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PubMedDate not supplied

Studies on the autonomic nervous system with SK&F 92657, a new antihypertensive agent causing direct arterial vasodilatation and beta-adrenoceptor blockade.

The beta-adrenoceptor-blocking properties of SK&F 92657, D,L-3-[2-(3-t-butylamino-2-hydroxypropoxy)phenyl]-6-hydrazinopyridazine, were studied in both in vivo and in vitro. The pA2 against isoprenaline tachycardia (beta 1 effect) in isolated guinea pig right atria was 7.16 (6.14-7.87). In contrast, histamine-induced tachycardia was unaffected by SK&F 92657. The pA2 against isoprenaline relaxation of guinea pig tracheal muscle (beta 2 effect) was 7.03 (6.28-7.61). In vivo ED50's against isoprenaline tachycardia (beta 1) and vasodilation (beta 2) in anesthetized cats were 5.7 x 10(-8) and 6.2 x 10(-8) mol/kg, i.v., respectively. Increases in heart rate caused either by activation of autonomic reflexes or by stimulation of efferent cardiac sympathetic nerves were also antagonized by SK&F 92657. The beta-adrenoceptor blockade caused by SK&F 92657 was shown to be competitive both in vivo an vitro and to be equally effective on beta 1- and beta 2-receptor populations. SK&F 92657 was a weak partial agonist in vivo and had only minimal local anesthetic activity. The compound had no direct effect on the functioning of the autonomic nervous system, apart from beta-blockade, but reflexes maintaining homeostasis were reduced because (1) SK&F 92657 is a beta-adrenoceptor antagonist preventing reflex increases in heart rate and cardiac output, and (2) it is a potent vasodilator counteracting reflex vasoconstriction. Postural reflexes were unaffected because SK&F 92657 selectively dilates arterial blood vessels.

Adrenergic beta-Antagonists↗
PubMed1983

Infant lesion effect: I. Development of motor behavior following neonatal spinal cord damage in cats.

This study was undertaken to determine the effect of spinal cord damage on motor development, and to determine whether there is greater survival of motor function in those motor patterns with a later onset of function than in those which are present at birth. The postnatal development of postural reflexes and locomotion was examined during the first 4 months of life in normal kittens and in those which had received a spinal cord lesion (at high cervical or low thoracic levels) at birth. The results suggest that there are some similarities in normal development, recovery of function after adult lesions and recovery and/or development of function after neonatal lesions. After neonatal lesions, just as after lesions in adults, reflex recovery appears to underlie recovery of locomotion. After spinal lesions, the pattern and sequence of motor development was identical to that seen in normal animals. Hindlimb motor development was normal for some time after the spinal lesion, but deficits appeared later. These observations suggest that postural reflexes and locomotion are not dependent upon ipsilateral descending input for their onset, but only for their maturation. Unexpectedly, tactile placing developed after neonatal spinal cord lesions. This represents sparing of function, for tactile placing is abolished and does not recover after the same lesion sustained in adulthood. Tactile placing is the last of the series of postural reflexes to develop. It depends on the last of the spinal pathways to develop, the corticospinal tract. Two aspects of this study support the hypothesis that later developing motor patterns will have a greater chance for survival and subsequent development than those which are present at birth. First, the immediate effects of spinal cord lesions on postural reflexes are more severe on those reflexes that are more mature at birth. Second, the spinal cord lesions produce more severe impairment of the more mature forelimb motor function than of the less mature hindlimb motor function. The hypothesis is not supported, however, when the long-term effect of spinal cord lesions on the maturation of motor behavior is considered. All postural reflexes and locomotion fail to mature fully, i.e. they retain characteristics of the immature responses.

Animals↗
PubMed1990

Hypothalamic lesioned rats given haloperidol mimic the behavior of intact rats given haloperidol plus morphine.

Lateral hypothalamic (LH) damage produces rats which exhibit sensory neglect, somnolence and akinesia, while ventromedial hypothalamic (VMH) damage produces rats which exhibit sensory hyperesponsiveness (Marshall and Teitelbaum, 1977). Rats with large lesions of both LH and VMH are somnolent and akinetic but hyperesponsive to touch. When given haloperidol (5 mg/kg) the LH-VMH-damaged rats adopt an actively maintained splayed out posture, in which the limbs are abducted and extended and the body lies flat on the ground. While in this posture, reflexes of postural stability, such as buttressing against a displacing force, are partially inhibited. These postural characteristics are similar to those of normal rats given haloperidol (5 mg/kg) plus morphine (20 mg/kg) (Pellis et al., 1986).

