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Biomedical subjects

B E Levin

Publications and source records attributed to B E Levin.

At least 163 records · Page 9Linked to original sources

The relation of plasma norepinephrine and epinephrine levels over time in humans.

Plasma norepinephrine (NE) and epinephrine (E) levels were measured at 15 min intervals in 5 male and 7 female, healthy recumbent humans over periods of 4 h (n = 9), or 8 h (n = 3). Levels of both plasma catecholamines (CA) fluctuated both tonically and phasically over time. There was a pronounced downward ("tonic") trend in the levels of the 4 h subjects who had slept at home but no consistent trend was seen in the 8 h subjects who slept in the test bed overnight. The average (+/- S.E.) of median plasma NE levels was significantly lower (231.9 +/- 15.0 pg/ml) in the 4 h group than the 8 h group (356.9 +/- 6.7 pg/ml) probably due to the younger age of the 4 h group and the weakly positive correlation of NE levels with age. Plasma E levels showed no correlation with age and were not significantly different in the 4 h (111.6 +/- 27.0 pg/ml) or 8 h (98.2 +/- 13.7 pg/ml) groups. NE and E levels correlated well in 9 out of 12 subjects when the tonic trend was considered but levels correlated in only 6 out of 12 subjects when the tonic trend was removed and only phasic variations considered. Cardiovascular parameters showed inconsistent correlations to plasma CA in the 8 h subjects although plasma NE correlated positively with mean arterial blood pressure in all 3. These data suggest that resting plasma levels of both CA vary both tonically and phasically and correlate well in only some individuals, particularly when considered on a short-term, phasic basis.

Adolescent↗

Basal sympatho-adrenal function in quadriplegic man.

Plasma catecholamines (CA) were measured at 15 min intervals over a 4 h time period in 5 supine, chronic, quadriplegic male humans subjects. CA levels fluctuated over time through a wide range, often exhibiting brief bursts of very high CA levels which differed from the slower duration fluctuations seen in normal subjects. Spikes of increased plasma CA often, but not always, correlated with muscle spasms, urination or pain and were often accompanied by appropriate changes in blood pressure and heart rate. When examined over a 4 h period, the subjects' median plasma norepinephrine (NE) levels (305.5 +/- 26.8 pg/ml) were within the normal, age-corrected range while plasma epinephrine (E) levels (210.4 +/- 48.9 pg/ml) were higher than those seen in normal control subjects (89.0 +/- 6.9 pg/ml) tested under similar conditions. Also, plasma NE and E levels in the quadriplegics correlated positively in 3 out of 5 subjects which was similar to the balance in normal subjects. Therefore, resting sympatho-adrenal tone, as indicated by plasma catecholamine levels, in quadriplegics is not decreased, but is either normal or increased. Activation of these systems is probably under the control of local spinal reflexes which appear to be capable of maintaining many of the resting automatic functions of the individual.

Adrenal Glands↗

Dorsal column stimulation: Effect on human cerebrospinal fluid and plasma catecholamines.

Plasma and cerebrospinal fluid catecholamines were measured in three patients with multiple sclerosis who had dorsal column stimulators placed at the T5-7 levels. Stimulation for 3 minutes and 20 minutes increased release of plasma norepinephrine, epinephrine, and dopamine, as well as norepinephrine into the cerebrospinal fluid. Neither dopamine nor epinephrine was released into the spinal fluid during or after stimulation. Percutaneous stimulation did not release catecholamines into the plasma or spnal fluid, suggesting that these findings were not simply related to sensory stimulation or stress. Plasma catecholamine levels were inconsistently correlated with pulse rate changes during and after stimulation but not with blood pressure, although the changes in pulse rate and blood pressure were relatively small compared to changes in plasma catecholamines. This study suggests that plasma catecholamines and spinal fluid norepinephrine reflect central activation of sympathetic nervous system pathways and are more reliable indicators of sympathetic activity than changes in cardiovascular function.

Adult↗

The use of neurotoxins to characterize the rates and subcellular distributions of axonally transported dopamine-beta-hydroxylase, tyrosine hydroxylase and norepinephrine in the rat brain.

