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Biomedical subjects

A Salustri

Publications and source records attributed to A Salustri.

At least 91 records · Page 5Linked to original sources

Exercise echocardiography and technetium-99m MIBI single-photon emission computed tomography in the detection of coronary artery disease.

To compare the relative diagnostic value of exercise echocardiography with perfusion technetium-99m metoxyisobutylisonitrile single-photon emission computed tomography (SPECT) in detecting coronary artery disease (CAD), 75 patients with suspected CAD but a normal electrocardiogram (ECG) at rest were included in a prospective correlative study. Both the exercise echocardiograms and SPECT studies were performed in conjunction with the same symptom-limited bicycle exercise test. The development of either a new wall motion abnormality or a reversible perfusion defect after exercise, or both, were regarded as a positive test for the exercise echocardiographic and SPECT studies, respectively. The results of these 2 diagnostic tests were compared with coronary arteriography. Exercise echocardiography identified 35 (71%) and SPECT 41 (84%, p = 0.13) of the 49 patients with significant CAD (defined as greater than 50% diameter stenosis). Twenty-five of the 26 patients (96%) without significant coronary stenosis had negative exercise echocardiographic results and 23 of 26 (88%) had negative SPECT results. Exercise-induced new wall motion abnormalities showed a good correlation with reversible perfusion defects, and the results of the 2 methods were concordant in 65 of 75 patients (agreement = 88%, kappa = 0.75 +/- 0.14). Both the diagnostic accuracy of exercise echocardiography and SPECT were significantly higher than the exercise ECG (81 vs 64%, p less than 0.02 and 88 vs 64%, p less than 0.005). The sensitivity and specificity for detecting individual diseased vessels were 60 and 95% for exercise echocardiography and 67 and 94% for SPECT.(ABSTRACT TRUNCATED AT 250 WORDS)

Contrast Media↗

The comparative value of exercise echocardiography and 99m Tc MIBI single photon emission computed tomography in the diagnosis and localization of myocardial ischaemia.

To determine the relative value of exercise two-dimensional echocardiography and 99m Tc methoxyisobutylisonitrile single photon emission computed tomography (MIBI SPECT) for the detection of myocardial ischaemia, 103 consecutive patients with either proven or suspected coronary artery disease, who were referred for perfusion scintigraphy, were studied by a combination of the two techniques during the same symptom-limited upright bicycle exercise test. Appropriate echocardiographic images were recorded both at rest and immediately post-exercise and subsequently analysed by means of digital cine loop processing. Both echocardiographic and MIBI SPECT images were visually analysed. For each technique, three different responses to exercise were defined: normal (absence of rest and exercise abnormalities); ischaemic (transient scintigraphic perfusion defects and transient wall motion abnormalities during exercise echocardiography); and fixed abnormalities (fixed scintigraphic perfusion defects; echocardiographic wall motion abnormalities at rest without worsening after exercise). To allow a valid comparison of each technique in localizing ischaemia, the left ventricle was divided into the following six major regions for both methods: anterior, posterolateral, inferior, interventricular septum (subdivided in anterior and posterior septum) and apex. Eleven of the 103 patients had to be excluded from the final analysis because of unsatisfactory examinations: seven with non-interpretable exercise echocardiograms and four with non-interpretable MIBI SPECT images. The response to exercise was concordantly classified by both techniques in 84% of patients (k = 0.78). Exercise echocardiography revealed the presence of ischaemia in 38 and MIBI SPECT in 45 patients (agreement = 77%).(ABSTRACT TRUNCATED AT 250 WORDS)

Contrast Media↗

Comparison of exercise echocardiography with myocardial perfusion scintigraphy for the diagnosis of coronary artery disease.

The rationale of exercise echocardiography for the diagnosis of coronary artery disease is based on the detection of exercise-induced wall motion abnormalities by ultrasound. Some of the problems that had previously limited the widespread application of the test have been solved by the development of digital recording and side by side cine loop display of two-dimensional echocardiograms: thus, respiratory artifacts can be eliminated, the examination is faster, and the comparison between rest and stress images has become practical and reliable improving sensitivity. The sensitivity and specificity of exercise echocardiography vary from 70 to 100%, according to patient selection, the protocol, and the gold standard used. Few studies studied the value of exercise echocardiography as compared to the more established nuclear cardiology imaging. Data from these comparative evaluations show a strong correlation between the two techniques for identifying and localizing myocardial ischemia. With good equipment and after proper training, exercise echocardiography can provide both diagnostic and prognostic information for routine clinical care.

