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Biomedical subjects

G F Gensini

Publications and source records attributed to G F Gensini.

At least 19 recordsLinked to original sources
PubMed1992

Automated blood pressure determination during exercise test. Clinical evaluation of a new automated device.

The accuracy and reproducibility of a new automatic device (P) specially designed for noninvasive blood pressure monitoring during the exercise stress test were evaluated in 50 consecutive subjects (34 normotensives and 16 hypertensives). Automatic measurements were compared with those taken by a sphygmomanometer (RR). A good agreement between systolic pressure values obtained by the two methods was found (RR 159 +/- 30 mmHg, P 158 +/- 28 mmHg, mean difference = -1.53 +/- 13 mmHg, p = 0.166, ns). On the contrary the new device significantly underestimated diastolic pressure values (RR 89.3 +/- 13 mmHg; P 84 +/- 13 mmHg, mean difference -5.37 +/- 9.3, p < 0.001). In conclusion the new device seems able to measure systolic but underestimates diastolic blood pressure both in hypertensives and in normotensives during the effort test.

Adult↗
PubMed1992

[Diabetic disease and periodontal disease. Diabetes and periodontopathy].

Diabetic patients have been reported to be more susceptible to gingivitis and periodontitis than healthy subjects, and these diseases are commonly considered to be oral complications of diabetes. The influence of diabetes on the onset and development of periodontal disease has been studied for many years but clear agreement is still lacking on the nature of the relationship between diabetes and these oral disorders. In fact recent observational epidemiological studies suggest that diabetes should not be considered as the direct cause of periodontal disease but rather as a systemic promoting factor, able to produce conditions suitable for local agents producing gingivitis and periodontitis. The overriding oral problem in diabetes is infection, like with any of the dermal lesions in the diabetic. In fact periodontal disease is caused by specific bacteria (Bacteroides Gingivalis, Actinobacillus actinomycetemcomitans) growing in the periodontal pocket so that the bacterial products such as histolytic enzymes, endotoxins or exotoxins may exert a direct effect. Particular attention has been directed to the neutrophils and to their role in antibacterial defense. In fact a reduced phagocytosis, leukotaxis and leucocyte index have been reported in neutrophils from diabetics. The careful metabolic control was reported by most of the Authors to lower the incidence and to reduce the severity of periodontal disease. This may be related both to the improvement in leukocyte function and to a change in gingival fluid rendering it less suitable for bacterial growth. In diabetics also local factors, such as decreased pH of salivary fluid and a reduced salivary flow, seem to play an important role.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1991

Human prostacyclin platelet receptors in diabetes mellitus.

Conflicting data have been reported about the impaired sensitivity to the inhibitory effect of prostacyclin (PGI2) in platelets from patients with diabetes. In the present paper we investigated binding of and sensitivity to PGI2 of platelets from insulin dependent (IDDM) (n = 9), non insulin dependent (NIDDM) (n = 8) diabetics and two groups of ten healthy subjects of equivalent age in relation to platelet lipidic content. Platelet sensitivity to PGI2 (PGI2 IC50) was found not significantly changed in diabetics as compared to controls; similarly, no significant differences of the number of high affinity receptors for PGI2 in platelets from patients with IDDM and NIDDM were observed. Platelet sensitivity to PGI2 and PGI2 receptors were found to be significantly related to platelet cholesterol content (r = 0.89, p less than 0.001 and r = -0.80, p less than 0.001 respectively). In conclusion platelet PGI2 receptor changes are not detectable in diabetics in good metabolic control, but could take place when platelet lipid composition is altered.

Adolescent↗
PubMed1991

Platelet thromboxane A2 receptors in type I diabetes.

