Search PubMed⌕ Search

Biomedical subjects

R Nadeau

Publications and source records attributed to R Nadeau.

At least 109 records · Page 6Linked to original sources
PubMed1990

Alpha 2-adrenoceptor modulation of catecholamine and neuropeptide Y responses during haemorrhagic hypotension in anaesthetized dogs.

The acute effects of oxymetazoline, an alpha 2-adrenoceptor agonist, and idazoxan, an alpha 2-adrenoceptor antagonist, on the release of neuropeptide Y were evaluated during haemorrhage in pentobarbital-anaesthetized dogs. Plasma concentrations of neuropeptide Y and catecholamines (adrenaline, noradrenaline, and dopamine) were determined in samples simultaneously collected from aorta, portal vein, and adrenal veins. In control dogs, adrenal catecholamine output, aortic concentrations neuropeptide Y and catecholamines markedly increased during the hypotension period. However, adrenal neuropeptide Y output decreased significantly during this period. Portal venous noradrenaline and neuropeptide Y concentrations increased significantly. In dogs treated with idazoxan, catecholamine output from the adrenals increased to an extent similar to that observed in control dogs. However, the increase in noradrenaline and neuropeptide Y in aortic or portal venous blood during haemorrhage was significantly potentiated in the presence of idazoxan. Administration of oxymetazoline abolished this increase, but did not alter adrenal catecholamine or neuropeptide Y output. The present study demonstrates that neuropeptide Y is co-released with noradrenaline from sympathetic nerve fibers during haemorrhage. Since the release of neuropeptide Y appeared to follow a similar time course to that of noradrenaline release, the present observations suggest that haemorrhagic hypotension enhances both neuropeptide Y and noradrenaline release presumably through a common releasing mechanism. These results also indicate that, in peripheral sympathetic nerves but not in the adrenal gland, neuropeptide Y release is also modulated presynaptically by the inhibitory alpha 2-adrenoceptors in conjunction with the noradrenaline release.

Adrenergic alpha-Antagonists↗
PubMed1990

Comparative accuracy of the vectorcardiogram and electrocardiogram in the localization of the accessory pathway in patients with Wolff-Parkinson-White syndrome: validation of a new vectorcardiographic algorithm by intraoperative epicardial mapping and electrophysiologic studies.

The scalar electrocardiograms (ECGs) and vectorcardiograms (VCGs) of 41 patients with Wolff-Parkinson-White (WPW) syndrome were used to compare the accuracy of these techniques in the identification of the site of preexcitation. The location of the accessory pathway (AP) was determined by endocavitary electrophysiologic studies in all patients and the location was confirmed during intraoperative epicardial mapping in 28 of them. The ECGs were classified according to Gallagher's criteria and with Milstein's algorithm, whereas the VCGs were classified according to a new two-step algorithm. The presence of multiple accessory pathways and coexisting myocardial infarctions were major limitations in both the VCG and ECG classification procedures. In patients with a single accessory pathway, three AP localizations (right free ventricular wall, posterior, or left free ventricular wall) were identified with the first step of the VCG algorithm, with an overall sensitivity (96.5%), specificity (90.7%), and positive predictive values (80%) that were greater than those obtained with the ECG Milstein algorithm (77.1%, 91.5%, and 75%, respectively). The second step of the VCG algorithm made it possible to identify an AP location in one of the following sites: anterior right, lateral right, posterior right, posterior left, lateral left, or anterior left ventricle. The overall sensitivity, specificity, and positive predictive values were greater for the second step of the VCG algorithm than for the ECG criteria proposed by Gallagher (43.6% versus 39.3%, 92.1% versus 87.4%, and 51.5% versus 33.3%, respectively). It was concluded that the VCG seems to be more specific and sensitive than the ECG in the identification of the preexcitation site and should be given preference in the initial evaluation of the WPW syndrome.

