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Aging escalates baroreceptor reflex suppression by the posterior hypothalamus in rats.

To examine whether baroreceptor reflex regulation by the posterior hypothalamus becomes modified with age, we compared baroreceptor reflex sensitivity and hypothalamic responsiveness in 2- and 10-month-old rats anesthetized with urethane-chloralose. Hypothalamic regulation of baroreceptor reflex sensitivity was assessed by recording responses to intravenously infused phenylephrine and afferent aortic nerve stimulation after sham operation or electrolytic destruction of the posterior hypothalamus. Regardless of age, reflex bradycardia and sympathoinhibition elicited during pressor responses to phenylephrine, as well as all cardiovascular and sympathetic nerve responses to afferent aortic nerve stimulation, were stronger in rats with bilateral hypothalamic lesions than in age-matched, sham-operated controls. Distinctively, because baroreceptor reflex sensitivity differed with age only in sham-operated controls but not in lesioned rats, we concluded that age-related differences in baroreceptor reflex sensitivity had been abolished by posterior hypothalamic lesions. Other experiments were then performed to compare responses to graded electrical stimulation of the posterior hypothalamus in baroreceptor-intact rats. Pressor and sympathoexcitatory responses to hypothalamic stimulation were larger, and stimulus thresholds were lower at 10 than at 2 months of age thereby suggesting that hypothalamic responsiveness had increased with age. Our results are in accord with the interpretation that aging exacerbates the baroreceptor reflex suppression normally exerted by the posterior hypothalamus.

Aging↗

Mechanisms of reflex vasodilation: assessment of the role of neural reuptake of norepinephrine and release of histamine.

The mechanisms of reflex vasodilation were studied in an innervated canine hindlimb preparation which was perfused at a constant rate. Reflex vasodilation was produced by suddenly increasing the pressure in the trunk by the intravenous injection of norepinephrine, with consequent stimulation of the baroreceptors. When the basal vasoconstrictor tone exerted by the sympathetic nervous system on the systemic arterial bed was minimized, either by pretreatment with the alpha adrenergic blocking agent phenoxybenzamine or with reserpine, which depletes endogenous catecholamine stores, reflex vasodilation was virtually abolished. Administration of cocaine, a drug which blocks reuptake of norepinephrine by the nerve terminals, significantly reduced reflex vasodilation, the response after cocaine averaging 47% of the vasodilator response in the control period. Cocaine also potentiated the vasoconstriction caused by intra-arterially administered norepinephrine but attenuated the vasoconstriction induced by tyramine. The antihistamine, tripelennamine, had effects similar to those of cocaine. It is suggested, therefore, that reflex vasodilation results from a sudden decrease in the level of norepinephrine at the neuroeffector junction, which is a consequence of the cessation of norepinephrine secretion, together with continued and possibly augmented uptake. When the uptake mechanism is impaired, either by the administration of cocaine or tripelennamine, the magnitude of reflex vasodilation is diminished. It does not appear necessary to postulate active secretion of a vasodilator substance to account for reflex vasodilation.

Animals↗

Interaction of cardiopulmonary and somatic reflexes in humans.

Activation of cardiopulmonary receptors with vagal afferents results predominantly in reflex inhibition of efferent sympathetic activity, whereas activation of somatic receptors reflexly increases sympathetic activity to the heart and circulation. Previous studies in experimental animals indicate that there is an important interaction between these excitatory and inhibitory reflexes in the control of the renal circulation. The purpose of this study was to determine whether there is a similar interaction between somatic and cardiopulmonary reflexes in humans. The activity of the cardiopulmonary receptors was altered (reduced) with lower body negative pressure (-5 mm Hg), which causes a decrease in cardiac filling pressure and a small reflex increase in forearm vascular resistance without accompanying changes in arterial pressure. Activation of somatic receptors by isometric handgrip for 2 min at 10 and 20% of maximum voluntary contraction resulted in reflex vasoconstriction in the nonexercising arm. Lower body negative pressure at -5 mm Hg produced a threefold augmentation in the forearm vasoconstrictor response to isometric handgrip in the nonexercising arm. This increase in resistance was significantly greater (P < 0.05) than the algebraic sum of the increases in resistance resulting from lower body suction alone plus isometric handgrip alone. Furthermore, it occurred despite a greater rise in arterial pressure, which would be expected to decrease forearm vascular resistance through activation of arterial baroreceptors and through passive dilatation of forearm vessels. Thus, removal of the inhibitory influence of cardiopulmonary receptors by pooling blood in the lower extremities enhances the somatic reflex. These data suggest an interaction between cardiopulmonary and somatic reflexes in the control of forearm vascular resistance in man.

