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Biomedical subjects

T Stefenelli

Publications and source records attributed to T Stefenelli.

51 records · Page 3Linked to original sources
PubMed1990

[Angiologic, neurologic and orthopedic findings in vibration exposed chain saw operators].

The present study was designed to evaluate and correlate angiological, neurological and orthopaedic findings in lumberjacks, professionally exposed to vibration by chain-saws with a frequency of 40 to 120 Herz. Raynaud's phenomenon was diagnosed in 16 of 33 subjects. The nerve conduction velocity was delayed in 13 of 32 lumberjacks, the sulcus nervus ulnaris syndrome was diagnosed in 41%, the vibration threshold was abnormal in 10/32 cases. Orthopaedic examination and X-ray studies revealed spondylotic (59%) and spondyloarthritic (65%) alterations of the cervical spine; cysts in bones of the distal upper extremities were observed in 75% of cases. Frequency and severity of angiological, neurological, and orthopaedic pathological findings correlated with the total chain-saw operating time. However, there was no correlation between the presence of digital vascular hyperreactivity and the sulcus nervus ulnaris syndrome or changes in nerve conduction velocity.

Adult↗
PubMed1990

Calcium-dependent fluorescence transients during ventricular fibrillation.

Using surface fluorometry, calcium-dependent fluorescence transients were recorded during ventricular fibrillation in perfused rat and hamster hearts loaded with INDO 1-AM (fluorimetric reagent for calcium ion). Among a series of 203 consecutive isolated heart studies, 13 instances of ventricular fibrillation occurred. These arrhythmias developed during pretreatment with isoproterenol, dobutamine, norepinephrine, phenylephrine, digoxin, and 4 mmol/L calcium in the perfusate. Alternans behavior of calcium transients occurred in three cases; premature beats preceded ventricular fibrillation in six cases. Premature beats led to a further increase in the free intracellular calcium ([Ca2+]i) concentration, resulting in a stronger contraction with the subsequent beat and/or the initiation of ventricular fibrillation. Two distinct patterns of calcium transients were seen: ventricular fibrillation type 1 showed fast disorganized transients with small amplitude and an irregular, nonuniform tracing; type 2 revealed fast activity and multiform, polymorphous transients with marked changes in amplitude. Independent of the morphologic type of fibrillation, [Ca2+]i remained constant or even increased during an observation time up to 9 minutes. No intracellular hypocalcemia was observed. Isoproterenol pretreatment resulted in [Ca2+]i levels in the range of the end-diastolic calcium level of the last regular contraction. Fibrillating calcium transients after norepinephrine, dobutamine, phenylephrine, digoxin, high calcium, and fast pacing were in the previous end-systolic range. It is suggested that inotropic agents acting without a major elevation of cyclic adenosine monophosphate result in higher [Ca2+]i.

Animals↗
PubMed1990

Cardiac calcific deposits in patients with primary hyperparathyroidism: preliminary results of a prospective echocardiographic study.

To explain the incidence and significance of mitral and aortic valve calcification and calcific deposits in the myocardium, a prospective echocardiographic study was performed with 21 consecutive patients who had primary hyperparathyroidism (PHP) and with 21 age- and sex-matched control subjects with normocalcemia. Calcific deposits in the myocardium were seen in 13 patients (62%) with PHP, mainly in the interventicular septum, and in one control subject. Aortic valve calcification was observed in 12 patients (57%) with PHP and in one control subject. Calcification of the mitral valve was found in seven patients with PHP (33%) and three controls (14%). Calcification led to mild or moderate stenosis of the aortic valve in three patients with PHP and of the mitral valve in two patients with PHP. No stenosis was found in the subjects in the control group. Both calcification of the aortic and mitral valves and calcific deposits in the myocardium are common in patients with PHP and can be detected noninvasively by echocardiography. Because of the potential relationship of elevated calcium, calcification, and valvular heart disease, clinical evaluation of PHP should include echocardiographic studies before surgery is performed and during follow-up examination.

Adult↗
PubMed1989

Influence of positive inotropic agents on intracellular calcium transients. Part I. Normal rat heart.

This study, which was designed to evaluate the effects of positive inotropic agents on intracellular calcium transients ([Ca2+]i), is the first to analyze calcium transients in the whole heart. The positive inotropic agents that augment intracellular cyclic adenosine monophosphate (cAMP) (dibutyryl cAMP, amrinone, and isoproterenol) caused an increase in developed pressure and [Ca2+]i transients and a decrease in diastolic [Ca2+]i. On the other hand, the glycoside digoxin and the alpha-adrenoceptor agents, phenylephrine and dobutamine, also caused an increase in [Ca2+]i transients and developed pressure. However, unlike the agents that increase [cAMP]i, they induced an elevation in diastolic [Ca2+]i. With all the positive inotropic agents, developed pressure increased commensurately with the percentage changes in amplitude of the [Ca2+]i transients.

