The CNR program of preventive medicine--SP4 Objective 44. Non-invasive techniques for the evaluation of atherosclerotic plaque progression or regression.
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Arteriosclerosis↗
Biomedical subjects
M Mancini
Publications and source records attributed to M Mancini.
Energy balance and blood-pressure regulation. Update and future perspectives.
The relationship of blood pressure to body weight within populations is well documented: it is also generally accepted that the body mass index, as well as the change in body mass index over time, are predictive of risk for future hypertension. Short-term clinical trials suggest that satisfactory blood-pressure control can be more easily achieved in obese hypertensive subjects by a successful program of weight reduction. On the other hand, the pathophysiological aspects of the association between excessive weight and high blood pressure are still obscure; particularly the putative role of hyperinsulinemia, as well as exaggerated sympathetic activity, need to be confirmed. Recent evidence indicates that upper body fat predominance and low habitual physical exercise may be factors contributing to the increase in blood pressure, but the importance of still other factors, such as associated abnormalities of cell cation transport, has to be further elucidated. From the therapeutic point of view, there is a strong need for controlled trials to confirm feasibility and effectiveness of long-term programs of weight reduction as a means to control hypertension in the obese. Based on these considerations and the enormous potential for primary prevention, the problem of energy balance and blood-pressure regulation stands as a most important issue for future cardiovascular research.
Adult↗
[Factors influencing the development of proliferative diabetic retinopathy treated by laser therapy].
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Diabetic Retinopathy↗
Effects of sodium intake on blood pressure and adrenergic vascular reactivity.
The effects of dietary sodium restriction (approximately 2 g daily) on blood pressure (BP) and vascular reactivity to norepinephrine (NE) were evaluated in 12 patients with uncomplicated primary hypertension. BP was significantly reduced at the end of the treatment both at rest (153/100 +/- 19/7 vs. 142/93 +/- 19/5 mmHg) and during an exercise test on a bicycle. The pressor response to NE was significantly lower at the end of the low sodium period (reactivity index = 0.0044 vs. 0.0031; p less than 0.05): A twofold dose of NE was needed to increase mean BP by 20 mmHg (PD20) (from 273 +/- 120 to 450 +/- 218 ng/kg/min; p less than 0.05). Twenty-four-hour NE excretion increased significantly on a low-salt diet (40 +/- 14 vs. 49 +/- 16 micrograms/24 hr; p less than 0.05). The decrease in BP was inversely related to changes in PD20 (R = -0.60; less than p0.05). These results provide the evidence that the fall in BP is, at least in part, mediated by decreased end-organ responsiveness to adrenergic stimulation.
Adult↗
[Diet in the prevention of coronary disease].
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Coronary Disease↗
[Changes in the in vitro antibody formation in B lymphoproliferative diseases].
Peripheral blood mononuclear cells from three patients with multiple myelomas (M.M.), four patients with Essential Mixed Cryoglobulinaemia (E.M.C.) and four normal adults as controls were cultivated with or without poke weed mitogen (PWM); in vitro immunoglobulin (Ig) production was measured after seven days using the enzyme-linked immunosorbent assay method (ELISA). No significant differences in Ig production were noted between patients and controls: E.M.C. patients, on the other hand, displayed considerable spontaneous IgM production (without appreciable differences, however, between spontaneous and PWM-stimulated production). M.M. patients, on the other hand, displayed only scanty spontaneous IgM production and in two cases the PWM response was completely lacking. These results were then integrated and correlated with a parallel study of similar groups of patients and controls carried out with the aim of investigating modifications in the distribution of B and T lymphocyte subpopulations. Possible interpretations of the results are discussed.
Adult↗
Cross-over study of muzolimine and hydrochlorothiazide-amiloride in hypertensive patients.
Thiazide therapy is a widely used first line treatment for arterial hypertension. Its useful value, particularly in mild or moderate hypertension, is sometimes reduced by metabolic side-effects, as hypokalaemia and hyperuricaemia. In the present study the antihypertensive efficacy of a new, non-sulphonamide diuretic Bay g 2821 (muzolimine) was evaluated in comparison with the combination of hydrochlorothiazide-amiloride over a period of 4 weeks. A highly significant decrease in systolic and diastolic blood pressures was produced by both treatments. No decrease in serum potassium nor an increase in cholesterol, triglycerides, uric acid or glucose was detected during the 4 week treatment period. Subjective side-effects, such as headache and dizziness, were very rarely observed during Bay g 2821 treatment. The new diuretic appears, therefore, to be effective in the treatment of arterial hypertension without untoward side-effects.
