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C Rostagno

Publications and source records attributed to C Rostagno.

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

Aspirin effect on early and late changes in acute lung injury in sheep.

OBJECTIVE: There have been several studies that have already explored the potential beneficial role of cyclo-oxygenase (CO) inhibitors on oleic acid (OA)-induced lung injury in different species. These studies report no significant effect of CO inhibition, though thromboxane B2 (TxB2) was effectively blocked. However, recent studies indicate that pre-treatment with aspirin (ASA) preserve gas exchange in OA lung injury in dogs. Aim of our study has been to evaluate the potential beneficial effects of the pre-treatment with low doses of ASA on gas exchange, hemodynamics, respiratory mechanics, prostanoids and lung histology in OA-induced lung injury in sheep. DESIGN: 0.09 ml/kg of OA was administered into the right atrium of 14 anaesthetized sheep. Six received a bolus of ASA (10 mg/kg i.v.) 30 min before OA, the others saline as placebo. MEASUREMENTS AND RESULTS: Pulmonary and tissue gas exchange, pulmonary and systematic hemodynamics, respiratory system mechanics, TxB2 and 6-keto-PGF1 alpha, leukocytes and platelets concentrations were measured throughout the subsequent 3 h and lung histology was effected at end-experiment. The principal findings of our study are: 1) ASA reduces OA-induced early pulmonary vasoconstriction and bronchoconstriction, parallelled by a suppression of TxB2 generation; 2) the late increase in pulmonary artery pressure and airway resistance due to OA is not inhibited by ASA; 3) the early disturbance in pulmonary gas exchange is reduced by ASA, whereas the late severe deterioration is exaggerated by ASA; 4) the stability of tissue exchange ratio (R) at approximately 1 in ASA-group compared to its fall to approximately 0.7 in controls. CONCLUSION: Our findings suggest that ASA: 1) is only effective to treat the very transient TxB2-induced pulmonary vasoconstriction resulting in hydrostatic edema, and it is ineffective, even accentuates, the subsequent major pulmonary endothelial cell injury leading to alveolar flooding that is unrelated to TxB2; 2) has a transient protective effect on the TxB2-induced early bronchospasm; 3) has a biphasic behaviour on gas exchange, with a benefit which lasts only one hour and then results in a worse gas exchange; 4) has an immediate, stabilizing, persisting effect on R, contrasting with its transient effect on pulmonary hemodynamics and PaO2.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Age-related changes in the hemostatic system.

The increased incidence of arterial thromboembolism in the elderly has prompted investigation of age-related changes in the hemostatic system. Aging is associated with increased plasma levels of fibrinogen, factor VII and factor VIII, which have been shown to be risk factors for thrombotic disease in five large epidemiological studies. An increased responsiveness to different aggregating stimuli, elevated levels of beta-thromboglobulin and an increased production of thromboxane A2 were reported in the platelets of the elderly. These alterations are associated with modifications of platelet membrane lipid composition (namely an increase in the cholesterol/phospholipid ratio and a decrease in linoleic acid) with possible related changes in membrane fluidity. Moreover, a decrease in the number of platelet prostacyclin and thromboxane A2 receptors was observed with aging. Fibrinolytic activity is impaired in the elderly, probably due to an increase in plasminogen activator inhibitor 1. Interestingly, hypercoagulability has been demonstrated by an increase in the activation markers of the coagulation cascade (mainly fibrinopeptide A and prothrombin activation fragment F 1 + 2). Finally, clinical and experimental evidence suggests that endothelium could play a central role in hemostatic alterations which determine a thrombophilic state in the elderly.

Aged↗
PubMed1993

Predictive value for thrombotic disease of plasminogen activator inhibitor-1 plasma levels.

Plasminogen activator inhibitor-1 plays a major role in the fibrinolytic system as the main physiological inhibitor of both tissue-type and urinary-type plasminogen activators. The inhibitor is present in plasma in small amounts and derives mainly from endothelial cells. Positive correlations have been reported between plasma levels and different parameters, such as serum triglycerides, insulin plasma levels and body mass index. Moreover, high plasma inhibitor concentrations have been observed in different disease states, but it must be stressed that plasminogen activator inhibitor-1 behaves as an acute-phase reactant and measurement of plasma levels is not significant in the acute phase of the disease. A possible predictive value of inhibitor levels for thrombotic events such as deep vein thrombosis and ischemic heart disease has been studied. On the basis of available studies, the predictive value is not clear for venous thrombosis, whereas plasminogen activator inhibitor-1 levels can predict some coronary events, at least in subgroups of young patients with a first myocardial infarction. It remains to be established if treatments able to reduce plasma inhibitor levels lead to a decrease in the risk of thromboembolic events.

Female↗
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

Out-of-hospital symptomatic supraventricular arrhythmias. Epidemiological aspects derived from 10 years experience of the Florence Mobile Coronary Care Unit.