Animals↗
PubMed1989

Effects of unilateral loss of vestibular function on the vestibulo-ocular reflex and postural control.

Long-term recovery from surgically induced unilateral loss of vestibular function was studied in 14 patients. Seven patients underwent surgical extirpation or section of the vestibular nerve, and seven patients underwent labyrinthectomy without vestibular nerve section. The vestibulo-ocular reflex (VOR) and postural control were evaluated preoperatively and monitored for up to 4 years postoperatively with use of pseudorandom rotation (combined sinusoidal frequencies from 0.009 to 1.5 Hz) and moving platform posturography. Immediately following surgery all patients showed minimal reductions in the VOR gain constant, but marked reduction in the time constant, and marked increase in slow eye velocity bias. Bias returned to normal values within about 10 days, but time constants never returned to normal values. Results of standard Romberg tests in these patients were normal throughout the preoperative and postoperative periods. However, all patients showed marked postural control abnormalities in tests of the ability to maintain balance in unusual sensory environments in the immediate postoperative period. Seventy-five percent of the patients eventually recovered normal postural control. Postural control returned to near baseline performance with a time course similar to that of the VOR bias. However, postural control also continued to improve after the recovery of VOR bias was complete.

Adolescent↗
PubMedDate not supplied

Suppression of a somatosympathetic reflex by the gamma-aminobutyric acid agonist muscimol and by clonidine.

gamma-Aminobutyric acid (GABA) and GABA agonists, e.g., muscimol, reduce blood pressure and sympathetic outflow and inhibit the "carotid occlusion reflex." In contrast, muscimol exerted only marginal effects on postural reflexes in a prior study. The somatosympathetic reflex, i.e., potentials evoked in sympathetic nerves in response to sensory nerve stimulation, is a useful model for studying centrally acting drugs. Effects of muscimol on the reflex were examined in anesthetized normotensive rats. At doses which had previously been shown to reduce blood pressure but to produce only minimal attenuation of postural reflexes in conscious hypertensive rats, muscimol, administered intracerebroventricularly, reduced blood pressure and inhibited the somatosympathetic reflex in the present study. The time course of the evoked potential was not altered. Baroreceptor activation and intracerebroventricular clonidine also suppressed the reflex. The inhibitory effect of muscimol but not that of clonidine was prevented by pretreatment with the GABA antagonist bicuculline. Thus, the marked suppression of the somatosympathetic reflex by muscimol and by clonidine, in contrast to minimal effects on postural reflexes, point to the selectivity of their central inhibitory actions.

Animals↗
PubMed2004

Meta level concept versus classic reflex concept for the control of posture and movement.

Postural reflexes are replaced soon after birth by automatic reactions that allow for volition and cognition. It is still an enigma how this change in postural control is achieved. We suggest that the change involves the formation of a sensory processing level (meta level) that becomes interleaved in between the tight sensor-actuator coupling of the classic reflexes. We assume that the brain applies at this level intersensory interactions to reconstruct the physical stimuli which are causing the physiological stimuli and sensory signals. The thus derived estimates of the physical stimuli are then used as feedback signals in the posture control system. We present this concept on the background of the classic reflex concept and earlier attempts in the literature to overcome it. The earlier attempts were often motivated by the question how the brain prevents voluntary movements from being hampered by reflexive stabilisation of posture (so-called posture-movement problem). We compare our new concept with the classic reflex concept in a theoretical approach, by implementing both concepts into simple postural control models. In simulations of the two models we superimpose external perturbations (the physical stimuli) and a voluntary body lean movement. We show that it is possible to achieve successful stimulus compensation and unperturbed lean movement with both, the model derived from the new concept and the one of the classic reflex concept. With both approaches, the posture-movement problem does not arise. Based on preliminary considerations that include experimental findings from the literature, however, we conclude that the new concept provides more explanatory power than the classic reflex concept.