Adult↗
Plasma lipoproteins and lipoprotein lipase in young diabetics with and without ketonuria.
Plasma lipoprotein and lipoprotein lipase activity have been evaluated in young diabetics with and without ketonuria and in healthy controls of the same age. Fifteen (age range 7-23 years) newly detected diabetics (8 with ketonuria, 7 non ketonuric) have been examined before starting the treatment. Five healthy medical students (age range 19-21 years) have also been studied. Both ketotic and non ketotic patients showed an impaired insulin and C-peptide response to the glucose load in comparison to controls. Ketotic patients had low lipoprotein lipase activity (p less than 0.01) and high density lipoprotein (p less than 0.01); total plasma Triglycerides and VLDL Triglyceride and Cholesterol were higher than in controls. Plasma Triglyceride and VLDL Triglyceride and Cholesterol were inversely related to lipoprotein lipase activity. Low lipoprotein lipase activity, from adipose tissue and muscle, has been found to be associated with hypertriglyceridemia and reduced HDL Cholesterol in young diabetic patients with ketonuria.
Adolescent↗
Improved reactive hyperemia test after plasma exchange in familial hypercholesterolemia.
By using a non-invasive methodology of vascular diagnosis, ECG-triggered strain-gauge plethysmography, 5 patients with familial hypercholesterolemia (FH) (3 homozygous, 2 heterozygous) were evaluated before and during the 1st and 2nd week after plasma exchange (PE). In order to obtain data on the responsiveness to vasodilating stimuli in FH patients undergoing PE, reactive hyperemia test and peak flow determination were also performed. Resting arterial flow over the calf was found to be significantly enhanced after PE. Reactive hyperemia test demonstrated persistent improvement of peak flow following exchange. This study demonstrates useful hemodynamic effects of PE in patients with FH.
Adult↗
Pathophysiological interrelations of obesity, impaired glucose tolerance, and arterial hypertension.
There is a large amount of epidemiological and clinical evidence for associations among obesity, impaired glucose tolerance, and arterial hypertension; nevertheless, the pathophysiological mechanisms underlying these associations have not yet been elucidated. In this article, some working hypotheses are discussed, and original data are presented from two studies focusing on these pathophysiological interrelations. A case-control study of obese normotensive and hypertensive patients, matched for sex, age, and degree of overweight, has shown that obese patients with associated arterial hypertension have higher fasting serum insulin levels and reduced glucose tolerance compared with their normotensive peers. A second study compared subjects with impaired glucose tolerance with a control group of clinically healthy individuals of comparable sex, age, and body mass index, and it revealed that impaired glucose tolerance is associated with significantly higher blood pressure levels, independent of body weight. The results of the two studies together suggest that the association between hypertension and impaired glucose tolerance is independent of overweight; they also give some support to the hypothesis that hyperinsulinemia may contribute to the development of high blood pressure in obese patients.
Adult↗
Reproducibility of the new diagnostic criteria for impaired glucose tolerance.
Sixty-seven subjects with impaired glucose tolerance and 136 normoglycemic individuals defined according to the diagnostic criteria of the European Association for the Study of Diabetes were selected from among persons aged 40-59 years who participated in a health examination survey in Naples in 1980. A second oral glucose tolerance test was given under identical conditions between two and four months later with the participants having no knowledge of the results of the first test. Venous whole blood was utilized for blood glucose determination. At the second test, 93% of the control group were confirmed to be normoglycemic, but only 56% of the impaired glucose tolerance group were still intolerant. Reproducibility was poorest among subjects with blood glucose two hours after load of less than 140 mg/dl. Among these subjects, 47% reverted to normoglycemia at the second test. In contrast, 15% of those with blood glucose greater than or equal to 140 mg/dl two hours after load reverted to normoglycemia (chi 2 = 6.29, p less than 0.05). Subjects with impairment of glucose tolerance at the second test were reclassified according to the diagnostic criteria of the National Diabetes Data Group and the World Health Organization (WHO). Only 22 (46%) of the 48 individuals classified in the impaired glucose tolerance group according to the criteria of the European Association for the Study of Diabetes were so classified by the criteria of both the National Diabetes Data Group and WHO. The disagreement between the three diagnostic criteria was maximal in the lowest blood glucose range. It is concluded that the diagnosis of impaired glucose tolerance, despite the new diagnostic criteria, still has little reproducibility and uniformity.