Adult↗

Modulation of the mandibular stretch reflex sensitivity during various phases of rhythmic open-close movements in humans.

The muscle spindles of the jaw elevator muscles provide positive feedback to the alpha motoneurons. It is generally assumed that the feedback is modulated during chewing so that counterproductive forces of the jaw elevator muscles can be avoided during jaw opening. Our aim was to investigate the modulation of the muscle spindle input to the alpha motoneurons during various phases of open-close movements in man. To that end, subjects made rhythmic open-close movements at their natural chewing frequency. A force impulse (5 N, 10 ms), eliciting a jaw-jerk reflex, was unexpectedly applied. The impulse was applied to the mandible at 8 different phases during an open-close cycle, but only 1 impulse per cycle. Jaw movement and surface EMG of the masseter and temporal muscles on both sides were recorded during 3 cycles without an impulse and 3 succeeding cycles with an impulse. To examine whether the modulation of the mandibular stretch reflex sensitivity depends on the food resistance, we applied an additional external force on the mandible, counteracting closing of the jaw each cycle. Two experimental sessions were performed in random order, i.e., without force and with an additional force of 20 N. We observed pronounced reflexes at the onset of jaw closing, during the closing phase, and at occlusion. No or only weak jaw-jerk reflexes were present during jaw opening. The reflex amplitudes at occlusion were larger when an external force was present. This increase in reflex amplitude may be the result of an adjusted gamma motoneuron activity, from pre-motor inhibition, or from both. The reflex amplitudes elicited during jaw closing were not correlated with the phase of the movement.

Adult↗

A new approach to estimation of the number of central synapse(s) included in the H-reflex.

BACKGROUND: Among the main clinical applications of the H-reflex are the evaluation of the S1 nerve root conductivity such as radiculopathy and measurement of the excitability of the spinal motoneurons in neurological conditions. An attempt has been made to reduce the pathway over which H-reflex can be obtained in a hope to localize a lesion to the S1 nerve root, so the S1 central loop has been suggested. The main goal of this study is the estimation of the H-reflex number of synapse(s) for better understanding of the physiology of this practical reflex. METHODS: Forty healthy adult volunteers (22 males, 18 females) with the mean age of (37.7 +/- 10.2) years participated in this study. They were positioned comfortably in the prone position, with their feet off the edge of the plinth. Recording electrodes were positioned at the mid point of a line connecting the mid popliteal crease to the proximal flare of the medial malleolus. Stimulation was applied at the tibial nerve in the popliteal fossa and H, F and M waves were recorded. Without any change in the location of the recording electrodes, a monopolar needle was inserted as cathode at a point 1 cm medial to the posterior superior iliac spine, perpendicular to the frontal plane. The anode electrode was placed over the anterior superior iliac spine, and then M and H waves of the central loop were recorded. After processing the data, sacral cord conduction delay was determined by this formula: sacral cord conduction delay = central loop of H-reflex - (delays of the proximal motor and sensory fibers in the central loop). RESULTS: The central loop of H-reflex was (6.77 +/- 0.28) msec and the sacral cord conduction delay was (1.09 +/- 0.06) msec. CONCLUSION: The sacral cord conduction time was estimated to be about 1.09 msec in this study and because at least 1 msec is required to transmit the signal across the synapse between the sensory ending and the motor cell, so this estimated time was sufficient for only one central synapse in this reflex.

Adult↗

Spreading of sudomotor axon reflexes in human skin.

