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Biomedical subjects

S Iwase

Publications and source records attributed to S Iwase.

At least 19 recordsLinked to original sources
PubMed1992

Effect of L-threo-3,4-dihydroxyphenylserine on muscle sympathetic nerve activity in humans.

To clarify the effect of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), a precursor of norepinephrine (NE), the effect of this drug on microneurographically recorded muscle sympathetic nerve activity (MSA) from the tibial nerve was analyzed in ten healthy male volunteers. A single dose of 600 mg of L-threo-DOPS was orally administered and the effect of this norepinephrine precursor on MSA at resting and at upright standing positions, as well as the MSA responsiveness to head-up tilting was examined by comparing the data obtained after administration of the drug with those obtained under control conditions. The plasma NE levels were determined in two subjects. The results were as follows: (1) resting MSA increased significantly 80 min after administration of L-threo-DOPS and was accompanied by an increase in plasma NE levels; (2) standing MSA when treated with the drug was not significantly different from values obtained under control conditions; and (3) MSA responsiveness to orthostasis was reduced after L-threo-DOPS. We conclude from the activation of MSA by L-threo-DOPS that this drug raised blood pressure not only through an increase in metabolized plasma NE levels, but also through the enhancement of MSA by activation of descending noradrenergic or adrenergic pathways proximal to the recording site of the sympathetic discharge.

Adult↗
PubMed1992

Enhanced muscle sympathetic nerve activity during sleep apnea in the elderly.

To examine how muscle sympathetic nerve activity (MSNA) becomes modified during sleep apnea in the elderly, we analyzed polysomnographic recording simultaneously with microneurographically recorded MSNA. Subjects were three healthy elderly males aged 72, 75, and 76. MSNA was suppressed with deeper non-REM sleep stages in these elderly subjects. In all three subjects, sleep apnea for 10 s or longer was observed during sleep of 00:00-06:00. During sleep apnea, MSNA was enhanced concomitantly with a blood pressure fall and a reduction in saturation rate of oxyhemoglobin. With the termination of sleep apnea, MSNA was maximally enhanced with a transient elevation of blood pressure. We conclude that sleep apnea induces an enhancement of MSNA, which may be responsible for hypertensive episodes during sleep.

Aged↗
PubMed1992

Responses of muscle sympathetic nerve activity and cardiac output to the cold pressor test.

We measured muscle sympathetic nerve activity (MSA) to clarify the mechanisms of the blood pressure rise during cold pressor test (CPT), simultaneously with impedance cardiography and blood pressure wave measurement in 10 healthy subjects. MSA remained unchanged during the initial period of 0-30s of the CPT and increased remarkably during the later period of 30-90s of the CPT, while cardiac output exhibited a slight increase during the initial period but not during the later period. Mean blood pressure increased significantly throughout the entire period of CPT and reached the maximal level during 90-120s of the CPT. The mean blood pressure and total peripheral resistance during the CPT showed a linear correlation with MSA. In conclusion, an increase of cardiac output elevates blood pressure at the initial period of the CPT with little increase in MSA, while an increase of MSA plays an essential role to elevate the blood pressure at the later period of the CPT.

Adult↗
PubMed1992

[Laser-Doppler flowmetry].

Laser-Doppler flowmetry (LDF) is a non-invasive technique for measuring the tissue blood flow. It has been shown in the skin that LDF discloses blood flow fluctuations due to vasomotor nerve activity. LDF can give measurements of blood flow at various sites of different tissue. Furthermore, LDF may enable selective measurement of blood flow at different depths within the tissue, when the device and the probe are appropriately chosen. Thus, LDF is available for examining vasomotor responses at various tissue sites. For clinical application, a method for calibrating the LDF signal in absolute units should be established.

Autonomic Nervous System Diseases↗
PubMed1991

Involvement of a nuclear factor-kappa B-like protein in induction of the macrophage colony-stimulating factor gene by tumor necrosis factor.

