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Biomedical subjects

R W Russell

Publications and source records attributed to R W Russell.

At least 37 records · Page 2Linked to original sources
PubMed1990

Pretreatment with an irreversible muscarinic agonist affects responses to apomorphine.

The main aim of the present study was to investigate if responses to the direct dopamine agonist, apomorphine, could be modified by changes in the activity of cholinergic neurones. A novel approach was adopted in which these responses were assessed following reduction of muscarinic receptor concentration (mAChR) in the brain (assessed from [3H] QNB binding) by the alkylating derivative of oxotremorine, N-[4-(2-chloroethylmethylamino)]-2-pyrrolidone (BM 123). Stereotyped responses elicited by apomorphine were significantly reduced when QNB binding was 12% and 50% of control values. No changes in [3H] spiperone binding were found. There was significant hypothermia in the group with 12% QNB binding sites which was significantly increased by apomorphine. Body temperature returned to normal when QNB binding was 50% of control values. There was a significant decrease in activity when QNB sites were reduced to 12% of normal and vertical activity was still significantly reduced at 50% QNB binding, though horizontal activity was not then different from controls. These data are consistent with the hypothesis that changes in the function of mAChR modify responses elicited by dopamine receptor stimulation in both the striatum and other brain regions.

Animals↗
PubMed1990

Global in vivo replacement of choline by N-aminodeanol. Testing a hypothesis about progressive degenerative dementia: II. Physiological and behavioral effects.

We have examined the progressive effects of replacement of dietary choline with NADe for a period of 120 days on a broad spectrum of behavioral and physiological functions known to involve the cholinergic system. The magnitudes of these effects tended to increase with time on the NADe diet, but those related to learning and memory were largely confined to the 60-120-day period. Neurochemical effects were concomitant with the replacement of Ch by NADe, being consistent with a hypocholinergic state as found in such progressive degenerative dementias as Alzheimer's disease. As cholinergic functioning was progressively impaired, basic physiological ("vegetative") processes appeared not to be affected. Apparently the rate at which the hypofunctional state developed was sufficiently slow for adjustments to occur, allowing the animal to adapt at a survival level to neurochemical changes. More complex behavioral functions were affected progressively, cognitive processes (e.g., learning and memory) being most sensitive and showing the least adaptability. We propose that the syndrome generated by NADe replacement of Ch represents an experimental model of progressive degenerative dementia.

Alzheimer Disease↗
PubMed1990

Cerebral venous thrombosis: new causes for an old syndrome?

The range of disorders affecting the cerebral veins and sinuses is increasing and now includes blood disorders, abnormalities in the patterns of blood flow, and infiltrative or inflammatory conditions, all of which may promote thrombosis. We describe 10 patients with cerebral venous thrombosis: two had protein S deficiency, one had protein C deficiency, one was in early pregnancy, and there was a single case of each of the following: dural arteriovenous malformation, intracerebral arteriovenous malformation, bilateral glomus tumours, systemic lupus erythematosus, Wegener's granulomatosis, non-Hodgkin's lymphoma. The recognition of such diverse aetiology may be importance since clinical features are non-specific, and may consist only of raised intracranial pressure, allowing confusion with 'benign intracranial hypertension'. The existence of effective treatment both for the thrombosis and for many of the underlying disorders makes early diagnosis essential. The prognosis of treated patients may be favourable.

Adolescent↗
PubMed1990

The natural history of non-arteritic anterior ischaemic optic neuropathy.

Seventy one patients with non-arteritic anterior ischaemic optic neuropathy were studied retrospectively. Sixty three (89%) were followed to the end of the study or death, mean follow up time was 5.3 years. Whilst twenty (28%) had diabetes or hypertension, in thirty nine (55%) no predisposing condition was identified. In those who had monocular disease at presentation (68), subsequent involvement of the second eye occurred in seventeen (25%), seven within the first year. Nineteen patients died within the study period. Of these, nine died from myocardial infarction and four from cerebrovascular disease. This is a significant increase above figures calculated from the Office of Population Census and Surveys (p less than 0.001 for all causes, p less than 0.002 for myocardial infarction and cerebrovascular disease). Such an increase in mortality has not been previously reported, and implies that this condition carries a more sinister systemic prognosis than is frequently supposed.

Adult↗
PubMed1990

A review of metabolism of labeled glucoses for use in measuring glucose recycling.

The fate of tritium from each carbon of D-glucose and the metabolism of L-glucose and 2-deoxy-D-glucose are known. Differences in metabolism of labeled glucoses can be used to quantify physical and chemical recycling of glucose. Only physical recycling is measured by [1-3H]-L-glucose, whereas [U-14C]-D-glucose measures total recycling. The difference between [1-3H]-L-glucose and [U-14C]-D-glucose, therefore, is chemical recycling. Recycling from extracellular binding sites and hepatic glucose 6-phosphate can be measured by difference between [1,2-3H]-2-deoxy-D-glucose and [1-3H]-L-glucose, and the difference in irreversible loss of the two will measure extrahepatic uptake of D-glucose. Recycling via Cori-alanine cycle plus CO2 is the difference in irreversible loss measured by using [6-3H]-glucose and [U-14C]-D-glucose. Recycling via the hexose monophosphate pathway can be determined by difference in irreversible loss between [1-3H]-D-glucose and [6-3H]-D-glucose. Recycling via CO2 and glycerol must be measured directly with [U-14C]glucose, bicarbonate, and glycerol. Recycling via hepatic glycogen can be estimated by subtracting all other measured chemical recycling from total chemical recycling. This review describes means to quantify glucose recycling in vivo, enabling studies of mechanisms for conservation and utilization of glucose.