BACKGROUND: Acetylcholine (ACh) activates both sudomotor fibers and primary afferent nociceptors. This leads to sudomotor and vasodilator axon reflexes, which can be diminished, for example, in neuropathies. In some neuropathies, however, there is increased axon reflex sweating, a response pattern that has never been observed for vasodilator flares. OBJECTIVES: To compare both types of axon reflexes and to elucidate possible differences. METHODS: In healthy young male subjects, sweat response and flare reaction in response to ACh were quantified. Constant-current iontophoresis (300 mC) of ACh was performed on the lateral lower legs. The sudomotor axon reflex was visualized with iodine starch staining, and the sweat response was quantified with capacitance hygrometry (quantitative sudomotor axon reflex test [QSART]). The vasodilator flare was visualized and quantified by laser Doppler imaging. All measurements were performed during and for 10 minutes after finishing the iontophoresis. RESULTS: The sudomotor axon reflex area increased from 30.6 cm2 at the end of the iontophoresis to 39.2 cm2 (p < 0.001) 10 minutes later, while QSART response had already decreased. Flare size and flare intensity remained nearly constant during the observation period. CONCLUSION: Despite fast cleavage of acetylcholine by cholinesterases, sudomotor axon reflexes spread in the skin, indicating a possible peripheral amplification of sweating.

Acetylcholine↗

The effect of induced hyperthermia on the blink reflex in multiple sclerosis.

In 76 patients with multiple sclerosis, the blink reflex was elicted electrically at normal body temperature and during induced hyperthermia to observe the effect on conduction within the reflex pathway through the brainstem. Special attention was directed to 31 patients with electrophysiologic evidence of reflex slowing, presumably because of demyelination in the reflex pathway. Hyperthermia did not induce any significant changes in mean reflex latency, amplitude, or duration in either the overall group of 76 or in the 31 patients with baseline blink reflex abnormalities. While the mean reflex latency did not change, 13 (33 percent) of 39 abnormal R1 responses from the 31 patients changed by 1.5 msec or more during hyperthermia, whereas change of similar magnitude was noted in only three (3 percent) of 90 normal R1 responses.

Body Temperature↗

The effect of antiemetics on pupillary reflex dilation during epidural/general anesthesia.

UNLABELLED: The effect of dopamine D2 receptor antagonists, such as chlorpromazine and haloperidol, on pupil size in awake subjects suggests that these drugs might also alter pupillary reflex dilation and pupil size during general anesthesia. Forty-seven patients undergoing lower abdominal surgery under combined epidural/general anesthesia were randomized to receive one of the 5 following open labeled drugs: 10 mL saline, 0.13 mg/kg ondansetron, 0.25 mg/kg metoclopramide, 0.5 mg/kg metoclopramide, or 0.02 mg/kg droperidol. Three measurements of reflex dilation were taken at 5-min intervals and after the last measurement (time 0) the drug was administered. Measurements were then taken 5, 10, 20, and 40 min after I.V. drug administration. Reflex dilation was induced by intermittent noxious stimulation of the C5 dermatome with a tetanic electric current (60-70 mamp, 100 Hz, 3-s duration) after a stable level of epidural analgesia had been established with 3/8% bupivacaine and maintained with a continuous infusion. Metoclopramide produced a small decrease in pupil diameter and transiently depressed reflex dilation, whereas droperidol decreased pupil size at 10 min and depressed reflex dilation throughout the 40-min study period. Maximal change in reflex dilation was -6.6 +/- 3.3 mm-sec after droperidol. Ondansetron had no effect on pupil diameter or reflex dilation. When pupillary diameter measurements are used to gauge opioid levels during experimental conditions or during surgical anesthesia, antiemetic medication acting on the dopamine D2 receptor should be avoided. IMPLICATIONS: Miosis is often considered an effect of opioid administration during general anesthesia, but other drugs, such as antiemetics, might produce a similar effect on the pupil. This study demonstrates that 2 antiemetics, droperidol and metoclopramide, constrict the pupil and block the pupillary dilation brought about by nociceptive stimuli.

Adult↗

Airway protective reflexes evoked by laryngeal instillation of distilled water under sevoflurane general anesthesia in children.