The effect of 6-hydroxydopamine (6-OHDA), colchicine and cytochalasin B on the transport and subcellular distribution of proteins, tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH) and norepinephrine (NE) were studied in the noradrenergic neurons of the rat locus coeruleus (LC). Four waves of transported 3H-labeled proteins and glycoproteins, defined by previous studies, as well as hypothalamic levels of TH, DBH and NE, were examined after injection of each neurotoxin into the ascending dorsal noradrenergic bundle. Blockade of subcellular components of TH, DBH and NE was compared to their endogenous hypothalamic distributions. 6-Hydroxydopamine variably blocked transport of all 4 waves of 3H protein and bilateral injections decreased hypothalamic levels of TH, DBH and NE by 58.2, 56.9 and 52.2% of controls, respectively. Cytochalasin B blocked transport of protein waves I (72--192 mn/day) and III (13--20 mm/day) and decreased hypothalamic levels of TH to 60.1% of control after bilateral injections. Colchicine blocked transport of waves I, II (24--48 mm/day) and V (1.4--2.9 mm/day) and blocked [3H]NE transport, while decreasing hypothalamic levels of DBH and NE to 56.6 and 69.3% of control after bilateral injections. Colchicine and 6-OHDA, but not cytochalasin B, caused a backup of DBH immunofluorescence proximal to the injection site. DBH and NE appeared to be transported primarily in particulate form, while TH transport was predominantly soluble in distribution. None of the toxins differentially affected the transport of one particular subcellular component of TH, DBH or NE. Based on the differential blocking effects of these toxins, DBH and NE appeared to be associated with wave II, and TH with wave III, travelling at 24--48 mm/day and 13--20 mm/day respectively.

Animals↗

Axonal transport of [3H]proteins in a noradrenergic system of the rat brain.

Proteins synthesized from [3H]leucine injected into the rat nucleus locus coeruleus (LC) were transported through the hypothalamus in 5 successive waves at rates of 72-192, 24-48, 13-20, 3-4 and 1.4-2.9 mm/day (waves I through V, respectively). Waves I through IV began axoplasmic transport in the LC within the first few hours after [3H]protein synthesis began in the LC. Wave V was delayed in onset for 1.7-3.7 days and was also probably transported through the contralateral hypothalamus. Wave IV was not transported within the LC-hypothalamic axons ascending through the dorsal noradrenergic bundle since its transport was not blocked by 6-OHDA lesions in this bundle, as was transport of the other 4 waves. Unilateral dorsal bundle lesions caused a well defined caudal backup of dopamine-beta-hydroxylase immunofluorescence and a fall in dopamine-beta-hydroxylase activity in the ipsilateral frontal cortex and hypothalamus of 55% and 9%, respectively. Bilateral lesions caused only a significantly further reduction in hypothalamic levels indicating crossed innervation of the hypothalamus by the LC of 27%. Waves I and II have been classified as rapid transport and contained 33% of the transported [3H]protein. Wave V was slowly transported and contained 51% of the transported [3H]protein, while wave III was intermediate in rate and contained 16% of transported [3H]proteins.

Adrenergic Fibers↗

The clinical significance of spontaneous pulsations of the retinal vein.

A search for spontaneous retinal venous pulsations was carried out in 218 subjects. Spontaneous venous pulsations were present in 87.6% of 146 unselected subjects 20 to 90 years of age and absent in 100% of 33 patients with raised intracranial pressure without papilledema and ten patients with papilledema. Lumbar puncture in nine patients with raised intracranial pressure established the upper level at which spontaneous pulsations disappear as 190 mm H2O, and no pressure above 180 mm H2O was found in 29 patients with venous pulsations present prior to lumbar puncture. There was no correlation between the presence or absence of venous pulsations and blood pressure. Some normal subjects with absent pulsations showed definite pulsations on subsequent examinations. These findings confirm that the presence of spontaneous venous pulsations is a reliable indicator of an intracranial pressure below 180 to 190 mm H2O, while the absence of pulsations may be found with normal intracranial pressure and is therefore not a reliable guide to raised intracranial pressure.

Adult↗

Further evidence of a possible association between house dogs and multiple sclerosis.

The present study was undertaken because of the recent report of an association between familial multiple sclerosis (MS) and prior ownership of a small pet. Forty-five patients with sporadic MS were retrospectively compared with 45 closely matched controls and were found to have owned a significantly greater number of indoor dogs prior to the onset of MS. Importantly, the MS patients had also had more exposure to neurologically ill dogs in the five years before the onset of symptoms. These new data further support the hypothesis that house dogs may serve as an animal vector in MS.

Animals↗

Axonal transport of [3H]fucosyl glycoproteins in noradrenergic neurons in the rat brain.