The macrophage colony-stimulating factor (M-CSF) is required for the growth and differentiation of mononuclear phagocytes. Previous studies have demonstrated that tumor necrosis factor (TNF) induces transcription of the M-CSF gene in human myeloid cells. The present work examined the effects of TNF on cis-acting elements in the M-CSF promoter. Deleted forms of the M-CSF promoter were linked to the chloramphenicol acetyltransferase (CAT) gene and transfected by electroporation into HL-60 promyelocytic leukemia cells. The results demonstrate that an enhancer responsive to TNF stimulation is located between positions -406 and -344 upstream to the transcription start site. The fragment from positions -419 to -304 was cloned 5' to the heterologous thymidine kinase (TK) promoter and linked to the CAT gene. Both orientations of this fragment enhanced TK-promoter activity in TNF-treated HL-60 cells. The results of gel mobility shift assays with the -419 to -304 fragment demonstrate binding of a constitutive nuclear protein. A TNF-inducible protein also bound to this fragment and resulted in a different mobility pattern. Binding of the TNF-induced nuclear protein to the -419 to -304 fragment was inhibited by an oligonucleotide containing the nuclear factor-kappa B (NF-kappa B) consensus sequence. DNA footprinting demonstrated protection of an NF-kappa B binding site at positions -377 to -368. Methylation interference assays showed that the TNF-induced protein made contact points with guanine residues in the same NF-kappa B sequence. Taken together, the findings provide evidence for involvement of an NF-kappa B-like factor in transcriptional regulation of the M-CSF gene.

Base Sequence↗
PubMed1991

Long-acting alpha 1-adrenoceptive sympathomimetic agent suppresses sympathetic outflow to muscles in humans.

To clarify the effect of a long-acting selective alpha 1-adrenoceptive sympathomimetic agent on sympathetic outflow to muscles (muscle sympathetic activity, MSA) in humans, 5 mg of midodrine hydrochloride was injected intravenously in ten healthy male subjects aged 19-25. Spontaneous MSA was significantly suppressed as well as plasma norepinephrine level without changing heart rate, or systemic blood pressure. The suppression continued for more than 90 min, and this is supposed to be due to negative feedback action on the baroreflex loop. The absence of significant changes in heart rate or systemic blood pressure in healthy subjects suggests that hemodynamic homeostasis is maintained by reducing the MSA in response to a long-acting sympathomimetic agent, like midodrine hydrochloride, which constricts peripheral vessels directly.

Adrenergic alpha-Agonists↗
PubMed1991

Age-related changes of sympathetic outflow to muscles in humans.

Muscle sympathetic nerve activity (MSA) was recorded microneurographically from the tibial nerve in 40 healthy male subjects aged 18 to 75. Passive and graded head-up tiltings were loaded on the subjects. The effects of aging on the resting activity of muscle sympathetic nerve in supine position at rest (burst number per minute), increase in MSA from the resting level by orthostasis (slope of the regression line between sine of the tilt angle and MSA bursts per minute), and the MSA in upright standing position were analyzed. The resting MSA increased with age, and a significant positive correlation was observed between age and resting activity (Y = -6.83 +/- 0.876X, r = .882, p less than .001). The MSA was enhanced by head-up tilt linearly with the sine of the tilt angle, and a significant negative correlation was observed between age and the MSA increase by orthostasis (Y = 57.6 - 0.582X, r = . 843, p less than .001). Standing MSA increased significantly but less remarkably than resting MSA. It was concluded that aging increases the resting activity, but there is less increase in the standing activity of sympathetic outflow to muscles in humans.

Adolescent↗
PubMed1991

Changes in muscle sympathetic nerve activity during sleep in humans.

We microneurographically recorded muscle sympathetic nerve activity (MSA) during sleep in 12 healthy volunteers while simultaneously recording EEG, EOG, ECG, respiration, and blood pressure and determined the number of pulse-synchronous MSA bursts per minute (burst rate) for non-rapid eye movement (nonREM) sleep and rapid eye movement (REM) sleep. MSA decreased during nonREM sleep with progressively deeper sleep stages. During REM sleep, the burst rate of MSA increased and was associated with marked fluctuations in arterial blood pressure. During sleep stage 2, MSA bursts occurred approximately 1 second after spontaneous K-complexes. We conclude that (1) the decreases in MSA during nonREM sleep stages may indicate sleep-stage dependent central suppression of MSA activity; (2) increases in MSA during REM sleep suggest instability of the autonomic nervous system; and (3) a common pathway may exist for MSA bursts and K-complexes.

Adolescent↗
PubMed1991

Postprandial hypotension: microneurographic analysis and treatment with vasopressin.

To clarify the mechanism of postprandial hypotension (PPH), we made microneurographic analyses of patients with PPH and 10 healthy controls by recording multi-unit vasoconstrictive impulses of muscle sympathetic nerve activity (MSNA) directly from the tibial nerve fascicles during a glucose tolerance test. Oral intake of 75 grams glucose in 225 ml of water produced significant and prolonged hypotension in all patients and an increase in MSNA in all healthy subjects. Insulin and glucose responses were not significantly correlated with arterial blood pressure reduction. PPH was prevented by an infusion of vasopressin (0.3 U/min) given before glucose intake. These results suggest that PPH is caused by the lack of sympathetic compensation for the systemic hypotensive stress of splanchnic blood pooling that occurs after food ingestion, and that prior treatment with vasopressin reduces the portal venous flow by constricting the splanchnic vessels in patients with PPH.

