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Biomedical subjects

S E Robinson

Publications and source records attributed to S E Robinson.

At least 55 records · Page 3Linked to original sources
PubMed1995

Effect of continuous-wave ultrasound on blood flow in skeletal muscle.

BACKGROUND AND PURPOSE: The purpose of this study was to determine the effect of ultrasound on forearm, skin, and muscle blood flow. SUBJECTS: Twenty volunteers without known vascular problems (10 male, 10 female) participated. METHODS: All subjects received a treatment of continuous-wave ultrasound to the anterior forearm at a dosage of 1.5 W/cm2 for a duration of 5 minutes. The contralateral forearm served as the control and received identical treatment, except the ultrasound output remained at zero. Forearm blood flow was measured using venous occlusion plethysmography, and skin blood flow was measured using cutaneous laser-Doppler flowmetry before and after ultrasound administration, with the difference being muscle blood flow. RESULTS: No differences between the control arm and the ultrasound-treated arm were found for muscle, skin, and forearm blood flow. CONCLUSION AND DISCUSSION: These results suggest that administration of continuous-wave ultrasound at the prescribed dosage had no effect on skeletal muscle blood flow for up to 30 minutes posttreatment. Thus, muscle hyperemia is probably not the primary mechanism responsible for the clinical benefits seen following the use of ultrasound as a therapeutic modality.

Adult↗
PubMed1995

The effect of cocaine and other local anesthetics on central dopaminergic neurotransmission.

The effects of cocaine on dopaminergic function in the rat were compared with those of other local anesthetics having an esteratic linkage (dimethocaine, procaine) or an amide linkage (lidocaine). By means of reverse-phase HPLC with electrochemical detection and gas chromatography-mass spectrometry, levels of dopamine (DA) and its metabolites 3-methoxytyramine (3-MT) and dihydroxyphenylacetic acid were quantified in the striatum, nucleus accumbens and prefrontal cortex after i.p. injection of the drugs or saline. Time course and dose response studies determined the effects of the drugs on these parameters of dopaminergic function. These studies provide strong evidence that the three esteratic local anesthetics cocaine, dimethocaine and procaine all increase the synaptic presence of DA, as reflected in increased levels of 3-MT and the ratio of 3-MT to DA, in the striatum, nucleus accumbens and prefrontal cortex. Surprisingly, procaine had an equal or greater effect than cocaine and dimethocaine on 3-MT levels and the ratio 3-MT/DA. The effects of these drugs on dihydroxyphenylacetic acid, an indicator of intraneuronal metabolism of DA, were more variable. However, the amidergic local anesthetic lidocaine did not affect DA metabolism. Although the exact mechanisms behind the dopaminergic activities of procaine and dimethocaine remain unknown, it is clear that these drugs, as well as cocaine, activate dopaminergic systems in the intact animal.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Maternal and fetal brain and plasma levels of cocaine and benzoylecgonine after acute or chronic maternal intravenous administration of cocaine.

The effect of repeated i.v. administration of cocaine HCl (1.5, 3 or 6 mg/kg daily) from gestational day 8 through gestational day 18 was studied on maternal and litter parameters in the pregnant female Sprague-Dawley rat. These doses of cocaine had no significant effect on maternal weight gain or nutritional intake and did not significantly affect litter size. Levels of cocaine and its metabolite benzoylecgonine in the brain and plasma of the dams and their fetuses were measured on gestational day 18 at 1, 5, 20 or 60 min after a single injection or 11 daily i.v. injections of cocaine (6 mg/kg). The shape of the time courses for cocaine differed somewhat between dams and fetuses, with fetal plasma concentrations of cocaine initially being lower than those of their dams and then by 5 min becoming equivalent to those of their dams. Although plasma concentrations of cocaine soon equilibrated between dams and fetuses, plasma concentrations of benzoylecgonine did not. Interestingly, brain concentrations of cocaine did not differ between dams and fetuses. The most remarkable finding was that the relative distribution of cocaine between brain and plasma differed after chronic vs. acute treatment, with a relative shift in the distribution of cocaine from plasma to the brain in the fetuses, and with the exception of the earliest time point measured, in the dams after repeated dosing.

Animals↗
PubMed1993

Prenatal exposure to methadone delays the development of striatal cholinergic neurons.