Animals↗
PubMed1987

Exaggerated postural vasoconstrictor reflex in Raynaud's phenomenon.

The central and local regulation of capillary blood flow in the finger was studied by the local xenon-133 washout technique in women with primary Raynaud's phenomenon, men with vibration induced white finger, and their respective sex matched controls. The vasoconstrictor response to venous stasis of 40 mm Hg elicited by local reflex was normal in both types of Raynaud's phenomenon. Change in posture from lying to sitting induced vasoconstriction in all groups, which was abolished by proximal nervous blockade. The vasoconstrictor response to sitting was augmented in both groups of subjects with Raynaud's phenomenon compared with their sex matched controls. These results show the existence of central and local postural vasoconstrictor reflexes in normal fingers. In both types of Raynaud's phenomenon there was hyperreactivity of the central sympathetic nervous system to orthostatic stress and normal function of digital arterioles and postganglionic sympathetic nerve fibres.

Adult↗
PubMed2005

Impairment and recovery of postural control in rabbits with spinal cord lesions.

The aim of this study was to characterize impairment and subsequent recovery of postural control after spinal cord injuries. Experiments were carried out on rabbits with three types of lesion--a dorsal (D), lateral (L), or ventral (V) hemisection (HS) at T(12) level. The animals were maintaining equilibrium on a platform periodically tilted in the frontal plane. We assessed the postural limb/trunk configuration from video recordings and postural reflexes in the hindquarters from kinematical and electromyographic (EMG) recordings. We found that for a few days after DHS or LHS, the animals were not able to maintain the dorsal-side-up position of their hindquarters. This ability was then gradually restored, and the dynamic postural reflexes reached the prelesion value within 2-3 wk. By contrast, a VHS almost completely abolished postural reflexes, and they did not recover for > or =7 wk. The DHS, LHS, and VHS caused immediate and slowly compensated changes in the postural limb/trunk configuration as well as gradually developing changes. After DHS, both hind limbs were placed in an abnormal rostral and medial position. After LHS, the limb on the undamaged side was turned inward and occurred at the abnormal medial position; LHS also caused a gradually developing twisting of the caudal trunk. VHS caused gradually developing extension of the ankle and knee joints. These findings show that ventral spinal pathways are of crucial importance for postural control. When a part of these pathways is spared, postural reflexes can be restored rapidly, but not the postural limb/trunk configuration. Spinal and supraspinal mechanisms responsible for postural deficits and their compensation are discussed.

Animals↗
PubMed1991

Baroreceptor reflexes in postural control of circulation in rabbits.

The present study was undertaken to evaluate reflex cardiovascular responses to postural stress in rabbits. The changes in mean arterial pressure (MAP) and heart rate (HR) were monitored in the supine position and following sudden passive head up tilt (HUT), and head down tilt (HDT) to 70 degrees. The results show a significant increase in MAP (18.57%, P less than 0.001) and HR (2.92%, P less than 0.02) with HUT; and a marked decrease in MAP (43.48%, P less than 0.001) and HR (8.21%, P less than 0.001) with HDT (as compared to the values in supine position). The changes in MAP were found to be more marked than those in HR. The depressor responses to HDT were more marked than the pressor responses to HUT.

Animals↗
PubMed1995

Age effects on reflex and postural responses to propriomuscular inputs generated by tendon vibration.

The effects of aging on two sensorimotor levels of propriomuscular function were investigated in a young (20- to 44-year-old) and an elderly (60- to 86-year-old) population by eliciting segmental reflex and postural responses via the same muscle spindle inflow generated by applying the same pattern of tendon vibration. The latency and amplitude of the reflex responses to vibration (tonic vibration reflex) of the biceps and triceps brachii did not depend on the subjects' age. No major age-related changes were observed in the deep reflexes of the lower limbs. The postural responses to the same vibratory stimulation applied to both the soleus or the tibialis anterior muscles (vibration-induced falling) did not show any changes in latency depending on either age or the visual conditions, whereas the intensity of these responses decreased both with age and when the use of vision was possible. Our results suggest that the two levels at which the same propriomuscular messages were processed are differentially affected by aging. The lower reflex level does not undergo any noticeable impairment, whereas the higher postural control level deteriorates in the elderly, which might be partly responsible for the balance problems which tend to occur more frequently with advancing age.