Animals↗
PubMed1989

Influence of positive inotropic agents on intracellular calcium transients. Part II. Cardiomyopathic hamster hearts.

To study the mechanism of dobutamine on end-stage heart failure, we assessed hemodynamic responses, high-energy phosphates (31P-NMR), and free intracellular calcium ([Ca2+]i) transients (surface fluorometry) during perfusion with 10(-6) mol/L dobutamine in Syrian cardiomyopathic hamsters with severe heart failure. These results were compared to perfusion of the heart with 10(-6) mol/L norepinephrine and 10(-6) mol/L isoproterenol. With the positive inotropic agents the rate-pressure product increased immediately (p less than 0.01 with dobutamine, norepinephrine; p less than 0.003 with isoproterenol); after 10 to 15 minutes of perfusion the rate-pressure product remained relatively stable with norepinephrine and isoproterenol but decreased with dobutamine (p = NS vs control values). [Ca2+]i-transients increased significantly in all groups. The end-diastolic [Ca2+]i decreased continuously with norepinephrine and isoproterenol (p less than 0.008; p less than 0.005) but increased during dobutamine by 19%. Alterations in coronary flow, pHi, high-energy phosphates, and the phosphorylation potential were not significantly different among the three catecholamines. In conclusion, in contrast to norepinephrine and isoproterenol, dobutamine depressed myocardial performance and increased end-diastolic [Ca2+]i in late heart failure.

Animals↗
PubMed1989

Humoral regulation during cold-induced coronary arterial spasm.

Previous attempts to define the etiology of coronary arterial spasm have been focused on mechanisms such as autonomic nervous dysfunction and/or enhanced platelet activation. In the present study, humoral regulation was investigated in patients with vasospastic angina and scintigraphically documented transient myocardial perfusion abnormalities after a peripheral cold pressor test. Serial changes in angiotensin II, epi- and norepinephrine as well as thromboxane B2 (the stable derivate of thromboxane A2), and malondialdehyde were determined at baseline (I), immediately after 5 minutes cold water hand immersion (II), and following 10 minutes recovery (III). Angiotensin II and epinephrine remained unchanged during observation (I vs II, II vs III: P = NS). Norepinephrine was elevated after cold (I vs II: P less than 0.001) and normalized after 10 minutes (I vs III: P = ns). Thromboxane B2 and malondialdehyde increased continuously (I vs III: P less than 0.05 and I vs III: P less than 0.002, respectively). Further radiothin-layer chromatography results indicate an activation of platelet function during myocardial ischemia. Our results do not establish a cause-effect relationship but, together with other evidence, they may suggest that thromboxane A2 is unlikely to be the cause of spasm. It might, however, play an important role in the maintenance of vasoconstriction.

Angiotensin II↗
PubMed1988

Increase of pulmonary vascular resistance during cold provocation in patients with variant angina.

This study was performed to evaluate pulmonary vascular reactivity in patients with angiographically documented coronary vasospasm. Right heart catheterization was performed in 8 subjects with vasospastic angina without evidence of Raynaud's phenomenon: heart rate, systemic and pulmonary arterial pressure as well as cardiac output were determined at rest, during cold provocation and after 20 minutes recovery. Data were obtained both before and during treatment with nifedipine. During cold provocation pulmonary vascular resistance was elevated significantly (P less than 0.02 compared with baseline); systemic vascular resistance tended to increase; nifedipine blunted both vasoconstrictor effects. Our results indicate an abnormal vascular response of the pulmonary arteries to cold provocation in patients with symptomatic coronary artery spasm and suggest a primary vasospastic disorder with coronary and pulmonary manifestation.

Adult↗
PubMed1988

Prinzmetal's angina during cyclophosphamide therapy.

The first case of cyclophosphamide-induced myocardial ischaemia with electrocardiographically documented ST-segment elevation, T-wave inversion, arrhythmias, angina pectoris and cardiac decompensation is reported. The data suggest that cyclophosphamides induces myocardial ischaemia by eliciting coronary artery spasm.

Aged↗
PubMed1988

Acute vascular toxicity after combination chemotherapy with cisplatin, vinblastine, and bleomycin for testicular cancer.

Twenty-one consecutive patients with testicular cancer treated with bleomycin, vinblastine, and cisplatin (PVB) were evaluated for acute vascular ischaemic events during chemotherapy. Angina pectoris occurred in 8/21 (38%) patients, a median 5.6 weeks after initiation of chemotherapy and persisted for 2-7 days. Raynaud's phenomenon was detected in seven (33%) subjects, transient ischaemia of the toes was found in six (29%) patients, one patient complained of migraine, but none had major cerebrovascular accidents. Patients with and without angina pectoris and/or Raynaud's phenomenon did not differ in respect of age, histology of tumor or medication. Ischaemia occurred at any time during the course of chemotherapy. No correlation was found between dosage of drugs and time of onset of ischaemic reactions. However, arterial occlusive event is a frequent and common toxicity and a result of treatment with PVB.