Adult↗
Study with the competitive 5-HT2-serotonergic antagonist ketanserin.
In 10 patients with primary arterial hypertension of mild or moderate degree, ketanserin, a competitive antagonist of serotonin receptors, was given for a period of 4 weeks, 40 mg twice daily. In a control group, patients were given 100 mg twice daily of metoprolol for 4 weeks for each treatment. A randomized double-blind crossover model was used. Blood pressure and heart rate were measured at rest and during exercise testing on a bicycle; peripheral blood flow was measured by strain-gauge plethysmography. A slight reduction in resting systolic and diastolic blood pressure without change in heart rate was observed during treatment with ketanserin. Cardiac workload during exercise test did not change over the observation period. A slight increase in resting blood flow to the lower limbs, with a decrease in peripheral resistance was demonstrated by strain-gauge plethysmography.
Adult↗
Functionally thrombasthenic state in normal platelets following the administration of ticlopidine.
To elucidate the bleeding tendency that follows the administration of ticlopidine, we investigated the skin bleeding time and some ex vivo functions of platelets obtained from eight healthy volunteers before and 1 wk after daily administration of 500 mg of ticlopidine. We found the following: ticlopidine significantly (P less than 0.001) prolonged the skin bleeding time and impaired the binding of radiolabeled fibrinogen and von Willebrand Factor, the clot retraction and the aggregation of platelets in response to ADP, epinephrine, thrombin, ionophore A23187, collagen, or arachidonic acid. In contrast, the administration of this drug did not affect intraplatelet levels of cAMP, agglutination and binding of von Willebrand Factor in response to ristocetin, shape change in response to ADP, collagen, thrombin, or arachidonic acid, or binding of prostaglandin E1 to resting platelets. Secretion of ATP in response to ADP or epinephrine was completely inhibited, whereas secretion as well as thromboxane synthesis in response to high concentrations of collagen, arachidonic acid, calcium ionophore A23187, or thrombin was unaffected. Studies with monoclonal antibodies showed that the glycoprotein IIb-IIIa complex (the putative receptor for fibrinogen and von Willebrand Factor on the surface of platelets exposed to naturally occurring aggregating agents) was quantitatively unaffected by ticlopidine. This observation was further confirmed by densitometric scannings of Periodic Acid-Schiff-stained gels of platelet suspensions. The onset, as well as the cessation of the inhibitory effect of ticlopidine on platelets was very slow, and reached a maximum after a 3-5-d administration. In addition, ticlopidine appeared to be a much more potent inhibitor when administered to subjects than when added in vitro to platelets. Finally, abnormalities comparable to those found in volunteers taking ticlopidine were observed when platelets from untreated subjects were incubated in the plasma of ticlopidine-treated subjects. We conclude that ticlopidine induces a thrombasthenic state in normal platelets without affecting the glycoprotein IIb-IIIa complex quantitatively. Furthermore, our data suggest that one or more active metabolites rather than the native drug mediate the abnormalities of platelet function observed in ticlopidine-treated subjects.
Adenosine Triphosphate↗
Alteration of erythrocyte membrane lipid fluidity in human obesity.
The lipophilic probe 1,6-diphenyl-1,3,5-hexatriene was incorporated into erythrocyte ghosts of either normal or obese humans, and the polarization of fluorescence was measured between 0 and 40 C. The membrane lipid fluidity, evaluated by fluorescence polarization, was consistently higher in the ghosts from obese subjects. A strong correlation was found between increased 1,6-diphenyl-1,3,5-hexatriene fluorescence polarization and excess body weight. Measurements of cholesterol and phospholipids indicated increased cholesterol and decreased phospholipids in erythrocyte ghosts from obese subjects. These data suggest that alterations in lipid composition in erythrocytes of obese subjects are responsible for abnormal physical properties of plasma membranes, which, in turn, may cause altered enzymatic activities.