The transport of [3H]fucosyl glycoproteins has been investigated in the noradrenergic pathway from the locus coeruleus (LC) to the hypothalamus in the rat brain by use of local injection of L-[6-3H]fucose into the LC. Two discrete waves of 3H-glycoprotein pass through the hypothalamus in a caudorostral direction traveling at 4 mm/h (96 mm/day) and 2 mm/h (48 mm/day) respectively. Both waves appear to originate from the LC at approximately 2 h after the injection of [3H]fucose, a time when incorporation into glycoprotein has not yet peaked in the LC. Lesioning the LC-hypothalamic pathway with 6-OHDA, but not carrier solution, blocks both waves of 3H-glycoprotein demonstrating that transport occurs exclusively in the catecholamine axons within the pathway. DEAE-Sephadex chromatography combined with 6-OHDA lesions demonstrates clear differences in the character of 3H-glycoproteins in the two waves undergoing transport. The relative lack of labelling of hypothalamic glycoproteins in the interval before and after these waves suggests that relatively few rapidly transported glycoproteins contribute to the non-terminal axon membrane and are probably primarily transported to the nerve terminal. No evidence for slow axoplasmic transport of [3H]fucosyl glycoproteins is found.

Adrenergic Fibers↗

Axoplasmic transport of norepinephrine in the locus coeruleus-hypothalamic system in the rat.

The axoplasmic transport of norepinephrine (NE) between the nucleus locus coeruleus (LC) and the hypothalamus has been measured by three methods which employ the stereotaxic injection of [3H]catecholamines in the rat brain. [3H]NE is synthesized from [3H]dopamine (DA) injected into the LC and transported at a rate of 0.8-0.9 mm/h. This rate is probably an underestimate since it includes the time required for uptake and conversion of [3H]DA to [3H]NE prior to transport. Measurement of transport of [3H]NE between the posterior and anterior hypothalamus gives a rate of 2 mm/h which is independent of [3H]DA uptake and [3H]NE synthesis. This rate is in good agreement with the 1.9 mm/h figure calculated for [3H]NE transport in the system after LC injection of [3H]NE and represents a closer estimate of the true rate of axoplasmic transport than the 0.8-0.9 mm/h estimate. Transport of [3H]NE occurs through primarily ipsilateral NE fibers running in the median forebrain bundle and is blocked by 6-hydroxydopamine lesions in the bundle. Early appearing [3H]NE in the hypothalamus forms a relatively stable pool which is unaffected by median forebrain bundle lesions and is essentially unchanged by [3H]NE transported from the LC. This pool appears to be derived from non-specific spread of [3H]DA after injection, probably through the cerebrospinal fluid.

Afferent Pathways↗

Iatrogenic muscle fibrosis. Arm levitation as an initial sign.

Three patients had iatrogenic muscle fibrosis, without weakness or sensory loss. Deltoid muscle fibrosis produced the unique clinical sign of gradual, involuntary, and irreducible arm levitation. The third patient had both levitated arms and levitated legs, a result of injections in the rectus femoris muscles. Repeated intramuscular injections apparently resulted in muscle fibrosis and intramuscular nerve-twig damage. Pentazocine (Talwin) is a particularly offending agent. One patient showed an unusual tissue reaction to foreign material, which may have played a role in her muscle fibrosis. Nevertheless, dramatic recovery of muscle function followed surgical sectioning of the fibrous deltoid bands.

Adult↗

Loss of active avoidance of responding after lateral hypothalamic injections of 6-hydroxydopamine.

After injections of 6-hydroxydopamine (6-OHDA) along the medial forebrain bundle in the lateral hypothalamus, rats failed to acquire a one-way active avoidance response or failed to perform a previously acquired active avoidance response. Such rats, however, acquired a passive avoidance response and a conditioned taste aversion normally. Thus the effect of lateral hypothalamic injections of 6-OHDA was not a total loss of the capacity to acquire or perform conditioned responses, but was a failure to initiate forward movement in the presence of a conditional stimulus. Most of these rats could initiate a similar forward movement to escape from the unconditioned stimulus (foot shock). Failure to acquire or perform the active avoidance response was correlated with the loss of hypothalamic, striatal and forebrain catecholamines produced by lateral hypothalamic 6-OHDA injections. Identical injections of 6-ohda placed along the medial hypothalamus produced a similar loss of regional catecholamines, but medial 6-OHDA injections did not affect active avoidance responding. We interpret this dissociation between loss of catecholamines and the capacity for active avoidance responding to mean that medial 6-OHDA injections did not damage the same catecholaminergic terminal fields as lateral 6-OHDA injections and that the integrity of the terminal fields damaged by lateral 6-OHDA injections is necessary for active avoidance responding.

Amphetamine↗