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Biomedical subjects

M F Oliver

Publications and source records attributed to M F Oliver.

At least 73 records · Page 4Linked to original sources
PubMed1991

Sex difference in presynaptic adrenergic inhibition of norepinephrine release during normoxia and ischemia in the rat heart.

Using a perfused innervated rat heart model, we studied the sex difference in the sympathetic nerve stimulation-induced norepinephrine release and its presynaptic alpha 2-adrenergic inhibition in normoxic and ischemic conditions. During normoxic perfusion, the alpha 2-adrenoceptor antagonist rauwolscine resulted in a higher overflow of norepinephrine during nerve stimulation in females than in males (p less than 0.05). This more marked potentiation of norepinephrine overflow in females was accompanied by an increased chronotropic and inotropic response (p less than 0.01). During early stop-flow ischemia neural norepinephrine overflow was lower in female than in male hearts (p less than 0.005). Rauwolscine enhanced norepinephrine overflow more in females than in males (p less than 0.05), thereby eliminating the initial difference in norepinephrine overflow during ischemia between the two sexes. Ovariectomy attenuated the presynaptic alpha 2-adrenergic inhibition of norepinephrine release compared with sham-operated females (p less than 0.02). No sex difference was found in either cardiac norepinephrine content or nonexocytotic norepinephrine overflow induced by a 40-minute period of stop-flow ischemia. Thus, presynaptic alpha 2-adrenergic inhibition of myocardial norepinephrine release is greater in female than in male rats. This difference persists into the early phase of ischemia and is largely responsible for the lower neural norepinephrine release in the female heart. Female hormones may increase presynaptic alpha 2-adrenergic activity in the heart.

Adrenergic alpha-Antagonists↗
PubMed1991

Cholesterol and coronary disease--outstanding questions.

Established facts include the role of raised blood cholesterol in causing coronary atheroma and that a high dietary intake of saturated fat is a leading cause of coronary disease. It is also clear that reduction of hypercholesterolaemia in middle-aged males reduces CHD incidence, mostly that of non-fatal myocardial infarction. But there are many unresolved questions which should lead to a selective and moderate approach to the management of hypercholesterolaemia. These include lack of the exact knowledge of how raised cholesterol levels lead to atheroma; equivocal evidence of whether reduction of hypercholesterolaemia causes regression of atheroma; uncertainty about how far cholesterol levels can safely be reduced and whether the cost-benefit always justifies action; the fact that reduction of hypercholesterolaemia does not reduce total mortality and may increase non-cardiac mortality; and insufficient evidence as to whether the same policies for middle-aged men should be adopted for woman, the elderly and adolescents.

Adolescent↗
PubMed1990

Effects of safflower oil and evening primrose oil in men with a low dihomo-gamma-linolenic level.

Low levels of essential polyunsaturated fatty acids of the n-6 series are associated with coronary heart disease. Linoleic acid, but not gamma-linolenic acid requires the activity of delta 6-desaturase for its conversion to dihomo-gamma-linolenic and arachidonic acid. Evening primrose oil (EPO) and safflower oil (SO) are rich in linoleic acid, but EPO contains also 9% gamma-linolenic acid. The effect of EPO (10, 20 and 30 ml/day) and SO (20 ml/day) for 4 months on the deposition of linoleic acid metabolites in adipose tissue of 4 groups of 6-9 men with low adipose dihomo-gamma-linolenic acid was examined. EPO but not SO increased adipose dihomo-gamma-linolenic acid level from 0.080 +/- 0.005% to 0.101 +/- 0.005% (P less than 0.01; 20 ml/day for 4 months). Adipose dihomo-gamma-linolenic/linoleic acid ratio increased with EPO from 0.99 +/- 0.16 X 10(2) to 1.13 +/- 0.14 X 10(2) and fell on SO from 1.04 +/- 0.10 X 10(2) to 0.90 +/- 0.07 X 10(2) (P less than 0.01). Similar qualitative changes in the relative amount of dihomo-gamma-linolenic acid in serum triglyceride and cholesteryl ester fractions were observed. At the dose of 20 ml/day, SO and EPO did not differ in their effect on serum cholesterol (7.13 +/- 0.43 vs. 7.33 +/- 0.42 mmol/l (NS)), LDL-cholesterol (5.10 +/- 0.32 vs. 4.88 +/- 0.46 mmol/l (NS)) nor did the 2 oils differ in their effect on HDL-cholesterol. These results suggest that linoleic acid is not readily converted to dihomo-gamma-linolenic acid due to a low activity of delta 6-desaturase in these highly selected men. EPO was not an effective hypocholesterolaemic agent in this study.