The epidemiologic features and the relative incidence of symptomatic supraventricular tachycardias in out-of-hospital settings are unknown. Rhythm disturbances account for 20% of the interventions performed by the Florence Mobile Coronary Care Unit (MCCU). Between November 1979 and December 1989, the MCCU rescued 1239 patients with recent onset (less than 24 hours) symptomatic supraventricular arrhythmias. 809 had atrial fibrillation, 376 paroxysmal supraventricular tachycardia (PSVT), 36 atrial flutter and 18 different atrial dysrhythmias. Women showed an overall predominance, more evident in patients with PSVT, and the incidence of the arrhythmias increased with age. Preexisting heart disease was more frequent in atrial fibrillation (41.1%) and atrial flutter (33.4%) in comparison to PSVT (27.6%). Similarly, a higher incidence of associated cardiovascular events (AMI, acute coronary insufficiency, pulmonary edema) was found in patients with atrial fibrillation and atrial flutter. Palpitations were the main complaint in each group, however, in atrial fibrillation and atrial flutter they were frequently associated with chest pain or dyspnea.

Adult↗
PubMed1991

Evaluation of a mobile coronary care unit protocol in patients with acute onset chest pain.

This study was designed to assess the accuracy of a diagnostic protocol of the mobile coronary care unit (MCCU) of Florence for acute chest discomfort. During 1986, 706 patients with chest pain were seen by the MCCU. Of these, 324 of 376 (95.2%) of those hospitalized and 247 of 324 (76.2%) of the nonhospitalized patients were entered in the study. The MCCU diagnosis of acute myocardial infarction (AMI) was confirmed in 120 patients (80.3%). A false positive diagnosis of AMI was made in 27 patients (6.9%), while in 37 patients AMI was not diagnosed at the first MCCU clinical examination (false negative). The sensitivity in the diagnosis of AMI was 80.5%, the specificity 91.8%, and the diagnostic accuracy 89.1%. In the recognition of acute coronary syndromes (AMI + unstable angina), sensitivity and specificity were, respectively, 94.0% and 94.4%. The protocol of the Florence MCCU provides high accuracy in the diagnosis of AMI and acute coronary insufficiency; close adherence to the protocol can decrease the number and the costs of undue hospital admissions while protecting the safety of patients.

Acute Disease↗
PubMed1991

Pulmonary hypertension associated with long-standing thrombocytosis.

A case of thromboembolic pulmonary hypertension associated with long-standing thrombocytosis is presented. In this patient we found a significant local pulmonary platelet activation and thrombin generation as indicated by the existence of a transpulmonary gradient for thromboxane A2, beta thromboglobulin and fibrinopeptide A. Prolonged heparin and acetylsalicylic acid treatment resulted in improvement of clinical and hemodynamic conditions. These findings support the usefulness of anticoagulating and antiaggregating therapy in selected cases of pulmonary hypertension.

Adult↗
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↗
PubMed1991

[The mobile coronary unit of Florence: an evaluation of 10 years of prehospital cardiac care].

In order to reduce the high mortality from ischemic heart disease, a mobile coronary care unit manned by a cardiologist has been operating in Florence since 1979. From 1980 to 1989 there were 13,029 interventions, 8,718 (66.9%) of which were cardiac emergencies. 1,718 (19.7%) patients showed acute myocardial infarction while in 2,274 angina was diagnosed (26.1%). Acute pulmonary edema and paroxysmal supraventricular tachyarrhythmias accounted, respectively, for 6.2% and 18.3% of total cardiac emergencies; moreover there were 753 (5.8%) attempted resuscitations in sudden cardiorespiratory arrest from cardiac causes. In acute myocardial infarction, the median time between the onset of symptoms and mobile coronary care unit arrival was 85 minutes, and 69.9% of patients were reached within 3 hours from the onset of symptoms. Ventricular fibrillation, ventricular tachycardia and asystole were observed respectively in 80 (4.6%), 42 (2.4%) and 50 (2.9%) patients. Success rate of emergency treatment was 81.3% for ventricular fibrillation, 88.1% for ventricular tachycardia and 18% for asystole. Prehospital mortality was 4.06%. The ECG picture of the 753 patients found in cardiac arrest showed sustained ventricular tachycardia in 12 (1.6%), ventricular fibrillation in 198 (26.3%), bradyarrhythmia in 28 (3.7%), and asystole in 431 (57.2%). Cardiopulmonary resuscitation was successfully performed in 230 patients (30.5%). Finally, more than 50% of the patients with angina, 20% of the patients with acute pulmonary edema, and 70% of the patients with paroxysmal supraventricular tachyarrhythmia were adequately treated at home and needed no hospitalization. The ten years experience of Florence Mobile Coronary Care Unit suggests that a community wide emergency cardiac care system can significantly reduce the pre-hospital mortality and the time delays preceding thrombolysis and intensive care in acute myocardial infarction. Moreover, the cardiac "sudden death" can often be successfully treated. Most other cardiac emergencies may be adequately treated at home and unnecessary hospitalizations can be avoided.

Arrhythmias, Cardiac↗
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

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

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↗