Animals↗
PubMed1989

Effects of chronic in vivo replacement of choline with a false cholinergic precursor.

Chronic administration to rats of a diet in which all choline is replaced by NADe, an unnatural choline analog, results in a classical hypocholinergic syndrome characterized by progressive loss of learning and memory, hyperkinesis, hyperreactivity and hyperalgesia. Discontinuation of the artificial diet results in rapid elimination of NADe from both free and phospholipid-bound pools in all tissues studied, but the behavioral effects recede more slowly and incompletely. These results are consistent with a model in which choline and NADe compete in both acetylcholine and phospholipid synthesis, resulting in selective vulnerability of cholinergic neurons. Histological studies are in progress to determine whether microanatomical changes are also consistent with this model.

Animals↗
PubMed1989

Roles of neurotransmitter receptors in behavior: recovery of function following decreases in muscarinic receptor density induced by cholinesterase inhibition.

Cholinergic neurotransmitter levels were elevated in rat brain by reducing its inactivating enzyme, acetylcholinesterase (AChE), with an anti-AChE agent. Elevated levels result in decreases in cholinergic (muscarinic) receptors. Withdrawal of agent after 10 days of chronic treatment began a gradual return of neurochemical variables toward normal states, yet not fully achieving them within the following 29 days of the experiment. All behavioral and physiological variables measured showed significant effects at the start of the treatment period, developing tolerance at different rates as treatments continued. They also recovered differentially during withdrawal. Results are consistent with a theoretical model in which thresholds for normal functioning of different behavioral and physiological processes are associated with different receptor densities.

Acetylcholine↗
PubMed1989

Deactivation of tannin in high tannin milo by treatment with urea.

Experiments were conducted to determine the effectiveness of urea in deactivating tannin in high tannin milo. High tannin milo (Pioneer B 815, 3.4 +/- .3% tannin) was reconstituted with aqueous urea solutions to give combinations of 26, 30, and 34% moisture with 2, 3, and 4% urea (percentage of urea per dry weight of milo). All treatments were maintained at 25 degrees C and were effective in deactivating tannin with no differences among moisture or urea content. The average rate of tannin deactivation was 68 +/- 2% d-1. Temperature affected rate of tannin deactivation in milo reconstituted to 30% moisture and 3% urea when stored at 25 or 60 degrees C. Rate of tannin deactivation was 44 +/- 5 and 89 +/- 18% d-1 at 25 and 60 degrees C, respectively. Tannin in high tannin milo can be deactivated rapidly and completely by reconstitution with aqueous urea. These studies demonstrate that tannin is deactivated completely under conditions where urea is an effective preservative of high moisture milo.

Analysis of Variance↗
PubMed1988

Genetic and pharmacological models of cholinergic supersensitivity and affective disorders.

Increased muscarinic sensitivity has been associated with altered hormonal states (hypothyroidism and hyperadrenocorticism), chronic administration of muscarinic antagonists or antidepressants with muscarinic actions, selective breeding for anticholinesterase sensitivity, and certain inbred strains of rats and mice. Thus, both genetic and environmental factors may influence muscarinic receptor sensitivity. The reasonably detailed studies on the selectively-bred rats have revealed that the Flinders Sensitive Line (FSL) rats weigh less, are less active, are more sensitive to muscarinic agonists and to stressors, and have higher concentrations of hippocampal and striatal muscarinic receptors than 'normal', or the selectively-bred, Flinders Resistant Line (FRL) rats. Thus, there are a number of parallels between FSL rats and depressed humans. The FSL rats may be the first animal model of depression to mimic the actual trait of depression, and not just the state.

Acetylcholine↗
PubMed1988

Acute cerebral ischaemia: concurrent changes in cerebral blood flow, energy metabolites, pH, and lactate measured with hydrogen clearance and 31P and 1H nuclear magnetic resonance spectroscopy. III. Changes following ischaemia.

CBF has been measured with the hydrogen clearance technique in the two cerebral hemispheres of the gerbil under halothane anaesthesia. At the same time, intracellular pH and the concentrations of lactate and high-energy phosphates were measured in the brain using 1H and 31P nuclear magnetic resonance spectroscopy. Flow and metabolism have been followed during either a 15- or a 30-min ischaemic period (induced by bilateral carotid occlusion) and for up to 1 h of recovery. There was no significant difference between the flow characteristics of the two experimental groups. High-energy phosphate levels and pH returned to control within approximately 20 min of the end of the ischaemic period. Lactate clearance, following a 30-min occlusion, was slower than the recovery of pH. The concentration of free ADP, calculated from the creatine kinase equilibrium, was lower during the recovery phase than under control conditions.