Adult↗
PubMed1986

Morphine subtracts subcomponents of haloperidol-isolated postural support reflexes to reveal gradients of their integration.

Although cataleptic rats do not spontaneously orient, scan, or walk, they will cling, stand, right themselves in the air, and resist being displaced from a stable position (Schallert, Whishaw, De Ryck, & Teitelbaum, 1978). Morphine produces a state of immobility in which all reflexes used for stable static support (e.g., standing, righting, clinging, and bracing) appear to be inhibited (De Ryck, Schallert, & Teitelbaum, 1980). Addition of morphine to haloperidol abolished or reduced those reflexes used to defend against slow postural displacements (e.g., bracing) but left intact those used to protect against fast postural displacements (e.g., righting in the air). However, although intact, these responses to fast postural displacements were completely abolished by labyrinthectomy, showing that they were controlled only by vestibular inputs. During recovery from morphine's effects, the responses to slow postural displacements reemerged, revealing fractional subcomponents. Furthermore, the reorganization of the subcomponents proceeded along specific body gradients; for example, bracing and standing reemerged caudorostrally, while at the same time, righting and clinging reemerged rostrocaudally.

Animals↗
PubMed1991

Reversal of nostril dominance by posture.

Reflex reversal of differential air flow through nostrils (DAFTN) by the adoption of suitable lateral recumbent position was studied in male Nigerian subjects. The subjects who demonstrated more air flow through the left nostril initially in the supine position, adopted left lateral recumbent (LLR) position which brought the decongested left nostril to the down-side and the congested right nostril to the upside. Within 3 to 4 minutes after the adoption of LLR position, the air flow through the nostrils was equalised and by 11th minute the DAFTN was reversed, with more air flowing through the upsided right nostril. Return of the subjects to supine position could not result in the recovery to the initial pattern of DAFTN. It is suggested that reversal of DAFTN with adoption of suitable lateral recumbent position was a reflex effect due to the pressure stimuli to the lower lateral side of the body particularly around the shoulder region and effect was mediated through the sympathetic innervation to mucosal venous sinuses of the nostrils. Possibility of gravitational effect was ruled out.

Adolescent↗
PubMed1985

Carotid sinus reflexes during postural changes, naturally elicited fighting behaviour, and phases of sleep in the cat.

Reflex responses of mean blood pressure and of heart rate to either bilateral common carotid occlusion (CO) or unilateral carotid sinus dilatation (CSD) during rest and different behaviours have been compared in conscious cats. Unloading and loading the carotid sinus receptors elicited equal reflex responses both of mean blood pressure and of heart rate during control immobile behaviour (CO: +34 +/- 6 mmHg and +35 +/- 6 beats . min-1; CSD: -37 +/- 4 mmHg and -52 +/- 11 beats . min-1), standing on the hindlimbs (CO: +36 +/- 5 mmHg and +29 +/- 5 5 beats . min-1; CSD: -40 +/- 6 mmHg and -61 +/- 10 beats . min-1), fighting against an attacking animal (CO: +34 +/- 5 mmHg and +31 +/- 5 beats . min-1; CSD: -37 +/- 5 mmHg and -56 +/- 10 beats . min-1), quiet wakefulness (CO: +37 +/- 5 mmHg and +38 +/- 4 beats . min-1; CSD: -34 +/- 4 mmHg and -53 +/- 8 beats . min-1) and synchronised sleep (CO: +36 +/- 5 mmHg and +37 +/- 4 beats . min-1; CSD: -36 +/- 4 mmHg and -52 +/- 6 beats . min-1). Desynchronised sleep was associated with an identical response to CSD (-30 +/- 4 mmHg and -51 +/- 7 beats . min-1) but with a reduced (p less than 0.01) reflex response to CO (+18 +/- 3 mmHg These data indicate that carotid sinus baroreflexes largely maintain their ability to modulate pressure upwards and downwards when blood pressure has been reset at somewhat higher levels by standing and fighting and at somewhat lower levels by synchronised sleep. The selective depression of carotid occlusion responses during desynchronised sleep suggests a central or peripheral shift of the baroreflex stimulus-response curve or a selective central inhibition of the reflex response to baroreceptor unloading.

Animals↗