Coronary Disease↗

[The echo-dobutamine test for the diagnosis of myocardial ischemia. Study on 20 patients with normal kinetics at rest].

We have assessed the value of dobutamine stress echocardiography for the diagnosis of myocardial ischemia in 20 consecutive patients referred for chest pain, without a previous myocardial infarction and with a normal left ventricular wall motion at rest. The test was considered positive when wall motion abnormalities appeared during dobutamine infusion (from 5 to a maximum of 40 micrograms/Kg/min). The results were compared to the % diameter stenosis (%DS) quantitatively measured on coronary arteriography. "Significant" coronary artery disease was defined as greater than or equal to 50% DS. No significant side effects occurred in any patients during the test. Transient wall motion abnormalities were detected in 8 of the 12 patients with significant coronary artery disease (sensitivity = 66%) and in 1 of the 8 patients without significant coronary artery disease (specificity = 88%). All the patients with false-negative dobutamine stress echocardiography had distal stenosis or stenosis in a collateral vessel; moreover, all the patients with true-positive dobutamine stress echocardiography had proximal (7 patients) or middle (1 patient) stenosis. The results of this study show that dobutamine stress echocardiography is a safe and feasible test for the noninvasive diagnosis of myocardial ischemia.

Adult↗

Hyaluronic acid synthesis by mural granulosa cells and cumulus cells in vitro is selectively stimulated by a factor produced by oocytes and by transforming growth factor-beta.

In ovarian antral follicles cumulus cells (approximately 1,000/follicle) closely surround the oocyte, and mural granulosa cells (approximately 50,000/follicle) are distributed at the periphery. Previous work (Salustri, A., Yanagishita, M., and Hascall, V. C. (1990) Dev. Biol. 138, 26-32) showed that oocytes produce a factor(s) which stimulates hyaluronic acid (HA) synthesis by cumulus cells during expansion of the cumulus cell-oocyte complex. We now show that mural granulosa cells also respond in vitro to the oocyte factor(s) with greatly increased HA synthesis. As with cumulus cells, a factor(s) present in fetal calf serum is required to retain newly synthesized HA in the extracellular matrix. Unlike cumulus cells, follicle-stimulating hormone (FSH) is not required for maximal stimulation, in part because mural granulosa cells synthesize prostaglandin E2 which can substitute for FSH in promoting cumulus cell-oocyte complex expansion. Of several growth factors studied, only transforming growth factor-beta 1 (TGF-beta 1) stimulated HA synthesis in both cell types. However, the stimulation of HA synthesis by TGF-beta 1 was additive with that for the oocyte factor(s), and neutralizing antibodies to TGF-beta did not inhibit the response to the oocyte factor(s). The results indicate that the oocyte factor(s) and TGF-beta 1 are not the same and that they operate through different receptors in stimulating HA synthesis. Epidermal growth factor was able to replace FSH in amplifying the response of cumulus cells to the oocyte factor(s) and in stimulating synthesis of dermatan sulfate proteoglycans.

Animals↗

Mouse oocytes regulate hyaluronic acid synthesis and mucification by FSH-stimulated cumulus cells.

Mucification (or expansion) of the cumulus cells surrounding the oocyte is thought to depend on the direct action of gonadotropins in stimulating production and deposition of hyaluronic acid (HA) in the extracellular matrix. We now report that the oocyte is essential for this process. Either follicle-stimulating hormone (FSH) at 1 micrograms/ml or dibutyryl cAMP at 2 mM induces mucification of intact cumulus cell-oocyte complexes (COCs) in vitro, but fails to stimulate mucification of isolated cumulus cells. HA synthesis by FSH-stimulated cumulus cells is only approximately 3.5% of the value achieved by FSH-stimulated COCs. Isolated oocytes cultured with or without FSH do not synthesize detectable amounts of HA but induce isolated cumulus cells to increase HA synthesis approximately 13-fold in cocultures with FSH. Medium conditioned by isolated oocytes for 5 hr induces nearly the same level of HA synthesis by cumulus cells under the same culture conditions. FSH also stimulates cumulus cells to increase synthesis of dermatan sulfate proteoglycans (DS-PGs) approximately 3-fold, but this stimulation does not depend upon the presence of oocytes. The results indicate that oocytes produce a soluble factor(s) essential in combination with FSH to stimulate HA, but not DS-PG, synthesis by cumulus cells in vitro and that this factor(s) acts independently or downstream from the FSH-induced formation of cAMP.

Animals↗

Synthesis and accumulation of hyaluronic acid and proteoglycans in the mouse cumulus cell-oocyte complex during follicle-stimulating hormone-induced mucification.