The effect of prenatal exposure to methadone via maternal osmotic minipumps on the expression of acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) has been studied by light microscopy in the striatum of male and female rats. At postnatal day 10, rats of both sexes exhibit reduced intensity of ChAT-immunoreactive staining in striatal neurons in the methadone-treated group in comparison to either untreated or water-treated controls. Although the number and distribution of ChAT-immunoreactive neurons appear to be similar across all three groups, the size (cross-sectional area) of these neurons is significantly smaller in the methadone-treated animals. By postnatal day 22, there are no differences in the ChAT immunoreactivity of striatal neurons between the water-treated and methadone-treated animals. The size of these neurons in female animals of both treatment groups is significantly larger than those of male animals in the same groups at postnatal day 22. AChE histochemical staining is qualitatively similar between treatment groups in both age groups. Thus, prenatal exposure to methadone appears to produce a delay in the expression of ChAT in striatal neurons. It remains to be demonstrated whether these differences are a direct effect of methadone exposure or are a consequence of neonatal withdrawal.

Acetylcholine↗
PubMed1993

Hypothermia blunts acetylcholine increase in CSF of traumatically brain injured rats.

Activation of muscarinic acetylcholine (ACh) receptors contributes to the pathophysiological consequences of moderate experimental traumatic brain injury (TBI). Hypothermia (30 degrees C) provides protection in experimental TBI. We measured ACh levels in CSF and plasma 5 min after moderate fluid percussion TBI under normothermic or hypothermic conditions, because ACh in the CSF has been correlated with the severity of behavioral deficits after TBI. Three groups were examined: TBI with hypothermic brain (30 degrees C), TBI with normothermic brain (37 degrees C), or sham TBI with normothermic brain (37 degrees C). ACh concentrations in CSF were significantly higher in 37 degrees C TBI rats, but not in 30 degrees C TBI rats compared to shams. ACh concentrations in plasma did not differ between groups. These results suggest that a contributing factor to the neuroprotective effects of moderate hypothermia in TBI may be related to the reduction of excessive ACh levels in the central nervous system following injury.

Acetylcholine↗
PubMed1993

Does being in the military affect nurses' perceptions of work life?

This study was a causal comparative investigation of military and civilian nurses' perceptions of selected aspects of work life. The Work Environment Scale, the Maslach Burnout Inventory and the Michigan Job Satisfaction Scale were administered to civilian and military samples matched on selected demographic variables. MANOVA procedures failed to reveal significant differences on measures of burnout and morale. Although military nurses were significantly more satisfied with issues of pay and fringe benefits, civilian nurses reported significantly greater job satisfaction, peer cohesion, supervisory support, decision making, autonomy, task orientation and opportunity to be innovative. These findings and suggested changes are discussed with attention to differences between the military and civilian work setting.

Adult↗
PubMed1992

Blockade of acute hypertensive response does not prevent changes in behavior or in CSF acetylcholine (ACH) content following traumatic brain injury (TBI).

There is evidence that the blood-brain barrier (BBB) is breached following traumatic brain injury (TBI), allowing the unregulated entry of circulating neuroactive substances into the central nervous system. As the traumatic episode is typically associated with an acute hypertensive event, which in itself may alter BBB status, the effects of the blockade of TBI-associated hypertension on injury-associated behavioral and cerebrospinal fluid (CSF) neurochemical changes were assessed in rats. Animals were injected with either saline or hexamethonium 15 min prior to a moderate fluid percussion injury while under light methoxyflurane anesthesia. This dose of hexamethonium was demonstrated to block the hypertensive response to TBI. Pretreatment with hexamethonium prevented neither acute nor more enduring behavioral deficits observed after TBI. Hexamethonium did not prevent TBI-associated increases in CSF acetylcholine (ACh) content in separate group of rats sampled 12 min following TBI. Furthermore, histological inspection indicated that hexamethonium did not prevent TBI-induced disruption of the BBB, as assessed by intravascular horseradish peroxidase (HRP). Thus, blockade of the hypertensive response to TBI does not afford behavioral protection nor does it prevent changes in the BBB or CSF ACh content following TBI. TBI is in itself sufficient to modify behavior, neurochemistry and BBB function in the absence of hypertension.

Acetylcholine↗
PubMed1992

The effect of cobrotoxin on cholinergic neurons in the mouse.

