Toshiyoshi Matsukawa

Effect of heat stress on muscle sympathetic nerve activity in humans.

To elucidate the effect of heat stress on the sympathetic nervous system, we evaluated changes in muscle sympathetic nerve activity (MSNA), plasma arginine vasopressin (AVP), tympanic temperature, skin blood flow, cardiac output, mean blood pressure, and heart rate in 9 subjects in response to acute heat stress induced by raising the ambient temperature from 29 to 34 degrees C and then to 40 degrees C. With the heat exposure, MSNA was significantly increased with a significant increase in tympanic temperature. Skin blood flow and heart rate were also significantly increased, while mean blood pressure tended to decline and cardiac output tended to increase. The combination of the increased MSNA and skin blood flow may have caused the redistribution of the circulatory blood volume from the muscles to the skin, facilitating convection heat loss. The increases in MSNA counteracted the lowered blood pressure during heat exposure. Thus, the increased MSNA may play an important role both in thermoregulation and in the maintenance of blood pressure against heat stress.

Age-related changes in baroreflex control of heart rate and sympathetic nerve activity in healthy humans

To determine how the baroreflex control of sympathetic nerve activity is affected by aging, muscle sympathetic nerve activity (MSNA) from the tibial nerve was monitored using microneurography, and heart rate and blood pressure were recorded during the pressor or depressor responses to intravenous injections of phenylephrine or nitroglycerin in 39 healthy humans, aged 16 to 56 years. Although the baroreflex slope for heart rate showed attenuation with aging, the baroreflex slope for MSNA was not affected by aging. These data suggest preservation of the baroreflex control of sympathetic nerve activity despite attenuation of the baroreflex control of parasympathetic nerve activity by aging in humans.

Baroreflex control of muscle sympathetic nerve activity is attenuated in the elderly.

To determine whether the baroreflex control of sympathetic nerve activity is attenuated in the elderly, muscle sympathetic nerve activity (MSNA) from the tibial nerve was monitored using microneurography, and heart rate and blood pressure were recorded during the depressor (phase II) or pressor (phase IV) period to Valsalvas maneuver in 10 younger subjects and 7 aged subjects. The baroreflex slope for heart rate showed attenuation in the aged subjects during the pressor phase but not during the depressor phase, the baroreflex slope for MSNA was also attenuated in the aged subjects during the pressor and tended to be attenuated during the depressor phases. These data suggest impaired baroreflex function for both heart rate and sympathetic nerve activity in the elderly.

Altered muscle sympathetic nerve activity in hyperthyroidism and hypothyroidism

To determine whether sympathetic nerve activity is altered in hyperthyroidism and hypothyroidism we microneurographically measured muscle sympathetic nerve activity in patients with these thyroid dysfunctions and compared the results with those of normal controls. Patients with hyperthyroidism tended to have less muscle sympathetic nerve activity than normal controls, and patients with hypothyroidism had significantly greater muscle sympathetic nerve activity than normal controls (P < 0.05). In all subjects, there was a significantly negative-correlation between the serum concentration of free triiodothyronine or free thyroxine and muscle sympathetic nerve activity, and there was a significantly positive correlation between the serum concentration of thyroid-stimulating hormone and the muscle sympathetic nerve activity. These results suggest an inverse relationship between thyroid function and sympathetic nerve activity.

Effect of oral ethanol intake on muscle sympathetic nerve activity and cardiovascular functions in humans

The aim of the present study was to clarify the acute effect of alcohol drinking on muscle sympathetic nerve activity and other cardiovascular variables in young healthy human volunteers. Seven volunteers (25.0 +/- 4.7 years in age, weighing 59.9 +/- 5.9 kg) were instructed to lay down on a bed, and muscle sympathetic nerve activity (MSNA) was microneurographically recorded from the tibial nerve, simultaneously with an electrocardiogram, blood pressure with Finapres and autosphygmomanometer, cardiac output by impedance cardiography, and skin blood flow by laser Doppler flowmetry. After a 1-h rest, the subjects drank alcohol (0.6 g/kg) and were remained in resting position for 105 min. Blood ethanol levels indicated that they were moderately intoxicated. Heart rate constantly increased until 30 min after the ingestion, and maintained a peak level. MSNA was slightly but significantly suppressed just after the ingestion, and was gradually enhanced until the end of the experiment, showing a significant difference from the control level until 40 min in burst rate and until 25 min in total MSNA after the ingestion. Blood pressure showed an abrupt and transient increase at first, then gradual decrease until 30 min after the ingestion, and maintenance of the resting level until the end of the experiment. Cardiac output showed no constant tendency and no significant differences after the ingestion with wide interindividual variation. Skin blood flow increased 15 min after the ingestion.(ABSTRACT TRUNCATED AT 250 WORDS)

A new method of quantifying human muscle sympathetic nerve activity for frequency domain analysis.