To investigate how sevoflurane modifies airway protective reflexes in anesthetized children, we recruited patients younger than 12-yr-old for our study. Anesthesia was induced with inhaled sevoflurane in oxygen. The airway was managed with a laryngeal mask airway and the patient breathing spontaneously. Depending on the depth of anesthesia, the subjects were divided into two groups: Group 1 and Group 2 (1% and 2% of end-tidal sevoflurane concentration, respectively). Behaviors of the larynx were assessed mainly by the fiberscopic images of the larynx as well as respiratory flow and esophageal pressure. A small dose, 0.02 mL/kg of distilled water (minimum 0.2 mL) was instilled to the larynx through a channel of the scope to evoke an airway protective reflex from the larynx. The responses were categorized into passive (laryngeal closure, laryngospasm, and apnea) and active (cough, expiration reflex, and swallowing reflex) responses. Ten subjects were included in each group. In both groups, the primary responses were passive; however, in Group 1, active reflexes were also observed in 8 of 10 subjects; no subjects in Group 2 had active reflexes (P < 0.01). We concluded that, in children, the depth of general anesthesia with sevoflurane modified airway protective reflexes.

Anesthesia, General↗

Processing of mechanosensory signals in local reflex pathways of the locust.

The processing of mechanosensory signals responsible for the reflex adjustment of the posture or movement of the legs of the locust is described in terms of the actions and connections of identified neurones. Signals can be followed from the major classes of exteroceptors of a leg, through their various integrative stages in the central nervous system to their emergence as specific patterns in known motor neurones. Particular emphasis is placed on the integrative roles of two classes of local interneurones. The spiking local interneurones map the leg as a series of overlapping receptive fields and reverse the sign of the afferent input. The nonspiking local interneurones control the output of the motor neurones by the graded release of chemical transmitter and can adjust the gain of a local reflex depending on the position and movements of the joints of that leg. The reflex movements of one leg must not impair the stability of the animal and must therefore be influenced by events at the other legs. Populations of intersegmental interneurones convey sensory information from one segment to another to ensure such coordination. These interneurones do not produce stereotyped intersegmental reflexes but, instead, alter the performance of a local reflex in a distant leg by making synaptic connections with nonspiking local interneurones. These connections change the effectiveness of the outputs to the motor neurones and consequently the local reflex. The local interneurones therefore play a crucial role both in the production of local reflexes and in the integration of these actions with the movements of the other legs.

Afferent Pathways↗

Intersegmental reflex actions from a joint sensory organ (CB) to a muscle receptor (MCO) in decapod crustacean limbs.

In the walking legs of decapod crustaceans, intersegmental reflex actions originate from various joint proprioceptors. The activity of the 'accessory flexor' (AF) muscle, which with the myochordotonal organ (MCO) constitutes a muscle proprioceptor for the mero-carpopodite (M-C) joint, is modulated by the sensory discharge of a joint receptor (CB chordotonal organ) for the more proximal, coxo-basal (C-B) joint. Selective mechanical stimulation of the CB organ also reflexly modifies the motor activities of the main M-C flexor and extensor muscles (recorded as EMGs). 1. Dynamic CB stretch (as would occur during a dorso-ventral C-B movement - i.e. 'depression' of the limb) stimulates motor discharge to the M-C extensor muscle, while dynamic release of CB (as during a ventrodorsal C-B movement - or leg 'elevation') excites the accessory flexor as well as the main flexor muscle. 2. Successive M-C muscle responses to repetitive sinusoidal changes of CB length differ quantitatively according to the direction (stretch or release) of the first CB movement, in some cases increasing but more commonly 'adapting' with repetition. 3. Reflex discharge frequencies of the extensor, flexor and accessory flexor motoneurones increase with velocity of CB movement. 4. Eye illumination, and spontaneous or other sources of increased central excitability, generally increase the CB reflex drive to the flexor and accessory flexor muscles and, in parallel, decrease the reflex action on the extensor muscle. The results are discussed in terms of the role of proprioceptive reflexes in intersegmental co-ordination of the leg joints. In particular the significance of the reflex regulation of the myochordotonal receptors, and thereby the gain of the M-C resistance reflexes, is considered in the light of the observed 'co-activation' of main flexor and receptor muscle motoneurones.

Action Potentials↗

Analysis of the vagal reflex tracheal constriction in the dog.