Adult↗
PubMed1991

Muscle sympathetic nerve responsiveness to static contraction is not altered under hypoxia.

The purpose of this study was to determine if response in muscle sympathetic nerve activity (MSNA) to static muscle contraction alters or not during peripheral chemoreceptor stimulation with hypoxia. MSNA was recorded from the tibial nerve using a microneurographic technique in seven healthy subjects in a sitting position. They performed a static handgrip exercise (SHG) for 2 min under normobaric normoxia and hypobaric hypoxic conditions corresponding to an altitude of 4,000 m (460 mmHg). MSNA represented as burst rate and total sympathetic nerve activity (TSNA) (burst rate X mean burst amplitude) at rest increased by 7.7 bursts/min and by 60%, respectively, compared to those under normoxia. During the exercise, MSNA increased over control values before exercise both under normoxia and hypoxia. TSNA increased during the first and second minute of SHG by 19% (p greater than 0.05) and 35% (p less than 0.05) in normoxia and by 15 (p greater than 0.05) and 34% (p less than 0.05) in hypoxia over the control value, respectively, while the absolute intensity of MSNA during SHG was higher under hypoxia. The response of MSNA to SHG which showed algebraic sums was the same under normoxia and hypoxia, that might relate to consist of afferent pathways independent from carotid chemoreflex.

Adult↗
PubMed1991

[Effects of muscle relaxant E-0646 on human stretch reflex and responses].

The experiment examined the effects of a muscle relaxant E-0646 on short latency stretch reflex (SLR) and long latency stretch responses (LLRs) of lower leg muscles in 5 healthy male subjects, aged 24-41 years. An AC servomotor produced an ankle rotation of comfortably seated subjects in the direction to stretch the triceps surae muscle for the SLR and the tibialis anterior muscle for the LLRs. Following control measurements, after the oral administration of 50, 100, 150, and 300 mg of E-0646, the SLR and LLRs were recorded every 2 hours for 4 or 6 hours with simultaneous blood sampling to measure E-0646 plasma levels. Electromyograms (EMGs) of the soleus and tibialis anterior muscles were recorded with surface electrodes on each muscle belly. A precision potentiometer was used to measure the ankle angle. The soleus SLR, evoked by a torque pulse (7 msec duration) of one of 5 different amplitudes, decreased 2 hours after the 300 mg administration. A SLR decrease was also found in a simple relationship between the integrated SLR EMG and the angular velocity at 20 msec after the torque onset, in which the slope and intercept of the relationship changed. The plasma E-0646 level roughly correlated with the SLR decrease. No significant change of the SLR was observed when dosage was less than 150 mg. The LLRs of the tibialis anterior muscle were tested under the instruction "resist when perturbed" during a weak isometric contraction against a constant plantar flexion torque.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Low frequency components of the body's center of gravity and blood circulation.

The purpose of this study was to clarify how low frequency components of the body's center of gravity, mainly 1 minute waves (1-MWs), are related to the mechanism of compensation for the venous blood pooling in the legs during static standing in humans. The 1-MWs of foot pressure center, oscillations of body circumferences and other parameters were analyzed with cross-power spectral analysis. The 1-MW of the calf's blood volume propagated to the chest via the venous system. This was inversely synchronized with the 1-MW of the body's center of gravity. It was speculated that muscular pumping of the calf related to the 1-MW of the body's center of gravity might be compensating for the venous blood pooling in the legs.

Adult↗
PubMed1991

[Altered expression of protooncogenes during clinical course in an AML case transformed from MDS].

The changes of expression of oncogenes in the mononuclear cells of MDS case was studied during his clinical course, in series. His bone marrow was considered to maintain its function partly in initial stage, since both peripheral blood and bone marrow responded to clinical episodes. However, his hematopoietic function was gradually impaired with the disease evolution to AML. We examined the expression of four oncogenes in the mononuclear cells of his three clinical stages, early RAEB-t, RAEB-t and AML, to study the cause of transformation from MDS to AML. Early RAEB-t cells expressed all oncogenes studied other than c-myb, while only c-myc was weakly observed in RAEB-t. AML cells expressed c-myc, c-jun and c-myb, except for c-fms. The expression of c-fms and c-jun of early RAEB-t was considered to reflect the monocytosis induced by infections, and the expressions of c-myb and c-myc of AML cells were regarded as one of malignant signs of tumor transformation. These findings suggest that the evolutional transformation of MDS to AML was affected by the altered expression of oncogenes.