Adult↗
PubMed1990

Occlusion time dependency of regional noradrenaline release and cardiac arrhythmias during reperfusion of acutely ischaemic heart in the dog in vivo.

STUDY OBJECTIVE: The aim was to study the occlusion time dependency of reperfusion induced increases in regional cardiac noradrenaline release from the ischaemic area in relation to the incidence of ventricular arrhythmias. DESIGN: The left anterior descending coronary artery was ligated for 15, 30 and 60 min in three separate groups of dogs (n = 10 per group). Each occlusion period was followed by a 30 min reperfusion period. The coronary sinus and the epicardial vein running in parallel with the left anterior descending coronary artery were cannulated for measurement of noradrenaline and lactate. EXPERIMENTAL MATERIAL: 30 adult mongrel dogs, 22.5(SEM 1.1) kg, were used for the study. The animals were anaesthetised with sodium pentobarbitone. MEASUREMENTS AND MAIN RESULTS: During occlusion, epicardial venous blood noradrenaline concentrations remained unchanged up to 30 min, but increased from 0.133(0.027) ng.ml-1 to 0.289(0.069) ng.ml-1 after 60 min of occlusion (p less than 0.05). However, epicardial venous blood lactate concentrations increased immediately upon occlusion, and remained elevated (p less than 0.05) during the whole period of occlusion in all groups. Neither noradrenaline nor lactate concentrations in coronary sinus blood increased during occlusion. During reperfusion, nine dogs showed early ventricular fibrillation. The highest incidence of fibrillation (n = 5/10) was found in the 15 min occlusion group, but the difference was not significant between groups. Epicardial venous blood noradrenaline concentrations increased to 0.371(0.076) ng.ml-1, 0.470(0.178) ng.ml-1, and 1.824(0.713) ng.ml-1 upon reperfusion following 15, 30 and 60 min occlusion, respectively (each p less than 0.05). Maximum increases in epicardial venous blood noradrenaline concentrations during reperfusion were correlated with duration of preceding occlusion (r = 0.60, n = 21, p less than 0.01). Maximum increases in mean arrhythmic ratios observed during the first 10 min of reperfusion were proportionally related to mean epicardial venous blood noradrenaline concentrations. The increases in epicardial venous blood noradrenaline concentrations and the incidence of ventricular arrhythmias in the 60 min occlusion group were greater (p less than 0.05) than in the other two groups. CONCLUSIONS: This study shows that noradrenaline is released progressively from the ischaemic area during occlusion for 60 min. The amount of noradrenaline washed out upon reperfusion and the incidence of reperfusion ventricular arrhythmias both appear to be dependent upon duration of preceding occlusion. The results suggest that cardiac noradrenaline released locally from the ischaemic region may contribute to the genesis of reperfusion ventricular arrhythmias, but not to that of reperfusion ventricular fibrillation.

Animals↗
PubMed1990

Absence of prejunctional sympathetic effect of amiodarone in hearts of open-chest anesthetized dogs.

The effect of amiodarone (30 mg/kg p.o. each day for 3 weeks) on noradrenaline (NA) overflow into coronary sinus (CS) blood during left stellate stimulation (15 V, 2-ms square waves, 30 s duration at 1, 2, 4, and 8 Hz in random order) was investigated in an open-chest dog preparation. CS blood samples were taken before and during the stimulation period for plasma NA and hematocrit determinations. CS blood flow was monitored (extracorporal circulation with an electromagnetic flow meter) and used for NA output computation. The right atrium was paced throughout the experimental period. However, because AV block occurred at a high pacing rate in some amiodarone-treated dogs, pacing rate was lower in that group than in control dogs (132 +/- 13 vs. 161 +/- 10 min-1, ns). Mean arterial pressure was also lower in the treated group (95 +/- 9 vs. 110 +/- 13 mmHg, but increased in every dog upon stimulation (p less than 0.05). Basal left ventricular dP/dtmax was comparable in the two groups of dogs and increased in a similar fashion upon stimulation (p less than 0.05). The increase in plasma NA concentration upon stimulation was comparable between the control and the amiodarone-treated group (0.38 +/- 0.08 vs 0.40 +/- 0.12 ng/mL at 1 Hz and 12.7 +/- 3.1 vs 11.3 +/- 2.3 ng/mL at 8 Hz, ns). The increase in NA output was also comparable (7.0 +/- 1.6 vs. 10.7 +/- 5.4 ng/min at 1 Hz and 356 +/- 124 vs. 334 +/- 102 ng/min at 8 Hz, ns). Amiodarone did not alter the myocardial NA content. We conclude that amiodarone, administered orally for 3 weeks, does not interfere with neural NA release, or with the positive inotropic response, following sympathetic nerve stimulation in dogs.