We devised a preparation for measuring the vagal reflex tracheal constriction following the bronchoconstriction induced by histamine inhaled in the bronchial side in dogs. Properties of the vagal reflex tracheal constriction were investigated using this preparation. Histamine inhaled in the bronchial side caused the tracheal constriction following the bronchoconstriction. The tracheal constriction was inhibited by section of the bilateral superior laryngeal nerves or vagal cooling, respectively, but was not completely blocked. The combination of section of the bilateral superior laryngeal nerves and vagal cooling abolished the tracheal constriction. An i.v. administration of pentobarbital reduced both bronchoconstriction and tracheal constriction. These findings indicate that the tracheal constriction observed in the present study is mediated by the vagal reflex arc and that the extravagal pathway consisting of the recurrent and superior laryngeal nerves plays a role in a part of the afferent pathway of the vagal reflex airway responses. When the bronchoconstriction was completely abolished by isoproterenol inhaled in the bronchial side, the reflex tracheal constriction still existed. Transient inflation and deflation of the lungs caused reflex tracheal dilatation and constriction, respectively. We conclude that the vagal reflex airway constriction is due to complex effects which may be mediated by plural sensory receptors in the airways.

Animals↗

Intrathecal noradrenaline facilitates and inhibits the flexor reflex mediated by group II afferent fibers via alpha 1- and alpha 2-receptors, respectively.

The effects of intrathecal noradrenaline (NA) on the flexor reflex mediated by group II afferent fibers (group II flexor reflex) were investigated in anesthetized spinal rats. Low doses (0.01 and 0.1 mumol) of NA-HCl inhibited the group II flexor reflex, while high doses (1 and 10 mumol) facilitated it. In rats pretreated with the selective alpha 2-antagonist yohimbine-HCl (0.1 mumol), the effect of NA-HCl (0.1 mumol) shifted from inhibition to facilitation. Intravenous administration of prazosin-HCl (0.1 and 1 mg/kg, i.v.), a selective alpha 1-antagonist, dose-dependently antagonized the facilitation of the group II flexor reflex induced by NA-HCl in rats pretreated with yohimbine-HCl. The selective alpha 1-agonist methoxamine-HCl (1 mumol) and the alpha 2-agonist clonidine-HCl (0.1 mumol) facilitated and inhibited the group II flexor reflex, respectively. The effects of clonidine-HCl and methoxamine-HCl were almost the same as those of NA-HCl at doses of 0.1 and 10 mumol, respectively. NA-HCl (1 and 10 mumol) and methoxamine-HCl (1 mumol) increased the spontaneous electromyogram (EMG) spikes of the muscle tibialis anterior. The time course of the increase in the spontaneous EMG spikes was similar to that observed in the group II flexor reflex. These results suggest that NA facilitates and inhibits the group II flexor reflex via alpha 1- and alpha 2-receptors, respectively, and one of the mechanisms of the facilitatory effects is the elevation of excitability of the alpha-motoneuron.

Adrenergic alpha-Agonists↗

Neuronal excitation in the ventral tegmental area modulates the micturition reflex mediated via the dopamine D1 and D2 receptors in rats.

Involvement of the dopamine D(1) and D(2) receptors in the ventral tegmental area (VTA) in the micturition reflex was investigated using female Sprague Dawley rats under urethane anesthesia. Cystometrograms during continuous infusion of warmed saline into the bladder were recorded. When intervals of bladder contraction became constant, the excitatory amino acid DL-homocysteic acid (DLH) was microinjected into the VTA and changes in the cystometric parameters were observed. The selective D(1) antagonist SCH23390 (0.3 mg/kg) or D(2) antagonist eticlopride (0.1 mg/kg) was subcutaneously injected (s.c.) 15 min prior to the DLH treatment. A low dose of DLH (3 microg) facilitated the micturition reflex, whereas a high dose of DLH (30 microg) inhibited the micturition reflex. However, a middle dose of DLH (10 microg) did not show any effect. The facilitated micturition reflex induced by a low dose of DLH was inhibited by the selective dopamine D(2) antagonist eticlopride, but unaltered by SCH23390, a selective dopamine D(1) antagonist. In contrast, the inhibitory effect induced by a high dose of DLH on the micturition reflex was suppressed by SCH23390 but not eticlopride. These results suggested that the facilitated micturition reflex might be mediated via the dopamine D(2) receptors, while the inhibitory effects on the micturition reflex was mediated via the dopamine D(1) receptors.

Animals↗

Endogenous GABA does not mediate the inhibitory effects of gabapentin on spinal reflexes in rats.