1. Human platelet thromboxane A2 receptor expression on the membrane surface is possibly dynamically regulated by changes either in the ligand concentration or in membrane fluidity. An increased thromboxane A2 production and a decreased membrane fluidity has been reported in diabetic patients. 2. In the present study the binding characteristics of platelet thromboxane A2 receptors have been investigated in nine diabetic patients (type I) and in 15 healthy control subjects by a radioligand-binding method using 9,11-dimethylmethane-11,12-methane-16-[3-125I-4-hydroxyphenyl]-13, 14- dihydro-13-aza-15-tetranor-thromboxane A2 as the radiolabelled ligand. 3. The maximum concentration of binding sites was 163 (SD 35) fmol/10(8) platelets (n = 15) with 987 (SD 209) receptors/platelet in controls, whereas in diabetic patients the maximum concentration of binding sites was 74.2 (SD 28) fmol/10(8) (n = 9) with 447 (SD 172) receptors/platelet (P less than 0.001). The dissociation constants were 18 (SD 4) nmol/l and 21 (SD 6) nmol/l (not significant) in control subjects and in diabetic patients, respectively. Glycated haemoglobin, which is reported to reduce membrane fluidity, was found to be negatively correlated (r = 0.60, P less than 0.05) with thromboxane A2 receptor number in the diabetic patient group. On the contrary, a positive linear correlation between the equilibrium dissociation constant and glycated haemoglobin was found in diabetic patients (r = 0.75, P less than 0.01).

Binding Sites↗
PubMed1991

Acute reduction of TxA2 platelet binding sites after in vivo administration of a TxA2 receptor inhibitor.

1. Picotamide has been shown to interfere competitively with the thromboxane A2 (TxA2) platelet receptor. In the present study the effect of in vivo administration of picotamide on TxA2 human platelet receptors was investigated in 10 healthy subjects. 2. Picotamide (300 mg x 3 daily) or placebo were administered in a double-blind, cross-over, placebo controlled study, each treatment lasting 1 week with a 2 week interval period. TxA2 receptors were investigated by a direct radioligand binding assay method employing [125I]-PTA-OH as labelled ligand. Platelet studies were performed on the first day of treatment immediately before and 2, 4 and 8 h after the ingestion of the drug. The effects of chronic administration were assessed on the seventh day. 3. Two and 4 h after the administration of picotamide 300 mg orally platelet TxA2 receptors were significantly reduced from 1366 +/- 237 to 957 +/- 221 (P less than 0.05) and 753 +/- 119 receptors/platelet (mean +/- s.d.) (P less than 0.03). After 8 h platelet receptor population was restored (1362 +/- 324, NS). The same pattern was observed after 7 days of treatment. Thus picotamide seems to induce a short lasting down regulation of platelet TxA2 receptors.

Adult↗
PubMed1991

Age-related changes in red blood cell lipids.

Red blood cell (RBC) lipid composition was investigated in 81 healthy subjects aged twenty to sixty-nine years, having similar dietary habits, and living in the same geographic area in order to search for changes referable to aging. A significant increase in RBC cholesterol and total phospholipid content with aging was found (p less than 0.001), whereas no differences were observed in cholesterol/phospholipid molar ratio. Significant increases in palmitic acid 16:0 esterified in phosphatidylcholine and in stearic acid 18:0 esterified in phosphatidylethanolamine (p less than 0.001) were observed with aging. Moreover, a decrease in 18:2 n6 was observed in all three phosphoglyceride fractions investigated (p less than 0.001). These results suggest that modifications in RBC lipid composition occur with aging, possibly causing a reduction of membrane fluidity.

Adult↗
PubMed1991

[Changes in the wall motion of left ventricle in dipyridamole-induced ischemic cardiopathy studied by nuclear magnetic resonance. A comparison with myocardial scintigraphy with 99mTc MIBI].

