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Biomedical subjects

E Tadaki

Publications and source records attributed to E Tadaki.

15 recordsLinked to original sources
PubMed2000

Effects of prestimulus respiratory levels on inhibitory respiratory response by nociceptive muscular afferents.

We have previously shown that the inhibitory respiratory response, which we call post-stimulus suppression, is induced by nociceptive muscular afferents. This phenomenon is thought to be caused by a negative feedback induced by excessive afferent inputs. In the present study, we investigated whether augmented levels of prestimulus respiration would influence the magnitude of poststimulus suppression by recording the phrenic nerve discharges in chloralose-urethane anesthetized, vagotomized, paralyzed and artificially ventilated cats. The respiratory level was augmented by means of either hypercapnia, hypoxia or naloxone administration, all of which markedly facilitated the peak amplitude (PK) of integrated phrenic discharges, neural tidal volume. When the electrical stimulation of thin-fiber muscular afferents was performed at these augmented PK levels, the magnitude of poststimulus suppression in the PK was markedly attenuated without consistently altering the facilitatory response during the stimulation period. It seems that the facilitatory component of the augmented level of resting respiration may reduce the inhibitory component of poststimulus suppression. The results indicate that prestimulus respiratory activity is an important factor in determining the magnitude of poststimulus suppression.

Animals↗
PubMed2000

Morphine inhibits resting respiration, but it attenuates reflexive respiratory suppression in anesthetized cat through kappa-receptor.

Noxious stimulation of thin-fiber muscular afferents induces a reflexive respiratory suppression that we call "poststimulus respiratory suppression." In anesthetized, vagotomized, paralyzed, and artificially ventilated cats, morphine depressed the level of resting respiration (inhibitory effect on resting respiration) and attenuated the magnitude of the poststimulus respiratory suppression (excitatory effect on the reflexively modified respiration). These two kinds of morphine effects were antagonized by naloxone, suggesting the participation of opioid receptors. To clarify the opioid receptor subtypes responsible for these effects of morphine, three type-selective opioid antagonists-naltrindole (delta antagonist), gamma-funaltrexamine (mu antagonist), and Mr2266 (kappa antagonist)-were tested. The morphine-induced depression in the resting respiration was antagonized by pretreatment with the kappa antagonist, not with the mu or delta antagonist. Furthermore, the morphine-induced attenuation in the magnitude of the poststimulus suppression was also blocked by the kappa antagonist, but not by the mu or delta antagonist. In conclusion, (1) morphine inhibits resting respiration, but it attenuates the magnitude of the poststimulus respiratory suppression; (2) both these morphine effects are mediated by kappa opioid receptors. The possibility that the kappa(3) receptor, one of the kappa receptors subtypes, mediates the two kinds of morphine effects has been discussed.

Analgesics, Opioid↗
PubMed1990

Augmentation of muscle nociceptive respiratory reflex facilitation by vagal afferents.

Vagal influence on the facilitation of phrenic neural activity during respiratory phase-locked, gastrocnemius muscle nerve nociceptive electrical stimulation was examined in anesthetized, glomectomized, paralyzed, and artificially ventilated cats. (1) In the vagi-intact state, respiratory reflex facilitation was characterized by a sharp rise in peak amplitude, maximum rate of rise or slope, and mean rate of rise of integrated phrenic nerve activity. This was greater during inspiratory phase-locked (T1-locked) muscle nerve electrical stimulation than during expiratory phase-locked (TE-locked) muscle nerve electrical stimulation. "Evoked post-inspiratory phrenic activity" during the early expiratory phase was also observed during TE-locked muscle nerve electrical stimulation. (2) Bilateral vagotomy significantly attenuated the respiratory facilitation during both T1- and TE-locked muscle nerve electrical stimulation. In particular, the "evoked post-inspiratory phrenic activity" during TE-locked muscle nerve electrical stimulation was also attenuated or almost completely abolished. (3) Conditioning electrical stimulation of the vagus nerve revealed facilitatory reflexes which co-exist with inspiratory inhibitory reflexes. (4) The "evoked post-inspiratory phrenic activity" during TE-locked muscle nerve electrical stimulation, which was attenuated or abolished after vagotomy, was restored after vagal T1-locked conditioning stimuli combined with TE-locked muscle nerve electrical stimulation. The results suggest that vagal facilitatory reflexes augment the respiratory reflex facilitation during muscle nociceptive stimulation.