Amiodarone↗
PubMed1990

Corelease of neuropeptide Y like immunoreactivity with catecholamines from the adrenal gland during splanchnic nerve stimulation in anesthetized dogs.

The release of neuropeptide Y like immunoreactivity (NPY-li) from the adrenal gland was studied in relation to the secretion of catecholamines (CA: NE, norepinephrine; E, epinephrine) during the left splanchnic nerve stimulation in thiopental-chloralose anesthetized dogs (n = 16). Plasma concentrations of NE, E, and NPY-li were determined in the left adrenal venous and aortic blood. Adrenal outputs of NPY-li, NE, and E were 2.4 +/- 0.4, 1.4 +/- 0.2, and 7.3 +/- 1.7 ng/min, under basal conditions, respectively. These values increased significantly (p less than 0.05; n = 8) in response to a continuous stepwise stimulation at frequencies of 1, 3, and 10 Hz given at 3-min intervals during 9 min, reaching a maximum output of 4.6 +/- 0.9 (NPY-li), 240.2 +/- 50.2 (NE), and 1412.5 +/- 309.7 ng/min (E) at a frequency of 10 Hz. Burst electrical stimulation at 40 Hz for 1 s at 10-s intervals for a period of 10 min produced similar increases (p less than 0.05) in the release of NPY-li (4.8 +/- 1.0 ng/min, n = 8), NE (283.5 +/- 144.3 ng/min, n = 8), and E (1133.5 +/- 430.6 ng/min, n = 8). Adrenal NPY-li output was significantly correlated with adrenal NE output (r = 0.606; n = 24; p less than 0.05) and adrenal E output (r = 0.640; n = 24; p less than 0.05) in dogs receiving the burst stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1990

Plasma catecholamines in the aorta and the phrenicoabdominal vein in exercising dogs.

Plasma epinephrine and norepinephrine concentrations were measured in the aorta and phrenicoabdominal vein in five dogs at rest and during short-duration mild- and moderate-intensity exercise and during prolonged mild-intensity exercise. Plasma epinephrine and norepinephrine concentrations increased with exercise in both the aorta and the phrenicoabdominal vein. Plasma epinephrine concentration was much higher in the phrenicoabdominal vein than in the aorta (24-43 times). Plasma epinephrine concentrations in the aorta and phrenicoabdominal vein were significantly correlated (r = 0.88). This confirms that peripheral epinephrine concentration is a reliable index of the activity of the adrenal medulla during exercise. The epinephrine-to-norepinephrine ratio in the phrenicoabdominal vein was stable (4:1) throughout the experimental protocol, suggesting that the proportion of the two amines released by the adrenal medulla did not vary through this range of adrenal activity in dogs.

Adrenal Medulla↗
PubMed1990

Spatial domain analysis of late ventricular potentials. Intraoperative and thoracic correlations.