In most mammalian ovaries, the cumulus cell-oocyte complex (COC) expands at the time of ovulation by depositing an extensive extracellular matrix between the cumulus cells. This phenomenon can be reproduced in vitro by culturing COCs with follicle-stimulating hormone (FSH) and serum. Biosynthesis of hyaluronic acid (HA) and proteoglycans by mouse COCs in vitro was studied using [3H]glucosamine and [35S]sulfate as metabolic precursors. Radiolabeled complex carbohydrates were analyzed by ion exchange chromatography, specific enzyme digestion followed by high performance liquid chromatography, and gel filtration. The specific activities of [3H]hexosamines in the labeled molecules were determined by measuring the incorporation of 3H and 35S into chondroitin 4-sulfate disaccharides. When COCs were stimulated with FSH, HA biosynthesis increased 20-30-fold between 3-12 h later when expansion occurs, reaching a maximum rate of approximately 780 pmol (as glucosamine)/COC/h compared with the unstimulated rate of approximately 26 pmol/COC/h. The final concentration of HA in the expanded COC was calculated to be approximately 250 micrograms/ml. The effects of dibutyryl cyclic AMP (Bt2cAMP) on COC expansion and HA synthesis were similar to those of FSH, suggesting that the effects of FSH are mediated by cAMP. However, FSH significantly decreased the specific activity of the incorporated hexosamines while Bt2cAMP did not. Serum is necessary for the accumulation of HA in the COC matrix. HA synthesis in FSH-stimulated COCs was as high or higher in the absence of serum, but most was recovered in the medium and not in the COC matrix. The molecular size of the HA was greater than 2 million dalton in either case, suggesting that the serum did not alter physical properties of HA. Stimulation of proteoglycan biosynthesis by either FSH or Bt2cAMP was less pronounced (three to four times control) than for HA and was sustained throughout an 18-h culture period. A reduction of 80% in the deposition of newly synthesized PGs in the COC matrix by 0.5 mM beta-xyloside treatment did not affect the expansion of the cumulus.

Animals↗

Adenosine potentiates forskolin-induced delay of meiotic resumption by mouse denuded oocytes: evidence for an oocyte surface site of adenosine action.

Adenosine is present in the mouse follicular fluid and has been shown to interfere with oocyte maturation in vitro. To clarify the mechanism of adenosine action on meiotic arrest, we have characterized the synergistic action of this purine with forskolin on the meiotic resumption of mouse denuded oocytes. Forskolin delays meiotic resumption by approximately 1 hour; adenosine at concentrations ranging between 30-750 microM has no significant effect. Conversely, adenosine treatment together with forskolin produces a further delay in the resumption of meiosis. This adenosine effect is dose-dependent and mimicked by adenosine analogs like N6-phenylisopropyl adenosine (PIA), 2-chloroadensoine (2-CLA), 5'-N-ethylcarboxamide (NECA). Dipyridamole, which inhibits adenosine transport, does not prevent the meiosis-arresting synergistic effect of adenosine with forskolin. Adenosine causes a 50% increase of adenosine triphosphate (ATP) content in the oocyte. However, this increase is not directly responsible for the observed delay in oocyte maturation for the following reasons: (1) the dose response of inhibition of meiotic resumption does not correlate with the doses of adenosine producing an increase in ATP; (2) dipyridamole blocks the increase in intracellular ATP, but it has no effect on the adenosine inhibition of maturation; (3) adenosine analogs inhibit oocyte maturation but do not affect intracellular ATP levels. These results suggest that the synergism of adenosine with forskolin on meiotic arrest does not require uptake of the nucleoside nor its conversion to ATP and that the adenosine effects are exerted at the level of the oocyte plasma membrane.

Adenosine↗

[Effect of the acute administration of molsidomine in refractory congestive heart failure. A double-blind randomized non-invasive study].

The effect of vasodilator Molsidomine (M) vs placebo on left ventricular dimensions and function measured by echocardiography was evaluated in a randomized study on 23 patients (pts) with refractory congestive heart failure (R CF) (NYHA class III-IV). The pts were randomized in two groups: group A (12 pts) received M, group B received an identical appearing placebo. Adequate echocardiograms were obtained before and one hour after 2 tablets of M (4 mg) or P; left ventricular end-diastolic and end-systolic diameters (LVEDD and LVESD), mean rate of circumferential shortening and left ventricular fractional shortening were calculated on the echocardiograms obtained. At the same time mean arterial pressure (MAP) and heart rate were measured. In group A, the single-dose test induced a significant reduction in LVEDD (74.1 +/- 7.2 to 72.1 +/- 7.1 mm; p less than 0.01), in LVESD (64.4 +/- 8.4 to 61.6 +/- 7.4 mm; p less than 0.01) and in MAP (96.5 +/- 8.3 to 85.4 +/- 7.2 mmHg; p less than 0.05). No significant changes were noted in the other parameters. Moreover, changes of parameters evaluated in group A between pts with idiopathic cardiomyopathy and pts with ischemic heart disease showed no statistical differences. Thus, acute Molsidomine therapy is effective in reducing left ventricular diameters and MAP in pts with RCF without changes of echocardiographic contractility indexes.