By using multiple time-point constant-rate infusions of deuterium-labeled phosphorylcholine, appropriate kinetic parameters were obtained for use in the calculation of the turnover rate of acetylcholine (TRACh) in selected mouse brain regions. After obtaining these data, the relationship between the analgesic agent cobrotoxin (CT) and the activity of central cholinergic neurons was investigated by determination of TRACh in selected mouse brain regions 3 hours following intracerebroventricular (i.c.v.) injection of CT. There were no obvious changes in the concentrations of ACh and choline (Ch) in the cortex, hippocampus, hypothalamus, midbrain, striatum, or thalamus of the mouse after injection of an analgesic dose of CT (2 micrograms, i.c.v.). TRACh in the thalamus and the striatum were significantly increased, as compared to controls. On the other hand, i.c.v. injection of CT was found to significantly reduce TRACh in the hippocampus and midbrain. These results suggest that the activity of hippocampal and midbrain cholinergic neurons is suppressed by CT, whereas the activity of striatal and thalamic cholinergic neurons is increased by CT at a time when a maximum analgesic response to CT is expressed.

Acetylcholine↗
PubMed1991

Prenatal exposure to methadone affects central cholinergic neuronal activity in the weanling rat.

The effect of prenatal exposure to methadone via maternal osmotic minipumps was studied on brain regional acetylcholine (ACh) turnover and dopamine (DA), norepinephrine (NE), serotonin (5-hydroxytryptamine, 5-HT) and their metabolites in 21-day-old female and male rats. ACh content was not affected in any region studied. However, the turnover rate of ACh (TRAch) was increased significantly in the striata and parietal cortices of both sexes. Two gender-specific changes were observed: a profound decrease in hypothalamic TRACh in the females and an increase in hippocampal TRACh in the males. No changes were observed in TRACh in the medulla-pons or the frontal cortex of either sex. The reduction in TRACh was accompanied by a threefold increase in DA content in the hypothalamus of the methadone-exposed females. No other changes were observed in DA, NE, or 5-HT, save for increased 5-HT content in the medulla-pons of the male methadone-exposed rats. Thus, prenatal methadone exposure produces several lingering changes in cholinergic function, many of which were not apparent in the immediate postnatal period. Although striatal ACh content was no longer reduced in methadone-exposed rats, striatal cholinergic function remains disrupted. It remains to be proven whether these differences are a direct effect of methadone exposure or are a consequence of neonatal withdrawal.

Acetylcholine↗
PubMed1991

Nurse burnout: work related and demographic factors as culprits.

This study was an examination of the combined ability of perceived work environment, demographic, and work-related variables to predict burnout among 314 nurses at a large metropolitan hospital. The three dimensions of burnout measured were emotional exhaustion, depersonalization, and personal accomplishment. High work pressure and low work involvement and supervisor support predicted emotional exhaustion. Task orientation, work pressure, work involvement, and age predicted both depersonalization and personal accomplishment. Burnout among nurses on each of the three work shifts also was examined. Results are discussed from the perspective of how to decrease or to prevent burnout among nurses.

Adult↗
PubMed1990

The effect of prenatal exposure to methadone on neurotransmitters in neonatal rats.

The effect of prenatal exposure to methadone via maternal osmotic minipumps was studied on neurotransmitter content of 4-day-old male and female rats. Several sex-related differences were observed in brain regional neurotransmitter content. Prenatal exposure to methadone produced only selective changes in brain regional neurotransmitter content. Exposure to methadone in doses sufficient to produce maternal and fetal dependence selectively reduced striatal acetylcholine content and produced a sex-dependent change in hindbrain acetylcholine.

Acetylcholine↗
PubMed1990

The effect of M1 muscarinic blockade on behavior and physiological responses following traumatic brain injury in the rat.