Afferent Pathways↗
PubMed1988

Respiratory changes induced by activation of testicular afferents in dogs.

Reportedly, more than 90% of the testicular afferents of the dog are of the polymodal type. The possible involvement of these afferents in modulation of respiration was studied using anesthetized dogs, which had been vagotomized and with both common carotid arteries ligated. Electrical stimulation of the superior spermatic nerve at an intensity of 1/5 Tc (Tc: threshold intensity for C-fiber activation) induced no substantial changes in respiration, while above 1/2 Tc it induced an increase in minute expiratory volume (VE), or a decrease followed by an increase in VE. The pattern of respiratory change was converted from the former to the latter by increasing the stimulation frequency while maintaining the same intensity. Mechanical stimulation of the testis through a stimulator with a tip of 1 cm in diameter caused an increase of VE at 200 g and a decrease followed by an increase of VE above 500 g. Intra-arterial injection of bradykinin (3 x 10(-6) M), hypertonic saline (1.5 M) and high K+ solution (180 mM) to the spermatic artery induced similar respiratory changes. Pneumograms showed a shift in end-expiratory position even at stimulus intensities without significant VE changes. Phrenic nerve recordings from some artificially ventilated dogs, revealed an prolongation of the first expiratory phase followed by augmentation of phrenic activity, mostly an increase in respiratory rate. Comparison between afferent activities and reflex respiratory changes suggests that above described two types of respiratory changes are brought about by the activities of testicular polymodal receptors.

Animals↗
PubMed1987

Respiratory depression caused by either morphine microinjection or repetitive electrical stimulation in the region of the nucleus parabrachialis of cats.

In chloralose-urethane anesthetized, vagotomized, paralyzed and artificially ventilated cats, respiratory response to either repetitive electrical stimulation or microinjection of morphine in the rostral pons was studied by recording the phrenic nerve discharges. In the region of the nucleus parabrachialis (PBN) and its ventral reticular formation, electrical stimulation delivered in 20 successive expiratory periods caused the respiratory depression to last long after the termination of stimulation. This respiratory-depressant effect could be reversed by naloxone. By a single electrical stimulation delivered in most of these effective sites, a phasic phrenic excitation was consistently elicited in the period of both expiration and inspiration, and the reduction in expiratory duration could be observed when the stimulation was delivered in expiratory period. In the microinjection study of 2.66 nmol morphine in 0.1 microliter in the localized area of the dorsolateral portion of the PBN, a significant reduction in both respiratory outputs and the rate of increase in inspiratory activity could be induced within 1 min after the application. The respiratory depression thus caused by both methods was quite similar in several respiratory variables. Thus an involvement of the PBN region in long-lasting respiratory modulation mediated by endogenous opioid system is suggested.

Animals↗
PubMed1985

Naloxone-reversible respiratory inhibition induced by muscular thin-fiber afferents in decerebrated cats.

Stimulation of muscular thin-fiber afferents of cats causes two types of respiratory suppression: one is stimulus-locked suppression which is not affected by naloxone, and the other is naloxone-reversible respiratory suppression after cessation of the stimulation. Both types of respiratory suppression could still be evoked after decerebration of cats at the midcollicular level. The present experiment revealed that muscular thin-fiber afferents, presumably polymodal receptor afferents, caused respiratory inhibition mediated through an opiate system in the brain structure below the caudal part of the brain stem.

Animals↗
PubMed1983

Two different inhibitory effects on respiration by thin-fiber muscular afferents in cats.

In anesthetized, vagotomized, paralyzed, and artificially ventilated cats, respiratory responses to electrical stimulation of the gastrocnemius muscle nerve were studied by recording the phrenic nervous discharges. Besides intensity-dependent facilitation of respiration, electrical stimulation of the thin-fiber muscular afferents caused two different types of respiratory suppression, during and after the stimulation. The first suppressive phase ('initial suppression') was observed immediately after the start of stimulation above A-delta fiber threshold, and usually accompanied by a fall of blood pressure. The other suppressive phase ('after suppression') was observed within several minutes after the cessation of the stimulation. The intensity of stimulation required to evoke the 'after suppression' was much higher than that for the 'initial suppression', and was usually in the C fiber stimulation range. Naloxone did not affect the 'initial suppression', but abolished the 'after suppression'.