Adult↗
PubMed1987

[Myocardial ischemia with normal coronary vessels. Indication of a vasospastic etiology].

In a 43-year-old woman with ECG changes of an acute anterior and posterior wall infarct, associated symptoms and biochemical findings, coronary angiography demonstrated normal coronary arteries and a normal variant in the course of the left coronary artery. Vasospasms in another vascular bed (migraine) and highly positive 201-Thallium scintigraphy during acral cold provocation speak for coronary spasm as cause of the myocardial ischaemia in this patient.

Adult↗
PubMed1985

Cardial decompensation caused by hypertension and polyglobulia associated with multiple renal oncocytomas.

A 43 year old man was referred to the Internal Department for the examination of cardial decompensation, hypertension, polyglobulia and atrophy blanche of the lower legs. Clinical and supersonic examination revealed two tumors in the left kidney (diameter 8 and 3.5 cm) and some small tumors in the right kidney. Laboratory studies disclosed erythropoietin levels up to 170 mU/ml (standard 14-61 mU/ml) and a red blood cell count of up to 8 X 10(6)/ml. After recompensation, a radical left nephrectomy and the removal of three small tumors of the right kidney four weeks later was initiated. Postoperative erythropoietin levels and red blood cell count sank to the normal range leading to the reduction of antihypertensive therapy. The clinical course indicates a strong etiological connection between hypertension as well as polyglobulia with the multiple bilateral oncocytomas. Polycythemia also led to the atrophy blanche which had resulted from disturbances of microcirculation.

Adenoma↗
PubMedDate not supplied

Primary hyperparathyroidism and the heart: cardiac abnormalities correlated to clinical and biochemical data.

Comparing patients with primary hyperparathyroidism (PHP) to a normocalcemic control population, those with PHP have a higher incidence of cardiovascular disease and cardiac abnormalities. This study aimed at correlating cardiac findings (valvular and myocardial calcification, myocardial hypertrophy) with clinical data (age, sex, clinical manifestation, nephrolithiasis, nephrocalcinosis, hypertension, skeletal abnormalities, hypercalcemic syndrome) and biochemical data (serum calcium, serum phosphate, serum iPTH level, serum creatinine). A group of 132 consecutive patients with surgically verified PHP (94 women, 38 men; ages 15-86, mean age 57 +/- 16 years) were included in this study. Blood chemistry, clinical presentation, radiography, and echocardiography were carried out in all patients for univariate and multivariate analyses of all parameters. There was no statistical correlation between clinical symptoms, biochemical data, and cardiac calcific alterations. Typical skeletal manifestations (osteolysis/subperiostal resorption) and valvular calcifications were significantly correlated to left ventricular hypertrophy (p = 0.005). Cardiac abnormalities such as calcific myocardial deposits or mitral and aortic valvular calcifications do not correlate with laboratory findings and clinical presentation at the time of diagnosis. There was no biochemical or clinical variable that could predict the frequency or severity of valvular sclerosis or calcific deposits in the myocardium. However, PHP-related skeletal abnormalities and valvular calcification were predicting factors for left ventricular hypertrophy, a reversible cardiac manifestation of PHP. Myocardial hypertrophy is more often found with classic symptomatic PHP with osseous abnormalities.

Adolescent↗
PubMedDate not supplied

In vitro evaluation of the anticancer drug modulatory effect of hyaluronidase in human gastrointestinal cell lines.

In an attempt to establish whether the combination of anticancer drugs with hyaluronidase would result in enhanced cytotoxicity, we have tested a range of 6 continuous cell lines against 4 different chemotherapeutic drugs with or without the addition of various concentrations of the enzyme. Measurement of cytotoxic drug effects has been performed using the Bactec system, a new semiautomated radiometric technique. In only 15 of a total of 144 experiments (11%) was a significant hyaluronidase-mediated potentiation of the single agents' activity seen. In the large majority of experiments, the antiproliferative effect of the combined treatment was classified as additive or subadditive, while in 23% it was antagonistic. Evaluation of the drug modulatory mechanism of hyaluronidase suggested that the combined drug-hyaluronidase effects were independent of the nature of the drug, the exposure mode and the concentration of the enzyme employed. Among the various tumor cell lines tested there was a marked heterogeneity in the sensitivity to the combined effect (P less than 0.0001). In summary, we have not been able to confirm the promising results of early reports of in vitro and in vivo enhancement of the cytotoxicity of antitumor agents by hyaluronidase. Our data emphasize the need for further controlled clinical studies in order to prove or disprove this new therapeutic approach.

Adenocarcinoma↗