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Biomedical subjects

M Boddi

Publications and source records attributed to M Boddi.

At least 37 records · Page 2Linked to original sources
PubMed1993

Interleukin-1 beta and interleukin-6 release by peripheral blood monocytes in head and neck cancer.

In patients with advanced head and neck squamous cell carcinoma (HNSC), evidence of cell-mediated immunity and monocyte functional abnormalities has been reported. We studied the production of interleukin 1 beta (IL-1 beta) and interleukin 6 (IL-6) by peripheral blood monocytes from 22 patients with HNSC (12 larynx and ten oral cavity cancers) in comparison with monocyte cytokine production of age-matched healthy subjects. Pure monocytes were incubated with and without lipopolysaccharides (LPS) (10 micrograms ml-1) for 4 h at 37 degrees C and IL-1 beta and IL-6 concentrations were determined in supernatants by specific ELISA. There was no significant difference in IL-1 beta levels in monocyte supernatants from cancer in comparison to control subjects; conversely, a higher IL-6 production by unstimulated and LPS-activated cells from HNSC patients than from controls was found. No relationship was observed between cytokine production and cancer stage. The regression analysis evidenced a significant correlation between IL-1 beta and IL-6 monocyte-release in HNSC patients and in controls, so suggesting a possible autocrine control of IL-6 production by other cytokines.

Aged↗
PubMed1993

Silent ischemia in unstable angina is related to an altered cardiac norepinephrine handling.

BACKGROUND: Inferential evidence suggests that silent ischemia might be related to sympathetic activity. Study of [3H]norepinephrine kinetics is a suitable tool to assess the regional sympathetic activity. This method was applied to investigate whether silent myocardial ischemia in unstable angina is related to and depends on cardiac sympathetic overactivity. METHODS AND RESULTS: Patients with active unstable angina were compared with patients with inactive unstable angina, stable effort angina, and controls. Silent myocardial ischemia was evaluated by three 24-hour Holter monitoring periods on alternate days, and [3H]norepinephrine kinetics was assessed under rest conditions and following the cold pressor test. Simultaneously, catecholamine concentrations were measured in the aortic, coronary sinus, and peripheral venous blood. Different than the other groups (p = 0.0013), in patients with active unstable angina, the majority of silent ischemic episodes occurred without increase in heart rate. These patients had a positive coronary sinus-aorta norepinephrine gradient, both at rest and following the cold pressor test. [3H]Norepinephrine kinetics demonstrated an increased selective cardiac spillover, both at rest and, even more, after the cold pressor test. Reduced cardiac [3H]norepinephrine extraction also was found. A significant relation was found between the number of ischemic episodes or the overall duration of silent ischemia and norepinephrine spillover, both at rest and following cold application. CONCLUSIONS: During the acute phase of unstable angina (but not in the quiescent phase or in stable effort angina), a disorder in cardiac norepinephrine handling occurs. This results in a reflex cardiac sympathetic overactivity that plays a major role in the occurrence of silent myocardial ischemia.

Angina, Unstable↗
PubMed1993

Lupus anticoagulant and monocyte procoagulant activity in polyabortive women.

Monocyte stimulation may be induced by various agents. Monocytes generate procoagulant activity (PCA) in response to stimulation; they widely interact with the hemostatic system and participate in thrombin formation. Extensive placental thrombotic infarction has been implicated in fetal death in polyabortive patients with lupus anticoagulant (LA). We investigated 38 polyabortive women: 17 LA negative (LA-) and 18 LA positive (LA+). We compared the results with 25 clinically normal women. After four hours of incubation, the mean value of monocyte PCA in the LA+ women was significantly higher than in either the LA- or the control group (p < 0.0001). The monocyte PCA was out of the range of the controls in 9 of the 18 LA+ women. No correlation was observed between the levels of LA and monocyte PCA (r = 0.02; p = 0.94). No differences were found in monocyte PCA increase when induced by LA-, LA+ or control plasma; in all cases the increase was about five-six fold. Our results indicate that an increased monocyte PCA is present in some LA+ polyabortive women, thus suggesting that monocyte activation might be involved in the formation of thrombotic placental infarction and the consequent fetal loss in some patients. It might also suggest that these patients, in particular, could benefit from corticosteroid treatment, which is known to inhibit the formation of monocyte PCA.

Abortion, Habitual↗
PubMed1993

[The tissue renin-angiotensin systems].

Over the past 10 years, our understanding of the renin-angiotensin system has changed greatly, reflecting significant advances in this field. Studies in cell biology, the application of molecular biological techniques, and studies of angiotensin kinetics have provided evidence for the existence in various sites (cardiac, cerebral, renal, vascular and gonadal) of tissue-based renin-angiotensin system that function independently of the plasma renin-angiotensin system. These local systems contribute to the functional activity of their plasma counterpart through the local production of angiotensins I and II; at the same time, they are autonomous autocrine-paracrine systems with their own regulatory mechanisms. This multicentric organization of the renin-angiotensin system has physiologic and pathophysiologic implications. However, it also has important therapeutic consequences, since it follows that inhibition of the plasma renin-angiotensin system alone is probably not sufficient for therapeutic purposes.