For investigation of late potentials seen on the signal-averaged electrocardiogram, intracardiac and thoracic distributions of terminal activity were analyzed in 16 patients undergoing cryosurgery for ventricular tachycardia after remote myocardial infarction. The body surface potentials measured with 63 time-averaged unipolar leads were compared with epicardial and endocardial potential maps in six patients without and 10 patients with bundle-branch block. Intracardiac post-QRS activity, defined as extending beyond the thoracic QRS offset, was found in five of six patients without bundle-branch block (83%) and in five of 10 patients with bundle-branch block (50%), corresponding to 4 +/- 5% of the total number of electrograms in each patient. Fragmentation, double deflections, and single deflections were observed in 27%, 34%, and 39%, respectively, of these post-QRS electrograms. Post-QRS activation patterns that were stable from beat to beat showed slow propagation around or within areas of conduction block. Post-QRS activity was most often observed on both epicardial and endocardial surfaces (five of 10 patients). In the six patients without post-QRS activity, an area of late activity displaying low-amplitude deflections that were masked by the terminal activation of the normal myocardium was identified. Isopotential maps of the high-pass-filtered (55-Hz) thoracic and intracardiac signals demonstrated a close spatial correlation between the location, amplitude, and orientation of the potential extrema observed over the thoracic, epicardial, or endocardial surfaces during post-QRS activity. The thoracic patterns were generally dipolar with close extrema for anteroseptal or apical sites of post-QRS activity and more distant extrema for other sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Efficacy of oral sotalol in suppression of premature ventricular complexes and analysis of its beta-adrenergic blocking activity.

The efficacy of oral DL-sotalol in suppressing premature ventricular complexes was assessed by Holter recordings in 28 patients during short term (two weeks) and long term (two years) trials, and its beta-adrenergic blocking effects were evaluated by heart rate response to the Bruce treadmill stress test and plasma catecholamine increases upon active standing. Sotalol produced a significant decrease (more than 85%) in the number of premature ventricular complexes, during both short term (54%) of patients) and long term (39% of patients) trials. The doses employed in this study (320 mg/day) produced mild to moderate degrees of beta-adrenergic blockade as suggested by: a 20% reduction in the mean heart rate on 48 h Holter monitoring (P less than 0.0005); a 15 to 30% reduction in tachycardia induced by strenuous exercise; and a 12% reduction in standing-induced tachycardia. Under long term sotalol therapy the increase in plasma noradrenaline concentrations in response to active standing was not modified, but the increase in plasma adrenaline concentrations was greater than under baseline conditions (P less than 0.025). Both systolic and diastolic blood pressures significantly increased during long term sotalol administration (P less than 0.005 and P less than 0.025, respectively). However, blood pressure remained within the normotensive range during sotalol therapy. It was concluded that sotalol provides, at effective antiarrhythmic doses, a satisfactory level of beta-adrenergic blockade which during standing was associated with significant changes in adrenaline plasma increments.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Noninvasive evaluation of supraventricular tachycardias.

In this article we discuss the role of noninvasive methods in evaluation of supraventricular tachycardias. The limitation of Holter monitoring and exercise testing is discussed. A significant portion of the article is devoted to the role of esophageal recording, body surface potential mapping, and phase image analysis, areas that are often underutilized but that have potential in the diagnosis of supraventricular tachycardias.

Atrial Flutter↗
PubMed1990

Predictors of survival and sudden death in patients with stable severe congestive heart failure due to ischemic and nonischemic causes: a prospective long term study of 200 patients.