Adolescent↗
Effects of beta-receptor blockade on carbohydrate metabolism.
The effects of beta-blockers on glucose tolerance, insulin secretion and peripheral insulin sensitivity were evaluated by oral glucose tolerance test and euglycaemic insulin technique in six normoglycaemic patients with primary arterial hypertension at the end of 3-week treatments with placebo (one tablet twice daily) and propranolol (80 mg twice daily). Body weight did not change during the study (83 kg at the end of placebo, 83 kg at the end of propranolol), while blood pressure (150 +/- 9/97 +/- 8 mmHg on placebo, 138 +/- 8/89 +/- 8 mmHg on propranolol, P < 0.01) and heart rate (66 +/- 9 beats/min on placebo, 60 +/- 5 beats/min on propranolol, P < 0.05) showed a significant fall on the beta-blocker. No change was observed in glucose tolerance (incremental area for glucose 3462 +/- 1149 mg/dl per min on placebo, 3209 +/- 1695 mg/dl per min on propranolol), insulin secretion (incremental area for serum insulin 7579 +/- 4380 microU/ml per min on placebo, 7934 +/- 4351 microU/ml per min on propranolol) and peripheral insulin sensitivity (metabolic clearance rate 11 +/- 4 ml/kg per min on placebo, 13 +/- 6 ml/kg per min on propranolol). These data support the hypothesis that chronic treatment with adrenergic blocking agents does not induce any significant change in insulin secretion or peripheral insulin sensitivity.
Adrenergic beta-Antagonists↗
Increased binding of fibrinogen to platelets in diabetes: the role of prostaglandins and thromboxane.
Previous studies suggested a role for prostaglandins or thromboxane A2, or both in the exposure of fibrinogen receptors on normal platelets in response to several aggregating agents. Platelets from diabetics are known to be more sensitive to aggregating agents and to produce more prostaglandins and thromboxane than platelets from normal subjects. We compared fibrinogen binding to platelets from diabetic subjects with binding to platelets from normal subjects and determined whether aspirin (which inhibits the formation of prostaglandins and thromboxane) would inhibit the binding of fibrinogen to platelets from diabetic subjects and whether this correlated with its effects on platelet aggregation. We found the following: Aspirin suppressed thromboxane formation and rendered the platelets less sensitive to the induction of aggregation by adenosine diphosphate (ADP) or collagen. The amount of U-46619 [( 15s]-hydroxy-11-alpha, 9-alpha [epoxy-methano]-prosta[5Z,13E]-dienoic acid, a stable analog of prostaglandin endoperoxide/thromboxane A2) necessary to induce aggregation, was similar in normal and diabetic subjects and was unchanged after ingestion of aspirin. Binding of 125I-fibrinogen following stimulation of platelets by ADP or collagen was greater in diabetic (because more binding sites were exposed) than in normal subjects. However, following stimulation by U-46619, binding was similar in diabetic and normal subjects. Aspirin caused a reduction in the exposure of binding sites on both platelets from diabetic and normal subjects, so that (in this respect) platelets from diabetic subjects became more like those from normal subjects. Effects of the monoclonal antibody B59.2, which is specific for the platelet glycoprotein IIb-IIIa complex (the presumed receptor for fibrinogen on the platelet surface) were also studied. The amount of this antibody that bound to platelets was the same for normal and diabetic subjects both before and after aspirin and with or without stimulation by ADP or collagen. In addition, B59.2 inhibited aggregation and fibrinogen binding in both platelets from diabetic and normal subjects. The combined data suggest that the glycoprotein IIb-IIIa complex of platelets from diabetic subjects is similar to that of platelets from normal subjects and that the increased fibrinogen binding and aggregation of platelets from diabetic subjects in response to ADP or collagen is mediated by increased formation of prostaglandin endoperoxide or thromboxane A2, or both.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Thromboxane- and ADP-independent aggregation and exposure of fibrinogen receptors on platelets from patients with familial hypercholesterolemia.
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Adenosine Diphosphate↗