8,11,14-Eicosatrienoic Acid↗
PubMed1990

Introduction: lipids and coronary disease--resolved and unresolved problems.

To my mind, there are more unresolved problems regarding lipids and cardiovascular diseases than those which have been settled. While this may seem disappointing after 40 years of intensive research, the progress which has been made is remarkable and impressive. It is appropriate, therefore, to begin an introduction by outlining the issues which have been resolved and which are more or less internationally agreed. In doing so, I shall deliberately not digress into causes of coronary heart disease (CHD) other than lipids, even though other influences may be as or more important in relation to its pathogenesis.

Cholesterol↗
PubMed1990

Duodenal ulcer is associated with low dietary linoleic acid intake.

It has been suggested that the falling incidence and virulence of duodenal ulcer is related to increased dietary polyunsaturated essential fatty acid intake. The adipose fatty acid profile, which closely reflects dietary intake, was measured in 35 men with chronic duodenal ulcer and 35 matched control men. The mean percentage of linoleic acid in adipose tissue was significantly lower in the ulcer group (10.0 (0.7) v 12.3 (0.7)%, p less than 0.01) and this difference was found in both smokers and non-smokers. This finding suggests that the diets of duodenal ulcer patients are deficient in linoleic acid and this could be of aetiological importance.

Adipose Tissue↗
PubMed1990

Failure of the cholinergic modulation of norepinephrine release during acute myocardial ischemia in the rat.

The effect of ischemia on cholinergic presynaptic inhibition of exocytotic norepinephrine release was studied in the innervated perfused rat heart. In normoxic hearts, vagal nerve stimulation significantly reduced exocytotic norepinephrine overflow to 75% of control values. This inhibitory effect was not affected by 3 minutes of low-flow ischemia (67% of control overflow values), but was attenuated or abolished by 10-minute low-flow ischemia or by 1-, 3-, and 5-minute stop-flow ischemia (107%, 85%, 101%, and 120% of control overflow values, respectively). The alpha-adrenergic antagonist phentolamine could completely or partly restore the failure of vagally induced inhibition of norepinephrine overflow in hearts with 1-, 3-, and 5-minute stop-flow ischemia (72%, 73%, and 85% of control overflow values, respectively). The muscarinic agonist methacholine substantially inhibited norepinephrine overflow to 18% of control overflow values in normoxic hearts. This effect was also significantly attenuated by 10-minute low-flow ischemia or by 1-, 3-, and 5-minute stop-flow ischemia (46%, 38%, 53%, and 55% of control overflow values, respectively). The cholinesterase inhibitor physostigmine did not restore the methacholine-induced inhibition of norepinephrine overflow after 3-minute stop-flow ischemia to normoxic level (55% vs. 17%). These results indicate that myocardial ischemia interferes with endogenous and exogenous cholinergic presynaptic inhibition of norepinephrine overflow in the rat heart. The extent of this attenuation depends on the severity and duration of ischemia. Reduced exocytotic acetylcholine release, which is at least in part due to an enhanced adrenergic presynaptic modulation, and dysfunction of presynaptic muscarinic receptors are suggested as two possible mechanisms.

Animals↗
PubMed1989

Adipose fatty acid composition and the risk of serious ventricular arrhythmias in acute myocardial infarction.