This prospective study of 200 stable outpatients with New York Hospital Association (NYHA) class III congestive heart failure on maximal medical therapy was done to determine which factors affect survival, to record the incidence of sudden death, and to identify prognostic features which characterize patients at high risk of sudden death. Congestive heart failure was due to coronary artery disease in 151 patients (76%). After an average follow-up of 40 months, 96 patients (48%) had died: 30 (15%) suddenly, 41 (22%) of low output, and 25 (13%) of other causes. Of the 30 patients dying suddenly 12 had autopsies, and acute myocardial infarction was found in nine. Of the 41 patients dying of low output 15 had autopsies, and recent myocardial infarction was found in five. Nine of the 25 patients dying of other causes died of acute myocardial infarction. Multivariate stepwise analysis revealed that severity of ventricular arrhythmias (modified Lown classification), exercise tolerance and left ventricular ejection fraction were the most important determinants of survival. In patients with coronary artery disease, complex ventricular arrhythmias detected by ambulatory Holter monitoring were frequent in all groups and were not clinically useful in predicting which of these patients were at a higher risk of dying suddenly. In contrast, patients without coronary artery disease who died suddenly had a higher incidence of nonsustained ventricular tachycardia and a tendency towards more frequent ventricular arrhythmias in general. The authors conclude that in ambulatory patients with stable NYHA class III heart failure, the severity of ventricular arrhythmias is a predictor of survival.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Surgical treatment of the Wolff-Parkinson-White syndrome. Endocardial versus epicardial approach.

From 1983 to 1988, 51 patients with the Wolff-Parkinson-White syndrome underwent surgical ablation of an accessory conduction pathway, 25 by the classic endocardial approach and 26 by the epicardial technique supplemented by cryosurgery. In the endocardial and epicardial groups, the accessory pathway was in the left free wall in 22 and 18 patients, respectively, posterior septal in two and seven, and in the right free wall in one patient in each group. There was no early or late death in the endocardial group, and postoperative complications developed in five patients (20%). Pathway ablation was completely successful in 22 patients (88%), preexcitation recurred in two patients (8%), and one had recurrence of supraventricular tachycardia (4%). One of the failures occurred with a posterior septal pathway (50%), and the two others with a left free-wall pathway (9%). With the epicardial technique, there were no early deaths and one late death caused by atherosclerotic coronary artery disease. Five patients (19%) had postoperative complications. The pathway was ablated successfully in 22 patients (85%), preexcitation recurred in three patients (12%), and supraventricular tachycardia remained inducible in another patient despite disappearance of the delta wave. Three of those failures occurred with anterior left free-wall pathways (16%), but only one patient had recurrent supraventricular tachycardia (4%) requiring immediate reoperation, which was successful. In conclusion, although epicardial or endocardial approaches produced similar results, our observations suggest that left free-wall accessory pathways located high anteriorly may be ablated in a more reproducible way with the endocardial technique, whereas the epicardial approach appears easier for posterior septal pathways. We therefore believe that any surgeon beginning such surgery should be aware of the possibilities and limitations of each of the two techniques.

Adolescent↗
PubMed1990

[The origin of late potentials in patients with ventricular tachycardia after myocardial infarction].

In order to study the origin of late potentials, their distribution was analyzed in 16 patients who had undergone surgery for arrhythmia due to ventricular tachycardia following myocardial infarction. The potentials were measured in sinus rhythm using 63 unipolar leads placed on the chest before the operation, then on the epicardium and endocardium during the operation. Epicardial and/or endocardial activity extending beyond the QRS complex measured from unfiltered chest signals and characterized by slowed propagation at the edge or inside of necrotic regions, stable from one beat to the next, and showing simple (39 per cent), double (34 per cent) or fragmented (27 per cent) deflections on the electrocardiograms were observed in 5/6 patients without bundle-branch block and in 5/10 patients with block. Similar activity but which did not extend after the QRS was detected in the 6 other patients. For signals filtered at 55 Hz, a close correlation between the distribution of chest, epicardial and endocardial potentials was observed, thus allowing approximate location of the origin of late potentials from the chest. Anterior or apical sites corresponded to close extrema in the precordial region, whereas the other sites were associated with more distant extrema. An analysis of potential distribution thus gives a better understanding of the electrogenesis of late potentials as well as their detection on the chest.

Aged↗
PubMed1989

Effect of sotalol against reperfusion-induced arrhythmias in Sprague-Dawley and Wistar rats.

