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Biomedical subjects

D Evéquoz

Publications and source records attributed to D Evéquoz.

At least 19 recordsLinked to original sources
PubMed1997

Right ventricular myxoma mimicking recurrent pulmonary embolism after primary ligament reconstruction.

Recurrent pulmonary emboli may be due to numerous causes and deep vein thrombosis are not an unusual source of pulmonary emboli following surgery. In this case report, the diagnostic approach and implications of a right ventricular myxoma as a rare source in a young patient is described. A 27-year old healthy woman presented scintigraphically proven recurrent pulmonary emboli after primary ligament reconstruction. Following a long period of diagnostic work-up for thromboembolism after surgery, a transthoracic and transoesophageal echocardiography was performed to document a right ventricular myxoma. Both transthoracic and transoesophageal echocardiography are powerful diagnostic means in a cardiac work-up and were used in this patient for the documentation of a right ventricular myxoma mimicking deep vein thromboembolism after surgery. As consequence of this case report we recommend to investigate patients with recurrent pulmonary embolism and no detectable venous thrombosis by echocardiography and a need for cardiac catheterization is restricted to patients with possible coexisting coronary artery disease. Furthermore, this case report demonstrates a myxoma in the right ventricle occurring only in 3-4% of all myxomas.

Adult↗
PubMed1996

[Sudden cardiac death: definition, mechanisms and risk factors].

Sudden cardiac death is defined as natural death due to cardiac causes, heralded by abrupt loss of consciousness within one hour after the onset of symptoms. The mechanisms are the following: 1. ventricular fibrillation, 2. ventricular tachycardia and flutter with subsequent ventricular fibrillation, 3. torsade de pointe, 4. bradyarrhythmias and asystolic arrest. White the main risk factor is the presence of coronary artery disease, any organic or functional disease of the heart can predispose for sudden cardiac death. To evaluate the risk of sudden cardiac death noninvasive (Holter, echocardiography, exercise test and signal averaged (ECG) and often invasive (electrophysiological study) tests are necessary. The therapy is based on drugs (mainly beta blockers and amiodarone), coronary revascularization, catheter ablation techniques and the implantation of a cardioverter defibrillator; the latter appears to be the most promising approach.

Adolescent↗
PubMed1996

Hypertension does not affect intracellular calcium uptake in human platelets.

The relationship between the Ca2+ transport of platelet endoplasmic reticulum and hypertension was analyzed in 17 untreated patients exhibiting various degrees of hypertension. Each patient underwent a 24-h recording of ambulatory blood pressure. Platelets from patients were permeabilized with saponin and the rate of ATP-driven thapsigargin-sensitive Ca2+ uptake determined using the fluorescent Ca2+ indicator fluo-3. No relationship between blood pressure (systolic, diastolic, day, night) and the rate of Ca2+ uptake into the sacroplasmic reticulum of platelets was found. A weak but insignificant correlation between Ca2+ uptake and the heart rate was noted. Therefore, the increase in cytosolic Ca2+ of platelets in hypertension may not be due to changes of the activity of Ca2+ uptake into the sacroplasmic reticulum.

Adult↗
PubMed1996

Effects of neuropeptide Y on intrarenal hemodynamics, plasma renin activity and urinary sodium excretion in rats.

Neuropeptide Y (NPY) is a vasoconstrictor peptide possibly involved in the regulation of renal sodium handling and renin release. This investigation was undertaken to assess in conscious normotensive rats the acute effects of a non-pressor dose of NPY on renal plasma flow, glomerular filtration rate, sodium excretion and plasma renin activity. Experiments were also performed during concomitant beta-adrenoceptor stimulation with isoproterenol. NPY per se had no effect on the studied parameters. Renal plasma flow was increased by isoproterenol and was significantly higher when the beta-adrenoceptor stimulant was infused alone (13.4 +/- 2.1 ml/min, p < 0.05, mean +/- SEM) that when administered together with NPY (7.2 +/- 2.0 ml/min). This was also true for glomerular filtration rate (3.3 +/- 0.3 vs. 1.8 +/- 0.3 ml/min, p < 0.01) and plasma renin activity (6.3 +/- 1.7 vs. 2.1 +/- 0.4 ng Ang I/ml/h, p < 0.05). Our data however do not allow to deduce whether the inhibitory effect of NPY on isoproterenol-induced renin release is mediated by changes in intrarenal hemodynamics or a direct effect on juxtaglomerular cells.

Adrenergic beta-Agonists↗
PubMed1995

Beta-adrenoceptor stimulation increases neuropeptide Y release from sympathetic nerves in intact rats.

This study was undertaken to assess in conscious normotensive rats the effects of beta-adrenoceptor stimulation on plasma neuropeptide Y (NPY) levels. Wistar rats were subjected to adrenal demedullation on the right side and were either adrenalectomized or sham-operated on the left side. Eleven days later, the conscious rats were infused i.v. for 30 min with either isoproterenol (10 ng/min) or its vehicle. Plasma NPY levels were significantly lower (23.8 +/- 2.6 pM, means +/- S.E.M., n = 12, P < 0.01) in vehicle-treated medullectomized rats than in corresponding sham-operated controls (36.7 +/- 4.1 pM, n = 12). The medullectomized rats infused with isoproterenol showed plasma NPY levels (36.7 +/- 3.3 pM, n = 11) comparable to those of sham-operated rats having received the vehicle. These data therefore demonstrate that plasma NPY levels are lower in rats without adrenal medulla and that in these animals isoproterenol increases NPY release, most likely by activating pre-synaptic beta-adrenoceptors.

Adrenal Medulla↗
PubMed1995

[Beta blockers in antihypertensive treatment].

Beta blockers are drugs of first choice for the treatment of essential hypertension today and may be combined with other antihypertensive drugs or diuretics. Use of highly selective beta-1 receptor-blocking agents without intrinsic sympathomimetic activity is particularly recommended for hypertensive patients after transmural myocardial infarction who suffer from exercise-dependent myocardial ischemia. Highly selective beta-1 receptor-blocking agents have only little influence on the lipid metabolism; however, if prescribed in diabetic patients treated with insulin, in patients with cardiac failure or in asthmatic patients, close supervision is mandatory.

Adrenergic beta-Antagonists↗
PubMed1994

Differential vascular effects of neuropeptide Y(NPY) selective receptor agonists.

Neuropeptide Y (NPY) increases blood pressure either directly or indirectly by potentiating the effect of various vasoconstrictors. Only one (the Y1-receptor) of two subtypes of receptors (Y1 and Y2) is thought to mediate the vascular smooth muscle contraction. To test this hypothesis we challenged isolated rat mesenteric arteries that had a functional endothelium with (1-36) NPY and with specific Y1-receptor ([Leu31, Pro34] NPY) and Y2-receptor ([Ahx5-24, gamma-Glu2-epsilon-Lys30] NPY) agonists. The Y1-receptor agonist elicited a contractile response similar to that of NPY, whereas the Y2-receptor agonist had no effect on wall tension. We also found that the presence of a functional endothelium has no influence on the contractile response to NPY. From these data we conclude that the direct contractile effect of NPY in the mesenteric artery is mediated by stimulation of Y1-receptors and is not endothelium-dependent.

Acetylcholine↗