We present a new method for quantitative analysis of muscle sympathetic nerve activity (MSNA), expressed as muscle sympathetic burst area (MSBA). This technique is likely to be useful for inter-individual comparisons and for frequency domain analysis of MSNA. After standardization of MSNA so that the burst of highest amplitude in the integrated MSNA trace was 1000 units, MSNA was assessed by measuring the area of each burst in the integrated MSNA trace, with baroreflex latency of about 1.3 sec while triggered by consecutive R-waves of the ECG. We examined the relationship between MSBA and burst rate (burst number/min) or plasma norepinephrine levels at rest in 50 healthy subjects, aged 23-82 years. MSBA showed positive correlations with burst rate (r = 0.91, n = 50) and plasma levels of norepinephrine (r = 0.64, n = 22). During head-up tilting in 6 subjects, MSBA showed linear correlations with sine values of tilt angles and with plasma norepinephrine levels. These results suggest that MSBA is a useful index of MSNA for evaluating both intra-individual and inter-individual variations of MSNA.

Skin sympathetic nerve activity and event-related potentials during auditory oddball paradigms

Skin sympathetic nerve activity (SSNA) from the tibial nerve and event-related brain potentials (ERPs) were recorded simultaneously during auditory oddball paradigms with a counting task in 10 healthy subjects to elucidate the relationships between the autonomic nervous system and the cognitive process. After the target tones. SSNA bursts were observed more frequently than after the non-target tones. Moreover, the amplitudes of SSNA bursts elicited after the target tones were higher than those elicited after the non-target tones. However, when subjects ignored the series of tones, there was no significant difference between the incidence of SSNA bursts after rare tones and frequent tones. The P300 latencies for the target trials with SSNA bursts were shorter than those for the target trials without SSNA bursts. The average ERP wave forms for the target trials with SSNA bursts showed larger positive deflection in the early part of the P300 component than those for the target trials without SSNA bursts. We conclude that SSNA is generated in relation to the conscious cognitive process, as well as to the reactive automatic process to changes in repeating stimuli. The early part of the P300 component, possibly P3a, may be related to the mechanisms that generate SSNA.

Stellate Ganglion Block Is Associated with Increased Tibial Nerve Muscle Sympathetic Activity in Humans

Background Left stellate ganglion block has been shown to increase heart rate and blood pressure, possible because of blockade of afferent vagal fibers from arterial baroreceptors in the aortic arch. Because efferent muscle sympathetic nerve activity (MSNA) is influenced by the arterial baroreflex, the hypothesis that left stellate ganglion block increases efferent MSNA recorded from the tibial nerve of humans was tested. Methods Twenty healthy male volunteers were sequentially assigned to one of three groups: stellate ganglion block (n = 10), in which 7 ml 1% mepivacaine was injected into the left stellate ganglion; placebo (n = 5), in which 7 ml of saline was injected into the left stellate ganglion; and intramuscular injection (n = 5), in which 7 ml mepivacaine was injected into the left deltoid muscle. Direct intraneural microneurographic recording with a tungsten microelectrode was used to record MSNA in the left tibial nerve. MSNA, heart rate, and blood pressure were recorded before and after injection in all groups. An additional five volunteers were studied with transthoracic echocardiography to examine the effect of stellate ganglion block on preload changes. Results Tibial nerve MSNA increased after mepivacaine injection to the left stellate ganglion but was unchanged after saline injection to the left stellate ganglion or mepivacaine injection into the deltoid muscle. Heart rate increased significantly after the left stellate ganglion block but did not change significantly after saline injection to the left stellate ganglion or after mepivacaine injection to the deltoid muscle. Systemic blood pressure did not change significantly in all groups. Left ventricular end-diastolic area and left ventricular end-diastolic circumference did not change after stellate ganglion block. Conclusions Tibial nerve MSNA increased during left stellate ganglion block with mepivacaine.

Neural and humoral controlling mechanisms of cardiovascular functions in man under weightlessness simulated by water immersion.

To clarify how neural and humoral mechanisms operate to control cardiovascular functions in man under weightlessness, the response of sympathetic nerve activity was observed in healthy human subjects by means of microneurographic technique with the changes of several hemodynamic parameters and hormonal responses during thermoneural head-out water immersion. Muscle sympathetic nerve activity was markedly suppressed by head-out immersion, concomitantly with a reduction of the leg volume, an increase of the stroke volume and a reduction of total peripheral resistance. At the same time, plasma level of norepinephrine, vasopressive and antidiuretic hormones (ADH, aldosterone, renin activity, angiotensin I-II) were reduced, while vasodepressive and diuretic hormone (ANP) was markedly increased. The systemic blood pressure was maintained almost unchanged during head-out water immersion. The suppressive response of sympathetic nerve activity seemed to be age-dependent. This response was less prominent in the elderly than in young subjects. It is concluded that the suppressive response of muscle sympathetic activity plays an important role to maintain hemodynamic homeostasis under weightlessness to compensate for the cephalad fluid shift and the resultant increase of the stroke volume in cooperation with the hormonal responses.

Effect of metoclopramide on muscle sympathetic nerve activity in humans

The aim of this study was to determine the effect of metoclopramide on the sympathetic nervous system. Muscle sympathetic nerve activity was increased in two stages after metoclopramide injection. The initial increase in sympathetic nerve activity may result from the unloading of arterial baroreceptors because there was a negative correlation between mean blood pressure and muscle sympathetic nerve activity. The later increase in muscle sympathetic nerve activity may be attributed to the central activation of the sympathetic nervous system because there was a positive correlation between mean blood pressure and muscle sympathetic nerve activity. These results suggest that metoclopramide activates the sympathetic nervous system by two different mechanisms.