The relation between subcutaneous adipose tissue fatty acid composition and serious ventricular arrhythmias during acute myocardial infarction was studied in 2 groups of patients. In group 1 (n = 42), studied retrospectively, patients with ventricular fibrillation or tachycardia had a higher concentration of long-chain saturated fatty acids than those without (32.5 +/- 0.8% vs 29.7 +/- 0.4% [mean +/- standard error of the mean], p less than 0.01). In a prospective study, patients with arrhythmias (n = 106) had higher levels of long-chain saturated fatty acids (32.1 +/- 0.5% vs 30.7 +/- 0.4%, p less than 0.05) and of stearic acid (4.9 +/- 0.2% vs 4.4 +/- 0.1%, p less than 0.02) and a lower concentration of palmitoleic acid (7.3 +/- 0.3% vs 8.1 +/- 0.2%, p less than 0.005). When peak plasma creatine kinase concentrations were included with the individual fatty acid levels in a multiple logistic regression, only creatine kinase correlated significantly with ventricular arrhythmias (p less than 0.01). Thus, saturated fatty acids in cardiac membranes may lead to greater vulnerability to ventricular arrhythmias, although infarct size is the only statistically significant predictor after multiple regression analysis.

Adipose Tissue↗
PubMed1989

Effects of Maxepa on serum lipids in hypercholesterolaemic subjects.

The effect of dietary supplementation with 20 capsules/day Maxepa or olive oil on serum lipids has been studied in 21 hypercholesterolaemic patients using a double-blind crossover design. Platelet membrane eicosapentaenoic acid percentage rose by more than 10-fold after 2 months dietary supplementation with Maxepa. Total serum cholesterol was unchanged and there was a rise in LDL-cholesterol and HDL-cholesterol concentration in men, but no change in LDL-cholesterol, and a fall in HDL-cholesterol in women. In men and women there was a marked fall in total serum triglyceride, VLDL-triglyceride and VLDL-cholesterol levels. Thus, Maxepa is not an effective treatment for isolated hypercholesterolaemia.

Clinical Trials as Topic↗
PubMed1989

Effect of pindolol versus atenolol on lipid profile in hypertensive patients.

The effect of pindolol (a beta-blocker with intrinsic sympathomimetic activity, ISA) on fasting plasma lipid profile in 30 hypertensive patients was compared with atenolol (without ISA) in a crossover single blind study. Both drugs lowered blood pressure. HDL-cholesterol increased significantly with pindolol (from 1.15 +/- 0.05 to 1.34 +/- 0.05 mmol/l at 12 weeks, P less than 0.001), but not with atenolol. VLDL-cholesterol increased with atenolol (from 0.57 +/- 0.09 to 0.86 +/- 0.14 mmol/l at 12 weeks, P less than 0.002), while there was no change with pindolol. These changes in lipoprotein profile suggest a more favourable effect of pindolol than of atenolol on lipid profile.

Adult↗
PubMed1989

Blood pressure, cigarette smoking and heart attack in the WHO co-operative trial of clofibrate.

In the WHO sponsored trial of clofibrate and its follow-up, about 15,000 men were observed for a mean period of 13.2 years. As expected, incidence of heart attacks (HA) was directly related to serum cholesterol, blood pressure (BP) and cigarette smoking. The previously reported lower incidence of HA in men receiving clofibrate compared with controls was most noticeable in hypertensive heavy smokers (P less than 0.01). BP was slightly lower in smokers than non-smokers (P less than 0.01). The difference in BP was greater in the trial visit before HA. Smokers also had higher plasma fibrinogen levels (P less than 0.05). The combination of reduced diastolic BP, and therefore myocardial perfusion pressure, with an increased thrombogenic tendency, might explain the high incidence of HA in smokers. Clofibrate apparently reduced fibrinogen levels, which might account for its specially good effect in preventing HA in smokers. However, the ill effects of smoking are still evident at a lower level in the men taking clofibrate and the drug is no substitute for giving up the habit. Clofibrate is not recommended for widespread use, except in subjects with marked lipid and/or blood fibrinogen abnormalities after dietary measures have been tried.

Bezafibrate↗