Adult↗

Granulosa cells stimulate in vitro the expansion of isolated mouse cumuli oophori: involvement of prostaglandin E2.

Granulosa cells (2 X 10(6) per ml) obtained from pregnant mare's serum gonadotropin (PMSG)-primed mice induce within 24 h the expansion in vitro of cocultured mouse cumuli oophori. Experiments with conditioned media showed that the expansion-promoting action of granulosa cells is due to diffusible factor(s) released into the culture medium. Studies with prostaglandin synthetase inhibitors and direct measurements of prostaglandin E2 (PGE2) released by granulosa cells in the culture medium have also been performed. The results strongly suggest that the cumulus oophorus expansion-promoting action of granulosa cells is mediated by PGE2, and support the hypothesis (Downs and Longo, 1983) that granulosa cells might play a similar role in the mechanism of cumulus expansion in vivo. The suggestion is advanced that coculture with granulosa cells might be of help to allow physiologic expansion in culture of immature cumuli obtained from preovulatory follicles in in vitro fertilization programs.

Animals↗

Effect of follicle-stimulating hormone on cyclic adenosine monophosphate level and on meiotic maturation in mouse cumulus cell-enclosed oocytes cultured in vitro.

We have reported that in vitro treatment with follicle-stimulating hormone (FSH) delays by about 3 h spontaneous meiotic resumption in cumulus cell-enclosed mouse oocytes. In the present paper we show that the temporary meiotic block is accompanied by a transient increase of cAMP concentration in the oocyte. In cumulus cell-oocyte complexes stimulated with 1 microgram/ml FSH, cAMP significantly increases within 1 h both in the whole complex (from a basal value of 1.9 +/- 0.2 to 169 +/- 13 fmol) and in the enclosed oocyte (from 0.9 +/- 0.2 to 2.4 +/- 0.2 fmol), then progressively decreases to basal values. Stimulation by FSH does not cause any cAMP increase in denuded oocytes. As the concentration of cAMP in the cells decreases, the percentage of oocytes escaping the meiotic block imposed by FSH increases. If the complexes are cultured in the presence of 1 microgram/ml FSH plus 1 mM isobutyl-1-methylxanthine (1BMX), cAMP concentration increases approximately 250-fold in the complex, and 10-fold in the enclosed oocyte; the level of cAMP in the oocyte drops very rapidly (50% degradation in less than 2 min) if the oocyte is then transferred to IBMX-free medium. The data are discussed in terms of the possible role of cAMP transfer from cumulus cells to the oocyte in the regulation of meiotic progression in mouse oocytes.

1-Methyl-3-isobutylxanthine↗

Acetylcholine receptors in monkey and rabbit oocytes.

Membrane potential responses to acetylcholine (ACh, 10(-7)-10(-3 M) were investigated in monkey and rabbit ovarian oocytes. In monkey oocytes ACh most commonly elicited a short-latency hyperpolarization concomitant with a decreased membrane input resistance (Rin). Under voltage-clamp short-latency ACh currents had an equilibrium potential of approximately -40 mV. In rabbit oocytes responses to ACh consisted of an increase in Rin or of a depolarization with an equilibrium potential of approximately -15 mV. Curare, hexamethonium, and atropine (10(-5)-10(-3) M) did not block these ACh responses. Thus, the oocyte membrane in the rabbit contains ACh receptors that cannot be classified as either muscarinic or nicotinic.

Acetylcholine↗

A comparison of protein synthetic activity in in vitro cultured denuded and follicle-enclosed oocytes.

We have studied in vitro protein synthesis in mouse denuded and follicle-enclosed oocytes by measuring 3H-leucine incorporation into TCA-precipitable material. Thirty percent more radiolabelled TCA-precipitable material was found in follicle-enclosed oocytes. Since in our experimental conditions the internal specific activity of 3H-leucine does not differ in the two systems, and no appreciable transfer of labelled protein from follicle cells to the oocyte occurs, we conclude that follicle cells have a beneficial influence on the oocyte's protein synthetic activity.

Animals↗