To investigate whether magnetic resonance imaging (NMR) can detect alterations in LV contractility during myocardial ischemia, ten patients aged 32-72 with coronary artery disease underwent ECG gated NMR performed at 0.5 Tesla after intravenous infusion of high dose dipyridamole (DP) (0.7 mg/Kg) over 5 minutes. LV contraction in planes similar to echo short axis projection was imaged under condition, 3' and 15-20' after infusion of DP by fast multiphasic imaging (FMI), multiple angulated cine-NMR sequence with a temporal resolution of 50 m/sec. Entity and size of perfusion defects after DP were determined by Tc 99m MIBI myocardial scintigraphy. In all patients changes in LV contractility appeared at NMR in the same site of perfusion impairments revealed with MIBI. In 8 patients the alterations lasted even more than 20' after the first NMR scan. NMR provides the opportunity of performing long-lasting assessment of ventricular wall contractility and enables to exactly localize the site and extension of kinetic changes as well as their time of onset and time duration.

Contrast Media↗
PubMed1991

Anaerobic threshold in patients with exercise-induced myocardial ischemia.

The aim of the present study was to investigate the ventilatory anaerobic threshold in patients with exercise-induced myocardial ischemia. Ventilatory volumes and gas exchanges were measured during treadmill stress testing in 36 patients (11 with previous myocardial infarction) with electrocardiographic criteria of myocardial ischemia during the test and in 23 healthy, untrained control subjects of equivalent age. The anaerobic threshold was detected in 32 of 36 patients (89%) and in 22 of 23 control subjects (96%). The anaerobic threshold was significantly lower in patients than in control subjects (13.5 +/- 1.9 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). In the 21 patients without previous myocardial infarction, the anaerobic threshold was also significantly lower than in the control subjects (13.9 +/- 1.6 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). Among the 21 patients without previous myocardial infarction, the 12 with a low ischemic threshold, which occurred during the first three steps of the modified Bruce protocol, had an anaerobic threshold significantly lower than the other nine patients (13.1 +/- 1.5 versus 14.9 +/- 1.0 ml/kg per minute VO2, p less than 0.01). However, even in the patients with a moderate to high ischemic threshold, the anaerobic threshold was significantly lower than in the control subjects (p less than 0.001). These data show that the anaerobic threshold can be measured in the great majority of patients with exercise-induced myocardial ischemia. The low anaerobic threshold level indicates a relevant functional impairment in these patients.

Adult↗
PubMed1990

The prominent role of thromboxane A2 formation on early pulmonary hypertension induced by oleic acid administration in sheep.

The early increase of pulmonary artery pressure observed in different models of experimentally induced lung injury have been shown to be associated with the release of vasoconstrictive agents by activated platelets. The aim of this study was to evaluate the pattern of these metabolites, in particular TxA2, and the effects of the inhibition of their production by ASA on the modifications of pulmonary hemodynamics induced by oleic acid administration in sheep. Group I (8 sheep) was infused with oleic acid (0.09 ml/kg at 0.02 ml/min) while in group II (6 sheep) ASA (10 mg/kg i.v.) was administered 30 minutes before oleic acid infusion. In group I pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) were significantly higher at the end of the infusion while cardiac output (CO) significantly decreased in comparison to baseline values. A marked increase in plasma TxB2 levels paralleled pulmonary hemodynamic changes. Also plasma 6 keto PGF levels increased after OA infusion. The early increase in PAP and PVR was significantly lower in group II (p less than 0.005) while CO did not undergo any significant change. ASA pretreatment significantly blunted the rise of TxB2 concentrations and prevented the elevation of 6 keto PGFa. These results indicate that early pulmonary hypertension in oleic acid induced injury is mainly related to TxA2 released from platelets and leukocytes and that pulmonary hemodynamic changes are significantly inhibited by ASA pretreatment.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Effect of heparin, aspirin, or alteplase in reduction of myocardial ischaemia in refractory unstable angina.

399 out of 474 inpatients with unstable angina were monitored for 48 h and 97 of these were found to be refractory to conventional antianginal treatments and entered a randomised double-blind study. With the initial protocol heparin infusion or bolus were compared with aspirin; with a modified protocol, heparin infusion, the best of these three treatments, was compared with alteplase. Patients were monitored for 3 days after starting treatment and then observed clinically for 4 more days. On the first days of treatment heparin infusion significantly decreased the frequency of angina (by 84-94%), episodes of silent ischaemia (by 71-77%), and the overall duration of ischaemia (by 81-86%). Heparin bolus and aspirin were not effective. Alteplase caused small (non-significant) reductions on the first day only. Only minor bleeding complications occurred.

