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Biomedical subjects

D G Lambie

Publications and source records attributed to D G Lambie.

At least 19 recordsLinked to original sources
PubMed1987

Effects of ethanol ingestion on blood pressure reactivity.

We examined the acute effects of ethanol consumption on circulatory responses to the cold pressor test, to handgrip exercise and to intravenous infusion of methoxamine in eight normal male subjects. Ethanol consumption reduced systolic blood pressure responses to the cold pressor test and to handgrip exercise and depressed both systolic and diastolic blood pressure responses to infusion of methoxamine. The depressant effects of ethanol on blood pressure responses to methoxamine were considerably greater than the effects on the cold pressor test and handgrip exercise. Catecholamine concentrations during the cold pressor test and handgrip exercise were not significantly different with or without prior ethanol consumption. Alcohol has been shown to have an acute hypotensive action with all the stimuli.

Adult↗
PubMed1987

Respiratory responsiveness in male alcoholics after withdrawal.

Peripheral and central chemosensitivity were assessed in eight abstinent male alcoholic patients and in seven healthy normal male subjects. Hypoxic rebreathing (15% O2, 7% CO2) was used to stimulate the peripheral and central chemoreceptors together. Hyperoxic rebreathing (93% O2, 7% CO2) was used to examine the central chemoreceptor response independently of the peripheral chemoreceptors. Minute ventilation was examined in relation to end-tidal PACO2 under the two conditions. Neither peripheral nor central chemoreceptor responses were significantly altered in the alcoholic as compared to the control subjects. Abnormal chemoreceptor function is therefore unlikely to be an important factor in the development of abnormal respiratory events during sleep in abstinent alcoholic subjects.

Adult↗
PubMed1986

Effects of ethanol on cardiovascular and catecholamine responses to mental stress.

The purpose of this study was to examine the effects of ethanol on heart rate, blood pressure and plasma noradrenaline and adrenaline responses to mental stress, involving reactions to anxiety and excitement produced using a cognitive task with electric shock and a competitive electronic game respectively. Twenty subjects were studied, each subject acting as his own control by participating twice, with and without prior ethanol consumption. Mental stress was associated with significant increases in all variables except plasma noradrenaline during the cognitive task. Ethanol raised baseline heart rate and plasma adrenaline, but significantly reduced the responses of these variables to the cognitive task but not to the electronic game. Systolic blood pressure responses to both experimental stressors and diastolic blood pressure responses to the electronic game were also significantly reduced after ethanol. These results may reflect a tension-reducing effect of ethanol in situations associated with anxiety, but suggest a more general effect of ethanol on blood pressure reactivity.

Adult↗
PubMed1986

The effects of acute and chronic ingestion of ethanol on the autonomic nervous system.

Evidence is reviewed linking clinical effects of ethanol with actions on the sympathetic and parasympathetic nervous systems. The studies reported include a series of investigations by the authors. Acutely, ethanol causes peripheral vasodilation and may also result in changes in heart rate and blood pressure. Ethanol may contribute to acute problems which may present clinically, including micturition syncope, accidental hypothermia and facial flushing. However, increased sympathetic nervous activity plays a role in causing hypertension and other symptoms during ethanol withdrawal in chronic alcoholics. Some chronic alcoholics may have neuropathy involving sympathetic nerves, and this can result in distal sweating loss and occasionally in orthostatic hypotension. Also, hypothalamic lesions associated with Wernicke's encephalopathy may result in hypothermia. Neuropathy involving parasympathetic nerves in not uncommon in alcoholics with other evidence of nervous system damage, but it is generally asymptomatic. Occasionally, vagal neuropathy may cause disorder of gastrointestinal motility, and neuropathy affecting the sacral innervation may be a factor in alcoholic impotence.

Alcoholic Intoxication↗
PubMed1986

Factors which influence the effectiveness of treatment of epilepsy.

Despite recent advances in the management of epilepsy, some patients continue to have seizures which defy therapeutic intervention. To examine factors which may influence the successful application of therapy a survey was carried out of 103 patients, with a previous diagnosis of epilepsy, who had a seizure for which an ambulance was called. It was evident that anticonvulsants are not always used to their maximum potential or under optimal conditions. Problems which were identified in treatment included the widespread use of polypharmacy. Patients contributed to failure of seizure control by lack of compliance with therapy (29 patients) and by excessive alcohol consumption (19 patients).

Alcohol Drinking↗
PubMed1986

Comparison of mefenamic acid and propranolol with placebo in migraine prophylaxis.

The prophylactic effects of the antiprostaglandin agent mefenamic acid on migraine attacks were compared with propranolol or placebo in a double-blind crossover study of 29 patients. In the 17 patients who completed the trial the frequency of attacks and their total duration were significantly reduced during mefenamic acid therapy or propranolol therapy as compared to placebo. There were no significant effects of mefenamic acid or propranolol on average duration or severity of migraine attacks. The study suggests that mefenamic acid and propranolol are equally effective for migraine prophylaxis.

Adult↗
PubMed1985

No improvement in ethanol-induced memory deficits after administration of a vasopressin analog.

