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T Buratti

Publications and source records attributed to T Buratti.

12 recordsLinked to original sources
PubMed2001

Plasma levels of procalcitonin and interleukin-6 in acute myocardial infarction.

Estimation of cardiac morbidity in patients after major surgery is a difficult problem. In addition, infectious complications seriously decrease potential beneficial outcome after cardiovascular surgery. The present study assessed the use of a newer marker of the inflammatory response, procalcitonin, in the field of myocardial infarction, in conjunction with measurements of interleukin-6. Forty-four consecutive cases with acute myocardial infarction were included in the study 4+/-1.3 h after the onset of symptoms. Plasma levels of procalcitonin and interleukin-6 were obtained at admission, and after 3, 6, 12, 18, 24 and 48 h, using commercially available test kits. The range of levels of interleukin-6 and procalcitonin was about normal at admission. Interleukin-6 levels increased significantly following myocardial infarction, whereas procalcitonin were essentially unchanged, i.e. remained close to the normal level threshold of 0.5 ng/ml; only minor variability occurred with a mean peak level of procalcitonin of 1+/-0.4 ng/ml. Data demonstrate that, in contrast to the acute phase reactant interleukin-6, plasma levels procalcitonin are not significantly elevated during uncomplicated acute myocardial infarction. This observation may support the role of procalcitonin measurements in the differential diagnosis of infectious and cardiovascular complications after major surgery.

Acute-Phase Reaction↗
PubMed2000

Hepatocyte growth factor plasma levels after myocardial infarction are not affected by recombinant tissue-type plasminogen-activator therapy.

Hepatocyte growth factor (HGF), a cytokine involved in tissue regeneration, angiogenesis and lateral vessel growth, is secreted as a biological-inactive, single-chain precursor named pro-HGF. In case, of tissue injury pro-HGF is proteolytically cleaved at the extracellular locus by serine proteases. Results obtained from in vitro experiments showed that urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA) can cleave single-chain HGF. In this study we measured serum HGF levels in patients with acute myocardial infarction (MCI). Two groups of patients were compared. One group (n = 7) was treated with a conventional therapy and the other group (n = 7) was subjected to a thrombolytic therapy with recombinant tissue-type plasminogen activator (rtPA). Serum samples were collected at time of admission and subsequently 12-16 hours, 20-30 hours and 50-60 hours after onset of chest pain. At admission and before administration of rtPA, serum HGF levels peaked at 16.8 +/- 2.2 ng/ml in the lysed group and at 20.7 +/- 6.5 ng/ml in the non-lysed group. Levels then continuously declined, reaching lowest values 50-60 hours after onset of chest pain (3.2 +/- 1.3 ng/ml in the group treated with rtPA versus 4.4 +/- 0.9 ng/ml in the non-lysed group). No statistical significant difference could be detected between the two groups at any time. We suggest that serine proteases other than tPA are involved in HGF activation in vivo.

Acute Disease↗
PubMed1999

Thrombolytic therapy in adult meningococcal purpura fulminans with acute renal failure and severe perfusion deficits to the extremities.

OBJECTIVE: To investigate whether systemic administration of recombinant tissue plasminogen activator would improve organ perfusion in an adult patient with fulminant meningococcal disease. DESIGN: Descriptive case report. PATIENT: A 45-year-old female with meningococcal septic shock, purpura fulminans and multiple organ failure who was treated in an eight-bed medical intensive care unit of a University hospital. INTERVENTION: In addition to standard aggressive treatment, on each of three consecutive days the patient received recombinant tissue plasminogen activator infusions at a dose of 20 mg over 4 hrs. RESULTS: Urine output was recorded before, during, and after the recombinant tissue plasminogen activator infusions. In addition, the patient's peripheral perfusion status was documented by clinical assessment. The patient showed a dramatic improvement in urine output, as well as a perceived increase in skin perfusion after recombinant tissue plasminogen activator therapy. The amount of exogenous vasopressor and inotropic support required to maintain the patient's hemodynamic status also rapidly decreased. CONCLUSIONS: In this adult patient, recombinant tissue plasminogen activator therapy resulted in improved organ perfusion similar to that reported for paediatric patients. The findings indicate a need for controlled studies concerning the use of thrombolytics in severe meningococcal disease.