Administration, Oral↗
PubMed1990

Defective coronary prostaglandin modulation in anginal patients.

In order to investigate whether coronary vasodilating prostaglandins (PGI2 and PGE2) have a role in the pathophysiology of myocardial ischemia, 26 patients with angina pectoris and 23 control subjects (nonischemic patients) were studied by assessing coronary hemodynamics and prostaglandin formation in relation to sympathetic stimulation. Following a cold pressor test (CPT), coronary prostaglandin output markedly increased (p less than 0.001) and coronary vascular resistance (CVR) decreased (p less than 0.001) in all control subjects. In contrast, in anginal patients prostaglandins in the coronary sinus were undetectable and after CPT prostaglandin output did not increase, whereas CVR paradoxically increased (p less than 0.001). In control subjects the inhibition of coronary prostaglandin formation (by ketoprofen [1 mg/kg intravenously] or by aspirin [15 mg/kg intravenously]) caused a paradoxical increase of CVR following CPT (p less than 0.001). In anginal patients the inhibition of prostaglandins further exaggerated the increase of CVR after CPT (p less than 0.001). These results indicate that coronary vasodilating prostaglandin PGI2 and PGE2 play a role in modulating coronary vascular response to sympathetic stimulation induced by CPT. Their defective production in anginal patients may be responsible for the paradoxical increase in CVR following sympathetic stimulation.

Adult↗
PubMed1990

Physiologic role of coronary PGI2 and PGE2 in modulating coronary vascular response to sympathetic stimulation.

To investigate a physiologic role of coronary prostacyclin (PGI2) and prostaglandin E2 (PGE2) 30 patients who were not affected by coronary heart disease were evaluated for coronary hemodynamics and coronary PGI2 and PGE2 production. Inhibition of coronary prostaglandin biosynthesis by ketoprofen (1 mg/kg) or aspirin (15 mg/kg) administered intravenously did not significantly change coronary hemodynamics in resting conditions. In all patients cold pressor tests induced significant increases in coronary blood flow (p less than 0.001) and decreases in coronary vascular resistance (p less than 0.001) without changes in cardiac oxygen extraction and with consequent increases in calculated myocardial oxygen consumption. Simultaneously, a marked increase in coronary PGI2 (as 6-keto-PGF1 alpha) and PGE2 formation was observed (p less than 0.001). Both ketoprofen (1 mg/kg) and aspirin (15 mg/kg) administration completely abolished PGI2 and PGE2 formation that was induced by cold pressor test and caused a paradoxical increase in coronary vascular resistance (ketoprofen: p less than 0.02; aspirin: p less than 0.05). The results of this study support a physiologic role for the coronary prostaglandins in modulating coronary vascular response to sympathetic stimulation in nonischemic patients.

Adult↗
PubMed1990

Heparin and antiaggregating therapy in unstable angina.

Heparin and antiaggregating therapy represent an effective treatment of unstable angina. Aspirin is able to prevent myocardial infarction and death in patients with unstable angina, but is not able to control myocardial ischemia. On the contrary, heparin administered by continuous intravenous infusion (about 1,000 U/h) controls myocardial ischemia by very early lowering anginal attacks and silent ischemic episodes. Heparin intermittently administered (6,000 U i.v. four times daily) did not significantly affect anginal attacks and myocardial ischemia. Thrombolytic therapy alone (Alteplase 1.75 mg/kg) reduced, but not significantly, the number of anginal attacks. The reduction of myocardial ischemia induced by continuous infusion of heparin is associated with a decrease of fibrinopeptide A plasma levels, whereas the thromboxane B2 production by platelets seems to be irrelevant in order to obtain a reduction of myocardial ischemia. Thus thrombin formation seems to be a primary factor in the occurrence of refractory unstable angina and in the activation of platelets.

Angina, Unstable↗