Angiotensinogen↗
PubMed1991

Evidence for local platelet activation in pulmonary vessels in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease.

To investigate the relationships between local platelet activation in pulmonary vessels and pulmonary artery pressure circulating platelet aggregates and plasma beta-thromboglobulin (beta-TG) levels were evaluated in peripheral venous blood and blood from different sites of pulmonary circulation (right ventricle, pulmonary artery and arteriolo-capillary bed) in 29 patients with COPD. Fifteen had pulmonary hypertension and 14 normal pulmonary artery pressure. In normotensive COPD no significant differences could be found in platelet aggregation and beta-TG levels among different sampling sites. On the contrary in patients with pulmonary hypertension a significant increase of platelet aggregates and beta-TG levels was found in blood withdrawn from the arteriolo-capillary bed. A significant correlation was demonstrated between platelet aggregation and both mean pulmonary artery pressure and pulmonary vascular resistance. These results indicate that in patients with pulmonary hypertension secondary to COPD a local platelet activation in pulmonary vessels does occur and may contribute to the maintainance of elevated pulmonary vascular resistance.

Adult↗
PubMed1990

Effects of calcium channel blockers on platelet aggregation and thromboxane A2 formation: an in vivo double blind randomized study.

In this double blind cross over study against placebo the in vivo effects of diltiazem, nifedipine and verapamil on platelet aggregation and Thromboxane A2 (TxA2) formation were evaluated in eighteen healthy adults. No significant inhibition of platelet aggregation or TxA2 formation was found either after acute or short term (8 days) administration of the three calcium channel blockers at the usual therapeutical dosages. Our study indicate that diltiazem, nifedipine and verapamil are unable to significantly affect platelet aggregation and TxA2 formation in healthy subjects.

Adult↗
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

Cyclooxygenase and lipoxygenase metabolite synthesis by polymorphonuclear neutrophils: in vitro effect of dipyrone.

Functional activity of polymorphonuclear neutrophils (PMN) is associated with the metabolism of Arachidonic Acid (AA) released from membrane phospholipids. In this study the in vitro effect of dipyrone, a non steroidal anti-inflammatory drug, on the production of AA metabolites through cyclooxygenase (CO) and lipoxygenase (LO) pathways by stimulated PMN has been investigated. PMN isolated by counterflow centrifuge elutriator were greater than 98% pure and viable. Metabolite production was evaluated by RIA of Thromboxane A2 (TxA2), Prostaglandin E2 (PGE2), Leukotriene B2 (LTB4) and Leukotriene C4 (LTC4) after PMN stimulation with calcium ionophore A 23187 (20 microM). The levels of beta-thromboglobulin (RIA) lower than 5 ng/ml allowed us to rule out activation of residual contaminant platelets. In these experimental conditions, in the absence of dipyrone the products (ng/10(6) cells) of AA metabolism were LTB4 (3.51 +/- 0.22), LTC4 (0.81 +/- 0.08), TxB2 (0.144 +/- 0.025) and PGE2 (0.150 +/- 0.017). Incubation with dipyrone induced changes of PGE2 and TXB2 production in a dose dependent fashion (r = 0.83 and r = 0.87, p less than 0.001), obtaining already at the lowest drug concentration (5 micrograms/ml) a significant inhibition (33 and 40% for TxB2 and PGE2 p less than 0.005). No significant changes of LTB4 and LTC4 production have been observed. The results of this study indicate that dipyrone relevantly affects CO metabolite synthesis by stimulated PMN at concentrations comparable to those reached in therapeutic use. The inhibition of PGE2 synthesis which is present in inflamed tissues and actively participates in inflammatory reactions, could contribute to the therapeutic anti-inflammatory action of dipyrone.

Arachidonic Acids↗
PubMed1990

Transcutaneous oximetry monitoring during the early phase of exercise in patients with peripheral artery disease.

The present work was performed to test the sensitivity of transcutaneous oximetry in evaluating the first stage of peripheral artery disease in patients with few symptoms. Eighteen nondiabetic patients, stage II according to Fontaine and classified according to their walking capability and Doppler examination, were investigated. Ten healthy subjects served as controls. Measurements were performed with the subjects standing and during exercise on a treadmill. Postischemic hyperemia was also evaluated with strain-guage plethysmography. Standing values did not discriminate between patients and controls; on the contrary the pattern of the early phase of trancutaneous oximetry curves obtained during exercise allowed the investigators to distinguish the symptomatic patients with minimal symptoms. Accuracy and sensitivity of the method further increased when regional perfusion index was considered.

Blood Gas Monitoring, Transcutaneous↗
PubMed1989

Ability of whole blood aggregometer to detect platelet hyperaggregability.