Acute Kidney Injury↗
PubMed1999

Mediator-dependent effects of pentoxifylline on endothelium for transmigration of neutrophils.

In the present study, we investigated the effects of the anti-inflammatory drug pentoxifylline (PTX) on activation of endothelial cells for enhanced adhesion and transmigration of neutrophils by lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF), interleukin-1 (IL-1) and granulocyte colony-stimulating factor (G-CSF). To evaluate the mechanism by which PTX exerts its effect, human umbilical vein endothelial cells (HUVEC) were pretreated with theophylline, 2'-O-dibutyryl-3', 5'-cyclic adenosine monophosphate (db cAMP), and 3-isobutyl-1-methylxanthine, respectively, prior to stimulation. Pretreatment of HUVEC with PTX significantly antagonized TNF-, IL-1-, and G-CSF-activated transmigration of neutrophils. Additive stimulatory effects of PTX were seen with LPS. With the exception of theophylline, all other test cAMP-raising agents stimulated transmigration in similar fashion to PTX. Upon stimulation with TNF or LPS, HUVEC produced IL-8 and PTX affected this process in opposing fashions, with inhibition of the effects of TNF and augmentation of those of LPS. These results demonstrate that PTX differentially affects mediator-induced activation of HUVEC. The present IL-8 dependent and cAMP-regulated augmentation of LPS-induced stimulation of transmigration is the first description of an additive effect of PTX with a pro-inflammatory agent.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Association of high plasma antioxidant capacity with new lesion formation in carotid atherosclerosis: a prospective study.

BACKGROUND: In atherosclerosis, both reductions and elevations in plasma levels of antioxidants have been reported. This study investigated total antioxidant capacity of plasma from subjects with atherosclerotic disease. MATERIALS AND METHODS: The study population consisted of 48 men with or without carotid atherosclerosis. At baseline (1990) carotid arteries were evaluated by duplex sonography and plasma samples were obtained for testing antioxidant capacity by two different test systems. One assay system used neutrophils from healthy volunteers as a source of oxygen free radicals activating the non-fluorescent dichlorofluorescin diacetate in the presence of antioxidant containing plasma from study subjects. In the other test system, total plasma antioxidants were detected colorimetrically by using 2,2'-azino-di-(3-ethylbenzthiazoline sulphonate), metmyoglobin and superoxide in the presence of plasma. Carotid arteries were re-evaluated for the development of new plaques 5 years later (1995). RESULTS: Increased baseline total antioxidant capacity of plasma was significantly associated with the development of new atherosclerotic lesions during a period of 5 years. CONCLUSIONS: Endogenous antioxidant capacity of plasma is increased in patients with active atherosclerotic disease. As scavenging of oxygen free radicals is thought to protect from atherogenesis, elevated antioxidative capacity may represent an adaptive mechanism.

Adult↗
PubMed1998

Decreased levels of beta-endorphin in circulating mononuclear leukocytes from patients with acute myocardial infarction.

Lymphocytes can be activated to produce and release opioid peptides. We investigated the levels of immunoreactive beta-endorphin in peripheral blood mononuclear cells from 11 patients with acute myocardial infarction. The concentrations of beta-endorphin in mononuclear leukocytes of 30.2 +/- 6.9 pg/10(6) cells on admission were in the normal range of 20-40 pg/10(6) cells and decreased significantly to 6.9 +/- 1.9 pg/10(6) cells after 48 h (p < 0.05). Decreased levels of mononuclear leukocyte-associated beta-endorphin in acute myocardial infarction may be due to the release of endogenous opioid after stimulation by stress and acute-phase reactants and play a role in inflammation and pain.

C-Reactive Protein↗
PubMed1996

Inhaled nitric oxide.

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Administration, Inhalation↗