The novel antiepileptic drug gabapentin was designed as a structural analog of gamma-aminobutyric acid (GABA). However, its mechanism of action remains unclear. In the present study, we investigated the effect of gabapentin on spinal reflexes in anesthetized rats. The mono- and polysynaptic reflex potentials were recorded from the ipsilateral L5 ventral root after stimulation of the L5 dorsal root. The dorsal root reflex potential, an index of presynaptic inhibition, was recorded from the ipsilateral L4 dorsal root. In non-spinalized (intact) and spinalized rats, intravenously administered gabapentin reduced the mono- and polysynaptic reflex potentials in a dose-dependent manner. These inhibitory effects of gabapentin were not suppressed by the GABA(A) antagonist picrotoxin. Moreover, gabapentin also decreased spinal reflexes in spinalized rats depleted of spinal GABA with semicarbazide, an inhibitor of the GABA-synthesizing enzyme. The dorsal root reflex potentials were not affected by gabapentin. These results suggest that endogenous GABA does not mediate the inhibitory effects of gabapentin on spinal reflexes.

Acetates↗

EEG evaluation of reflex testing as assessment of depth of pentobarbital anaesthesia in the rat.

Electroencephalography (EEG) was applied to evaluate the validity of the paw pinch reflex as an indicator of anaesthetic depth in rats which are anaesthetized with a single intraperitoneal dose of pentobarbital. After induction of the anaesthesia, characterized by the rapid loss of the animals' ability to maintain upright posture, the EEG of 10 out of 11 rats was dominated by paroxysmal (burst suppression) activity, associated with unconsciousness. In seven out of 11 rats, the paw pinch reflex was lost after onset of paroxysmal electroencephalographic activity. However, the paw pinch reflex remained present in four out of 11 animals, demonstrating that the response is independent of cortical activity. In five out of seven rats, the EEG still showed paroxysmal activity when the paw pinch reflex was regained. However, in two other rats the EEG returned to a pattern similar to that shown by awake animals, 4 and 21 min respectively, before the reflex was regained. These data indicate that in the pentobarbital-anaesthetized rat, presence of the paw pinch reflex is not related to the level of depression of electrical activity in the cerebral cortex, and consequently is probably not related to the level of consciousness. Based upon these findings it is concluded that the paw pinch reflex is unreliable as a sole indicator of anaesthetic depth.

Analgesics, Opioid↗

The negative acoustic reflex in retrocochlear disorders.

The most frequent impedance abnormality of an acoustic tumor is an absent reflex. However, this finding also occurs with middle ear disorders and is therefore nonspecific. This study recorded the contralateral acoustic reflex of human subjects suspected of having an acoustic tumor. Many tumor subjects, by visual inspection of the impedance bridge balance meter, appeared to have an absent reflex. Most of these subjects, in fact, had small amplitude negative reflexes by offline analysis on an averaging computer. Recognition of these negative reflexes increases the specificity and sensitivity of the reflex test for acoustic tumors. We recommend reflex testing with averaging computer monitoring to ensure their recognition.

Acoustic Impedance Tests↗

The expiration reflex from the vocal folds.

The authors present their 30 years' experience with expiration reflex. The reflex can be elicited from vocal folds by mechanical, chemical or electrical stimulation of the superior laryngeal nerve of man and laboratory animals, except mice and rats. It manifests itself by a short, forcible expiratory effort without a preceding inspiration which is indispensable for cough effort. The role of expiration reflex is to prevent penetration of foreign bodies into airways, expelling phlegm and detritus from subglottal area. The initial inspiration before expiration is undesired and could lead to inspiration pneumonia. The reflex is well known to laryngologists as '"laryngeal cough." Its receptors are small in number, localised mainly in medial margin of vocal folds deep in mucosa which can explain their stability in pathological conditions of the larygx. Afferentiation of the reflex is via laryngeal nerve similarly to sneezing and cough. Expiration reflex is not co-ordinated by a single "centre" but rather by a network system in the brain stem. Its motor pattern is supposedly produced by "multifunctional" population of medullar neurones in Botzinger complex and the rostral ventral respiratory group involved also in the genesis of breathing and cough. However, in cats also other neurones may play a vital role in production, shaping and mediation of the motor pattern of respiratory reflex, localised in rostral pons, lateral tegmental field or in the raphe medullar midline.

Animals↗