol. 6. These results showed that the characteristics of the use-dependent inhibition of Vmax and conduction velocity induced by pirmenol are similar to those of slow kinetic drugs such as disopyramide rather than of fast ones.

Action Potentials↗
PubMed1990

Initial accumulation of paraquat in the heart leading to acute death.

When a large amount of paraquat (364 mg/kg) which caused death in several hours was orally ingested in rats, the herbicide concentration in blood continued to increase until the animal died. Furthermore, there was a correlation between the paraquat concentration in the blood, heart, liver and adrenal gland and the survival time. While the paraquat concentration in the heart had the most evident correlation in those tissues (r = -0.962), there was no correlation between the paraquat concentration and survival time in the lung or kidney. ECG of the rats which died in the early stages showed severe damage in the heart. It was found by histopathological studies that edema, congestion and hemorrhage occurred in the myocardium of rats that had died shortly after administration of a large amount of paraquat (364 mg/kg). These results suggest that a rapid accumulation of paraquat into the heart in the early stages may play an important role in the cause of acute death.

Animals↗