Animals↗
PubMed1988

Kinetics of metabolism of glucose, propionate and CO2 in steers as affected by injecting phlorizin and feeding propionate.

Effects of injecting phlorizin subcutaneously and/or feeding propionate on metabolism of glucose, propionate and CO2 were determined for four steers used in a 4 x 4 Latin square design. Isotope dilution techniques were used to determine a four-pool kinetic solution for the flux of carbon among plasma glucose, rumen propionate, blood CO2 and rumen CO2. Injecting 1 g of phlorizin twice daily for 19 d resulted in 7.1 mol glucose C/d being excreted in urine. The basal glucose production of 13.4 mol C/d was increased to 17.9 mol C/d with phlorizin. There was no change in glucose oxidation or propionate production. The percentage of plasma glucose derived from propionate was unaffected by phlorizin, but 54 +/- 0.4% of total propionate was converted to plasma glucose during phlorizin treatment versus 40 +/- 0.6% during the basal treatment. When propionate was fed (18.3 mol C/d) glucose production increased to 21.2 mol C/d from the basal value of 13.4 mol C/d, and propionate oxidation to CO2 increased to 14.9 mol C/d from the basal value of 4.1 mol C/d. Glucose derived from propionate was 43 +/- 5% for the basal treatment and 67 +/- 3% during propionate feeding. The percentage of propionate converted to plasma glucose and blood and rumen CO2 was not affected by feeding propionate. An increased need for glucose, because of glucose excretion during phlorizin treatment, caused an increased utilization of propionate for gluconeogenesis, but an increased availability of propionate caused an increase in glucose production without affecting the relative distribution of carbon from propionate.

Animals↗
PubMed1988

Secretory patterns and metabolic clearance rate of porcine growth hormone in swine selected for growth.

Eleven Landrace pigs (six boars and five gilts, 50 kg) representing lines selected for three generations for maximum weight at 200 d of age were compared to eight pigs (four boars and four gilts, 50 kg) representing contemporary randomly selected Landrace controls to determine the effect of selection for growth on the metabolic clearance rate (MCR) and plasma concentrations of porcine growth hormone (GH). To estimate MCR of GH, the disappearance of a bolus of porcine GH was monitored over 120 min following its i.v. injection. Blood samples also were collected every 15 min over a 6-h period before injecting GH to determine baseline and overall mean GH concentrations, mean peak amplitude and number of GH secretory episodes. Boars exhibited greater overall mean GH concentrations (4.80 vs 3.11 ng/ml; P less than .05) and had greater maximum GH concentrations associated with secretory episodes (16.11 vs 10.80 ng/ml; P less than .05) than did gilts. There were no differences between boars and pigs exhibited greater baseline GH concentrations (2.04 vs 1.25 ng/ml; P less than .01) than did those from the unselected Landrace line. Selected and control pigs exhibited similar (P greater than .15) overall mean concentrations of GH, frequency of secretory episodes, amplitude of GH peaks and MCR. These data demonstrate that pigs selected for heavier weight at 200 d of age had greater basal plasma GH concentrations than did unselected control pigs.

Animals↗
PubMed1987

Clinical features of ischemia in cerebral arterial border zones after periods of reduced cerebral blood flow.

The clinical syndrome of border-zone ischemia is described in eight patients. Cerebral damage in four occurred during or after cardiac surgery and the other four patients had each experienced a period of severe hypotension. Cerebral blindness and visual disorientation are the most regular features and are produced by ischemic lesions in the parieto-occipital region, the common border-zone territory between all three arterial territories. Some patients show bibrachial sensorimotor impairment and a disturbance of volitional saccadic eye movement caused by more anteriorly placed ischemia in the anterior-middle artery border zone. Some show a temporary dyslexia/dysgraphia and memory defect related to bilateral parietotemporal lesions in the middle-posterior border zone.

Adult↗
PubMed1987

Influence of atropine and N-methyl atropine pretreatments on behavioral and physiological effects of the irreversible muscarinic agonist, BM123.

The irreversible muscarinic agonist, BM123 (63 mu moles kg-1, IV), was shown to produce central and peripheral physiological signs characteristic of cholinergic agonists. It also induced hypothermia, elevated nociceptive thresholds, reduced locomotor activity and disrupted spontaneous alternation performance in rats. The centrally acting muscarinic antagonist, atropine (50 mu mole kg-1) prevented or reduced all the above effects of BM123 when given SC 40 min prior to the BM123 injection. In contrast, the peripherally acting muscarinic antagonist, N-methyl atropine, prevented only the peripheral effects and the elevated nociceptive thresholds. Habituation of activity during a 20 min session was observed in all groups despite different levels of general activity. These findings are consistent with a model in which atropine and N-methyl atropine compete with BM123 for reversible association with the muscarinic receptor. In the case of BM123 administered alone, the association results, first, in agonist effects and proceeds to form an irreversible complex. Our present results show that by competing with BM123 for mAChR sites during the initial, reversible state of the interaction, atropine blocks the cholinomimetic effects of the agonist during both this state and its otherwise subsequent irreversible state.

Animals↗