Dicyclomine (1 mg/kg or 10 mg/kg), scopolamine (1 mg/kg), or saline was administered intraperitoneally to rats 15 min prior to moderate fluid percussion brain injury. A variety of reflexes and responses were measured up to 60 min following injury, and body weight and several neurological measures were taken daily up to 10 days following injury. All 3 antimuscarinic treatments reduced the duration of transient behavioral suppression as assessed by these measures. It appears that blockade of the M1 muscarinic receptor can attenuate transient behavioral suppression associated with concussive brain injury. Thus, stimulation of M1 muscarinic receptors may mediate components of reversible traumatic unconsciousness following cerebral concussion. No differences were observed between saline and antimuscarinic treatments in the incidence or duration of apnea following injury. Scopolamine pretreatment significantly elevated heart rate prior to injury, but had no significant effect on the responses of heart rate and blood pressure to experimental concussion. Both doses of dicyclomine significantly reduced resting heart rate, but unlike scopolamine, significantly enhanced the cardiovascular response to fluid percussion injury. Antimuscarinic treatment significantly reduced body weight loss and certain motor deficits, including beam balance and beam walk performance, following concussive head injury. Scopolamine and both doses of dicyclomine appeared to be equally effective in reducing long-term deficits. Data from these experiments indicate that at least some of the long-term behavioral deficits following moderate levels of brain injury may involve the binding of acetylcholine to M1 muscarinic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The effect of acetylcholine depletion on behavior following traumatic brain injury.

Rats were injected with either saline; A-4 (40 mg/kg, i.p.), a bis tertiary amine derivative of hemicholinium-3; or A-5 (50 micrograms/kg, i.p.), a bis quaternary amine derivative of hemicholinium-3, 1 h prior to moderate fluid percussion brain injury. A variety of reflexes and responses were measured up to 60 min following injury, and body weight and several neurological measures were taken daily up to 10 days following injury. Pretreatment with either A-4 or A-5 significantly attenuated components of transient behavioral suppression, as well as more enduring deficits in body weight and beam walk and beam balance performance. A-4 administered prior to fluid percussion was found to reduce striatal, but not pontine, acetylcholine content. A-5 did not significantly reduce acetylcholine content in either area. Both A-4 and A-5 pretreatment prevented a significant increase in acetylcholine content in the cerebrospinal fluid following fluid percussion injury; however, only A-5 significantly reduced plasma acetylcholine content. These results confirm cholinergic involvement in the production of both transient and longer-lasting behavioral deficits following traumatic brain injury. Furthermore, traumatic brain injury may allow plasma constituents to gain access to the central nervous system.

Acetylcholine↗
PubMed1990

The effect of cholinergic manipulations on the analgesic response to cobrotoxin in mice.

Intracerebroventricular (i.c.v.) injection of cobrotoxin (CT), a neurotoxin isolated from the venom of Naja naja atra, produced an antinociceptive response in mice as measured by the tail-flick test. This effect of CT was blocked by systemic administration of atropine, but not by methylatropine or naloxone. Depletion of central acetylcholine (ACh) by hemicholinium-3 (HC-3) blocked the antinociceptive action of cobrotoxin. These results suggest that central cholinergic neurons are important for the mediation of the antinociceptive properties of cobrotoxin.

Acetylcholine↗
PubMed1989

The effects of morphine and traumatic brain injury on central cholinergic neurons.

This study examined the effects of morphine and fluid percussion traumatic brain injury (TBI) on the activity of cholinergic neurons in specific areas of the rat brain 12 min after injury. Acetylcholine (ACh) turnover, used as an index of cholinergic neuronal activity, was determined using gas chromatography-mass spectrometry. Although morphine administration alone in general did not significantly affect ACh content and turnover in specific brain areas, morphine administered prior to TBI either prevented injury-induced changes in ACh turnover (dorsal pontine tegmentum) or actually reduced the rate constant for ACh utilization (kACh) and the turnover rate of ACh (TRACh) following injury (thalamus, amygdala, cingulate/frontal cortex, and hippocampus). Thus, the protective effects of morphine against enduring behavioral deficits following TBI may involve the inhibition of central cholinergic neurons.

Acetylcholine↗
PubMed1989

Life stress and lymphocyte alterations among patients with rheumatoid arthritis.

The relation between life stress and immune parameters was investigated for 33 female rheumatoid arthritis (RA) patients interviewed during three routine monthly clinic checkups. Life stress from major and minor events, coping efficacy, and self-reported psychological distress were assessed, and immunofluorescence of T-cells and B-cells was performed on the blood drawn during each visit. Small stressful events were positively related to the proportion of circulating B-cells, psychological distress was inversely related to proportion of circulating T-cells, and major life events were associated with lower T-helper/T-suppressor cell ratios.

Adaptation, Psychological↗