Anemia, Refractory, with Excess of Blasts↗
PubMed1990

Identification of sudomotor activity in cutaneous sympathetic nerves using sweat expulsion as the effector response.

In a warm environment at ambient temperatures between 25 degrees and 38 degrees C (relative humidity 50%-60%) the relationship between sympathetic activity in cutaneous nerves (SSA) and pulses of sweat expulsion was investigated in five young male subjects. The SSA was recorded from the peroneal nerve using a micro-electrode. Sweat expulsion was identified on the sweat rate records obtained from skin areas on the dorsal side of the foot, for spontaneous sweating and drug-induced sweating, using capacitance hygrometry. Sweat expulsion was always preceded by bursts of SSA with latencies of 2.4-3.0 s. This temporal relationship between bursts of SSA and sweat expulsion was noted not only in various degrees of thermal sweating but also in the sweating evoked by arousal stimuli, or by painful electric stimulation. The amplitude of the sudomotor burst was linearly related to the maximal rate of increase of the corresponding sweat expulsion, the amplitude of the expulsion and the integrated amount of sweat produced for the duration of the expulsion. The results provide direct evidence that sweat expulsion reflects directly centrally-derived sudomotor activity.

Adult↗
PubMed1990

Skin sympathetic activity in the tibial nerve triggered by vibration applied to the hand.

The effect of vibration applied to the hand on skin sympathetic activity (SSA) in the lower limbs was studied in five healthy subjects. SSA from the right tibial nerve at the popliteal fossa, plethysmogram from the right index toe and perspiration from the sole of the right foot were measured when vibration of 100 m/s2 at 60 Hz was applied to the left palm for 1 min. The SSA response to vibration exposure differed among subjects, but every subject showed an increase in SSA from the tibial nerve when vibration was applied to the hand. Decrease in amplitude of plethysmogram from the toe was also found in all subjects. One subject displayed a remarkable increase in perspiration on the sole of the foot together with a great increase in SSA. The present findings indicated that even vibration exposure of the hand triggers sympathetic activity in the tibial nerve innervating the foot, and causes vasoconstriction of the toe and perspiration on the sole of the foot.

Adult↗
PubMed1990

Changes in muscle sympathetic nerve activity and calf blood flow during static handgrip exercise.

To test the function of sympathetic vasco-constrictor nerves on blood flow in resting limbs during static muscle contraction, muscle sympathetic nerve activity (MSNA) to the leg muscle was recorded from the tibial nerve microneurographically before, during and after 2 min of static handgrip (SHG). Simultaneously, calf blood flow (CBF) was measured by strain gauge plethysmography. An increase in MSNA, a decrease in CBF and an increase in calf vascular resistance (CVR) in the same resting limb occurred concomitantly during SHG. However, the increase in CVR was blunted in the second minute of handgrip when MSNA was still increasing. The results indicated that the decrease of CBF during SHG reflects the increase in MSNA, while the dissociation between MSNA and CVR at the later period of SHG may be related to metabolic change produced by the vasoconstriction.

Adult↗
PubMed1990

Heat-induced finger vasoconstriction controlled by skin sympathetic nerve activity.

Finger blood flow (BF) and skin sympathetic nerve activity (SSA) to the glabrous side of the hand were measured during immersion of the hand in a water bath in which temperature (Tw) was raised every 10 min by steps of 2 degrees C from 35 or 37 to 41 degrees C. The experiments were conducted during the summer in rooms in which ambient temperature was 28-32 degrees C or 35 degrees C. The nine healthy male subjects were wearing summer clothes. Finger BF through vessels located deep in the skin was measured by using laser-Doppler flowmetry (ALF-2100, Advance). With the use of a tungsten microelectrode SSA was recorded directly from the median nerve at the wrist or antecubital fossa of the tested arm. With finger vessels already dilated at Tw of 35 or 37 degrees C, finger BF decreased, with a concomitant increase in the SSA bursts as Tw rose to 39-41 degrees C. We confirmed in one subject that anesthetic blockade of the median nerve at the site proximal, but not distal, to the recording site blocked responses to the step rise in Tw in the SSA bursts and in finger BF. From these results we conclude that, with the subject in a warm state, blood vessels of the finger respond to local heating with vasoconstriction, and this finger vasoconstriction is evoked reflexively, largely through the increased sympathetic outflow to the resistance vessels of the finger.

Adult↗