Animals↗
PubMed1983

Post-stimulus facilitatory and inhibitory effects on respiration induced by chemical and electrical stimulation of thin-fiber muscular afferents in dogs.

In anesthetized, vagotomized, paralyzed, and artificially ventilated dogs, respiratory responses to both electrical stimulation of the muscle nerve and chemical stimulation of muscular (polymodal) receptors by means of intra-arterial injection of NaCl solution were studied by recording phrenic nervous discharges. During the period of stimulation both types of stimulation caused intensity-dependent facilitation of neural respiratory outputs. After cessation of stimulation, facilitation persisted for a long time (more than 5 min) with a lower intensity stimulation; however, suppression was observed with a higher intensity stimulation. The present results suggest that afferent inputs from the muscular polymodal receptors activate long-acting central mechanisms for enhancement or suppression of respiration.

Animals↗
PubMed1981

Naloxone effects on the blood pressure response induced by thin-fiber muscular afferents.

Naloxone effects on the blood pressure level and on the blood pressure responses induced by thin-fiber muscular afferent stimulation were studied in anesthetized, bilaterally vagotomized and carotid sinus nerve-denervated dogs under artificial ventilation. Repetitive pulses of 8 Hz with various intensities were applied to the gastrocnemius nerve for 1 min while monitoring the compound action potentials. The mean arterial pressure significantly (P less than 0.001) rose by 10.95 +/- 1.78 mmHg (mean +/- S.E.) about 5 min after a naloxone injection. Compared with the reflexive response in the control period, the depressor effect significantly decreased by 3.80 +/- 1.06 mmHg, and the pressor effect significantly increased by 3.63 +/- 0.73 mmHg for 30 min after the injection of naloxone. No correlation was found between naloxone effects on the blood pressure level and on the reflex response, indicating an involvement of different mechanisms with these naloxone effects. We suggest that endogenous opiates might participate in the regulation of the blood pressure level, as well as of the blood pressure responses caused by thin-fiber muscular afferents.

Afferent Pathways↗
PubMed1981

Hemihidrosis due to skin pressure with particular remarks on the intensity and area of the pressure stimuli.

Sweating of symmetrical areas of the torso was measured by means of both the filter paper method and electrohygrometric method. Spontaneous sweating rates of the left and right side of the upper and lower chest and the back were statistically highly correlated. Reduction of sweating by pressure application to the unilateral subaxillary region ("pressure hemihidrosis") was studied quantitatively with 12 combination of pressure stimuli, i.e., 1, 2, 3 and 4 kg weights applied to disks with a surface area of 2, 6 and 16.6 cm/, respectively. The amount of reduction in sweating rate was proportional to both the intensity and the surface area to pressure applied. It was revealed that hemihidrotic effects induced from the unit area of pressure stimulation was statistically highly correlated to the pressure intensity.

Adult↗
PubMed1980

A possible participation of endogenous opiates in respiratory reflexes induced by thin-fiber muscular afferents.

In anesthetized, vagotomized, paralyzed, and artificially ventilated dogs, naloxone effects on respiratory responses induced by thin-fiber muscular afferents were studied by recording phrenic nerve discharges. Naloxone augmented respiratory outputs, before, during, and after the stimulation. Two different types were found in the returning phase of the respiratory response by thin-fiber muscular afferent stimulation: respiratory outputs were supressed below the pre-stimulus level within several minutes after the cessation of the stimulus in some cases, while in the other cases they remained above the pre-stimulus level. In the latter cases, naloxone did not change the pattern of returning phase of the response, on the other hand, in the former cases, the after-suppression was significantly reduced by naloxone. The present results suggest that endogenous opiates play a role in setting the level of respiratory outputs and that in addition to facilitatory effects on respiration, thin-fiber muscular afferents drive a negative feedback system via neurohumoral mechanisms.

Afferent Pathways↗