Acute ingestion of ethanol impairs memory, an effect which might be related to ethanol-induced inhibition of vasopressin release. This was studied using tests of memory and cognitive function in 26 normal subjects before and after ethanol ingestion. Equal numbers of subjects received randomly, by double-blind intranasal administration, placebo or 1-desamino-8-D-arginine vasopressin prior to ethanol ingestion. Administration of the vasopressin analog did not reverse the ethanol-induced deficits in memory and cognitive function.

Administration, Intranasal↗
PubMed1985

Non-compliance with anticonvulsant therapy as a cause of seizures.

Compliance with anticonvulsant therapy was assessed in 95 epileptic subjects with uncontrolled seizures. Following a seizure for which an ambulance was called, patients were interviewed and questioned on their medication taking. Compliance was also determined from measurement of anticonvulsant concentrations in saliva, and from intervals between collection of drugs from pharmacy. Compliance failure was found to be instrumental in precipitating 29 (31%) of seizures for which the ambulance was called. At the time of interview, 35 (37%) subjects were not taking their medication regularly in accordance with prescribing instructions. In addition to forgetting medication, many subjects deliberately stopped or changed doses of drugs. Other causes of non-compliance which were indentified included patient misunderstanding of prescribing instructions. Compliance with therapy was positively related to perceived benefit from anticonvulsant therapy.

Adolescent↗
PubMed1985

Alcoholic brain damage and neurological symptoms of alcohol withdrawal--manifestations of overhydration.

Central nervous system damage is a major complication of alcohol abuse. Vitamin deficiency, particularly thiamine deficiency, has a role in producing pathological and psychological changes of alcoholic brain damage, but it is likely that alcohol has a direct toxic effect on the brain. It is proposed that neuropathological abnormalities seen in alcoholics, and also neurological symptoms during alcohol withdrawal, may reflect cerebral edema caused by alcohol. The neurological symptoms of alcohol withdrawal show a similarity to those seen in hyponatremia or water intoxication. It is suggested that alcoholics show overhydration particularly during withdrawal and that pathological changes in the alcoholic brain are related to cerebral edema. Cerebral edema in withdrawing alcoholics may be caused by inappropriate section of vasopressin (antidiuretic hormone).

Alcoholism↗
PubMed1985

Beta-adrenoceptor responsiveness and plasma catecholamines as determinants of cardiovascular reactivity to mental stress.

Twenty-five normotensive men were subjected to two periods of mental stress involving a cognitive task and a competitive electronic game. Plasma catecholamines, heart rate and blood pressure were measured before and during mental stress. Responsiveness to beta-adrenoceptor stimulation was also determined in each subject by measurement of heart rate responses to bolus injections of isoprenaline. Both periods of mental stress were associated with significant increases in systolic and diastolic blood pressures, heart rate and plasma adrenaline, but not plasma noradrenaline. Heart rate responses to mental stress varied widely, with increases ranging from 1 to 48 (mean +/- SD 13.5 +/- 10.6) beats/min for the cognitive task and from 2 to 49 (20.4 +/- 14.0) beats/min for the electronic game. Systolic blood pressure responses also varied widely and showed significant positive correlations with heart rate responses. Significant relationships were found between heart rate responses to both forms of mental stress and cardiac sensitivity to isoprenaline, subjects with low responsiveness to beta-adrenoceptor stimulation tending to have smaller heart rate responses to mental stress than subjects with high responsiveness to beta-adrenoceptor stimulation. Relationships were also found between plasma adrenaline responses and heart rate responses to mental stress, although these did not reach significance. Considerably improved relationships were found when heart rate responses were correlated with a single variable generated from the product of the adrenaline response and the inverse of the dose of isoprenaline required to raise heart rate by 25 beats/min. It is concluded that wide variation is shown between different individuals in responsiveness to beta-adrenoceptor stimulation and that this is an important factor in the variability between individuals in heart rate and systolic blood pressure responses to mental stress. Both catecholamines and adrenoceptor-mediated responses to catecholamines should be examined when determining the physiological basis for differences in cardiovascular reactivity to mental stress between individuals or groups.

Adult↗
PubMed1985

Sleep apnoea in alcoholic patients after withdrawal.

Respiration during sleep was studied in 16 withdrawn alcoholic patients and in 12 control subjects. The alcoholic patients had increased numbers of central (P less than 0.01) and of obstructive (P less than 0.05) apnoea and of hypopnoea episodes (P less than 0.01) as compared with controls. Significant positive associations were found between the frequencies of central apnoea (P less than 0.05) or hypopnoea (P less than 0.01) and clinical evidence of central nervous system damage in the alcoholic patients. Hypopnoea also showed a significant association with vagal neuropathy (P less than 0.05), assessed by tests of cardioreflexes. We conclude that abnormal respiratory events are common in abstinent alcoholic patients and that they are likely to be at least partly related to nervous damage.

Adult↗
PubMed1985

Autonomic responses to glucose ingestion in elderly subjects with orthostatic hypotension.