In this study the reliability of platelet aggregation in whole blood (WB) was investigated in clinical conditions associated with thromboembolic complications. Spontaneous (SPA) and collagen-induced platelet aggregation were evaluated both in whole and diluted blood by the impedance method and in platelet-rich plasma (PRP) by the Born aggregometer in 18 healthy subjects, 15 patients with ischemic heart disease (IHD), and 15 patients with insulin-independent diabetes. SPA occurred more often in WB than in PRP, and in WB the occurrence of SPA was significantly more frequent in the patient groups (4 of 15 patients with IHD and 6 of 15 diabetic patients) than in the controls (1 of 18). WB aggregation induced by collagen was significantly higher in patients with IHD and in diabetic patients than in controls (P less than 0.01), whereas diluted WB and PRP aggregation were not statistically different from controls either in patients with IHD or in diabetic patients. WB aggregation values were found to be related, although not very closely, to megathrombocyte count (r = 0.31, P less than 0.05) whereas not at all to platelet count or hematocrit. No relationship was observed between WB aggregation and disease severity (angiographic lesions and number of ischemic attacks) in patients with IHD and between WB aggregation and HbAlc values in diabetic patients.

Blood Cell Count↗
PubMed1989

[Right ventricular thrombosis in association with dilated cardiomyopathy: diagnosis by echocardiography and nuclear magnetic resonance].

Thrombus formation in right chambers is an uncommon event which usually follows an acute right myocardial infarction or a thromboembolic disease. In subjects with dilated cardiomyopathy, thrombus formation is common in the left ventricle; so far right ventricular thrombosis has not yet been reported. In this report we describe a case of cardiomyopathy with right ventricular thrombosis as detected by echocardiography and nuclear magnetic resonance.

Cardiomyopathy, Dilated↗
PubMed1988

Radioimmunoassay of thromboxane B2 in plasma: methodological modifications.

Thromboxane B2 (TxB2) determination is usually performed by using commercial 3H-RIA kits. However, the low amounts of TxB2 present in plasma are not detectable without previous extraction. The aim of this study is the evaluation of 1) plasma protein interferences on the binding and separation steps of bound from free analyte and 2) charcoal efficacy in different experimental conditions. Our results indicate that plasma proteins do not influence the antibody binding, but significantly reduce the efficacy of precipitation of kit dextran-charcoal, so that the supernate radioactivity rises with the protein amount increase (r = 0.99 p less than 0.001). Such greater number of counts in the samples determines a lower estimation of TxB2 concentration in plasma when the calibration curve is set up in buffer. Our findings suggest that, in order to measure low amounts of plasma TxB2 without extraction, it is useful: 1) to refer to a calibration curve set up in buffer-diluted plasma, 2) to use the uncoated charcoal concentration allowing the lowest stripping and 3) to perform all steps at 4 degrees C.

Charcoal↗
PubMed1987

Acute reversible reduction of PGI2 platelet receptors after iloprost infusion in man.

Platelet sensitivity to PGI2 and platelet PGI2 receptors were investigated in eight subjects with peripheral artery disease (stage IV according to Fontaine) treated for 14 consecutive days with six hour iv infusion of Iloprost (Schering, FRG) 2 ng/kg/min. Platelet studies were performed on the 1st, the 2nd, the 7th and the 14th day of therapy, immediately before infusion (between 8.00 and 9.00 a.m.), at the end and 6 and 18 hours (the following morning) after the end of the infusion. Platelet sensitivity to PGI2 was assessed by determining the PGI2 inhibitory dose 50(ID 50) on platelet aggregation induced by 5 microM ADP. PGI2 platelet receptors were investigated by a direct radioligand binding assay. PGI2 ID 50 after the infusion was significantly higher than that at baseline(p less than 0.01) and six hours later the baseline sensitivity was restored. After the six hour Iloprost iv infusion a significant reduction in the number of high affinity PGI2 platelet receptor (HAR) was observed (p less than 0.005) without any change in their affinity for the ligand. Six hours after the end of the infusion the number of the HAR was still significantly reduced (p less than 0.05). The following morning the receptor number of HAR was restored. The baseline values of PGI2 HAR, when reassessed after seven and fourteen days of treatment, were not significantly different from those recorded on the first day of therapy. These data indicate that the reduction of platelet PGI2 sensitivity following short-term Iloprost infusion is rapidly reversible and is related to a contemporary down-regulation of PGI2 platelet receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1987

Effects of indenolol on blood pressure, lower limb blood flow, adrenergic reflexes, and plasma renin activity.

The antihypertensive effects of indenolol, a new not-cardioselective beta-blocking agent, were evaluated in patients with WHO grades I and II essential hypertension (range 160/95 to 200/115 mm Hg) in a double-blind, placebo-controlled study after acute (12 patients) and 2-week treatment (seven patients). Indenolol (30 to 120 mg) reduced blood pressure in a dose-dependent fashion. Maximum reduction was 26 mm Hg for systolic and 17 mm Hg for diastolic pressure. Hypotensive activity commenced within 10 minutes, peaked in 60 minutes, and persisted for about 7 hours. Lower limb vascular resistance (strain-gauge plethysmography) was significantly lowered, thus suggesting an intrinsic sympathomimetic activity. Heart rate was progressively reduced at 30 and 60 mg without any additional effect at 120 mg. Indenolol did not alter adrenergic reflexes (standing, cold application, and hand-grip) and did not induce any side effect. In conclusion, indenolol possesses an antihypertensive activity associated with reduction of vascular resistance.

Adrenergic beta-Antagonists↗