The cardiovascular and plasma catecholamine responses to oral glucose (50 g) ingestion were investigated in five elderly subjects with orthostatic hypotension and five elderly control subjects. All the orthostatic hypotension subjects showed blood pressure falls after glucose ingestion, as compared to only one of the control subjects. Significantly greater falls in the orthostatic hypotension as compared to control patients were observed for systolic blood pressure (P less than 0.01) at 60 and 90 min following glucose and mean blood pressure (P less than 0.05) at 60 min following glucose. The orthostatic hypotension subjects did not have evidence of reduced heart-rate or plasma catecholamine responses to the glucose ingestion. It is concluded that, in elderly patients with orthostatic hypotension, disorder of blood pressure control may also cause hypotension associated with eating.

Aged↗
PubMed1985

No effect of ethanol ingestion on beta-adrenoceptor-mediated circulatory responses to isoprenaline in man.

The acute effects of ethanol on circulatory responses to isoprenaline and atropine were investigated in 21 and 15 normal male subjects respectively. Each subject acted as his own control by participating twice, once after consumption of ethanol (1.0 ml kg-1, 20% v/v in orange juice) and once after orange juice. Ethanol increased baseline heart rate and forearm blood flow, but had no effect on heart rate and forearm blood flow responses to isoprenaline, or on heart rate responses to atropine. Baseline blood pressure and blood pressure responses to isoprenaline were also unaffected by ethanol. It is concluded that acute ethanol ingestion has no physiologically significant effect on beta-adrenoceptor responsiveness as assessed by the cardiovascular responses to bolus doses of isoprenaline.

Adult↗
PubMed1985

Drugs and folate metabolism.

Folates are a group of compounds which are required in the diet and are important in DNA, amino acids and possibly also amine metabolism. The biologically active folates are in the tetrahydro form. Tetrahydrofolates are produced from unreduced dietary folates by the enzyme dihydrofolate reductase. A number of drugs such as aminopterin, methotrexate (amethopterin), pyrimethamine, trimethoprim and triamterene act as folate antagonists and produce folate deficiency by inhibiting this enzyme. With other drugs which produce low serum and tissue concentrations of folate such as anticonvulsants, antituberculosis drugs, alcohol and oral contraceptives, the mechanism of this effect is uncertain. Possible mechanism include reduced absorption, prevention of release of folate from tissue stores, altered plasma protein binding, or increased folate metabolism in the liver. Treatment with folic acid antagonists such as methotrexate readily causes megaloblastic anaemia; this can be prevented by therapy with folinic acid (5-formyltetrahydrofolate). The role of other drugs in producing megaloblastic anaemia is less certain, e.g. it occurs in less than 0.75% of patients receiving anticonvulsants. The possible neurological and psychiatric effects of folate deficiency are also uncertain. However, in patients with folate deficiency who have neuropsychiatric symptoms, neuropathy or myelopathy, and normal vitamin B12 levels, it may be of value to try therapy with folic or folinic acid.

Amines↗
PubMed1984

Effects of ethanol ingestion on alpha-adrenoceptor-mediated circulatory responses in man.

The acute effects of ethanol on pressor responses to graded intravenous infusions of noradrenaline (24, 48, 90 ng kg-1 min-1) and methoxamine (0.2, 0.4, 0.8, 1.6, 2.0 mg/min, 1 min each) were each investigated in eight normal male subjects. The effects of ethanol on blood pressure, heart rate and plasma catecholamine responses to lower body negative pressure were also examined in six normal male subjects. Each subject acted as his own control by participating twice, once after consumption of ethanol (1.0 ml/kg, 20% v/v, in orange juice) and once after an equivalent volume of orange juice. Ethanol consumption significantly reduced the diastolic blood pressure response to infusion of noradrenaline. This occurred despite a significantly greater increase in plasma noradrenaline concentrations during infusion after ethanol. The systolic and diastolic blood pressure responses to infusion of methoxamine were both significantly reduced after ethanol. During lower body negative pressure, prior consumption of ethanol resulted in a greater fall in systolic blood pressure and a smaller rise in diastolic blood pressure. Plasma noradrenaline responses to lower body negative pressure were significantly increased after ethanol. It is concluded that acute ethanol ingestion depresses alpha-adrenoceptor-mediated vasoconstriction, with resulting impairment of blood pressure control.

Adult↗
PubMed1984

Disability in multiple sclerosis and the provision of social and medical services: findings in Wellington, New Zealand.

A study of the incapacity and socioeconomic scales in 120 patients with multiple sclerosis (MS) living in Wellington, New Zealand, is described. The questionnaire has been compared by different health professionals. There was good correlation between the observations of different professionals on incapacity analysis and this may be improved by reducing the questions to six. The findings on the socioeconomic scale, however, cannot be predicted accurately from the incapacity scale. The socioeconomic survey revealed major improvement in patient support in New Zealand during the last decade. We consider that our New Zealand findings indicate the value of field officers concerned with co-ordination of services and provision of information for patients with MS. Future research should be directed towards assessment of support systems.

Activities of Daily Living↗