The effect of (+/-)-sotalol (a beta-blocker with class III antiarrhythmic activity) against reperfusion-induced arrhythmias was studied in artificially ventilated, open-chest, Sprague-Dawley and Wistar rats. Coronary artery occlusion was produced for 5 min and reperfusion allowed for 10 min. A somewhat different arrhythmic profile was observed between saline-treated rats of the 2 strains studied, with more Sprague-Dawley rats experiencing an irreversible ventricular fibrillation (VF) upon reperfusion, compared to Wistar rats, in whom a combination of reversible ventricular tachycardia (VT) and VF was more frequently observed. No difference in action potential characteristics and ventricular effective refractory period determined in vitro, nor in myocardial noradrenaline content, was found between the 2 strains of rats. (+/-)-Sotalol (5 and 10 mg/kg, IV) showed marked beta-blocking activity and reduced the mean duration of VT-VF in both strains studied. It also produced similar increases in action potential duration and refractory period in vitro in these 2 strains. In a different series of experiments, the antiarrhythmic action of the racemic form was compared to that of (+)-sotalol using Wistar rats. (+)-Sotalol had much less beta-blocking activity, and was found to be similarly effective against reperfusion-induced VT-VF. It is concluded that the antiarrhythmic effect of sotalol against reperfusion-induced arrhythmias may not be related to beta-adrenergic blockade but probably to class III type activity. Despite differences in the profile of reperfusion-induced arrhythmias between Sprague-Dawley and Wistar rats, both strains were sensitive to the antiarrhythmic action of (+/-)-sotalol.

Animals↗
PubMed1989

Opposite effects of lidocaine and diltiazem on electrophysiologic alterations in acutely ischemic porcine myocardium.

To investigate the actions of lidocaine and diltiazem on the ischemic alterations associated with the onset of acute ischemic arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine (2.4-3.8 micrograms/mL of plasma) or diltiazem (390-510 ng/mL) in open-chest anesthetized pigs. Sixty-one unipolar electrograms were continuously recorded in the ischemic zone. Isochronal maps and isopotential maps were determined by computer analysis. The magnitude of beat-to-beat alternation of unipolar waveforms was described by the difference between the time integrals subtended by electrograms of consecutive beats. Activation times were prolonged by ischemia and the ST segment became elevated. Delay and ST elevation developed at a faster rate in the presence of lidocaine than under control conditions, but were reduced by diltiazem. ST-T alternation was not significantly different between control and lidocaine occlusions, but the incidence of negative T waves and that of ventricular tachycardia degenerating to fibrillation were higher in lidocaine occlusions than in control occlusions. In contrast, unipolar waveform alternation and negative T waves were virtually abolished by diltiazem, even at fast pacing rates (180-210 beats/min) at which diltiazem did not reduce ST elevation. Ventricular arrhythmias also were abolished by diltiazem. Thus, lidocaine and diltiazem produce opposite effects on the ischemic alterations most closely associated with the initiating mechanism of tachycardia. This could be related to differences between these drugs with regard to their actions on transmembrane currents during repolarization.

Animals↗
PubMed1989

Plasma atriopeptin during exercise in dogs under beta-blockade.

The purpose of this study was to describe plasma atriopeptin concentrations at rest and in response to moderate treadmill exercise (10 min, 4 km/h, 26% slope) performed with or without nonspecific beta-adrenergic blockade (1 mg/kg iv propranolol) in 10 mongrel dogs [19 +/- 2 (SE) kg]. A small (20%) but significant (P less than 0.05) increase in plasma atriopeptin concentration was observed from rest (43 +/- 5 pg/ml) to exercise (52 +/- 6 pg/ml) without beta-blockade. Propranolol significantly reduced heart rate at rest (89 +/- 7 vs. 104 +/- 7 beats/min) and during exercise (96 +/- 10 vs. 176 +/- 11 beats/min), and this was associated with a larger increase in plasma atriopeptin concentration during exercise (rest 46 +/- 6 pg/ml; exercise 171 +/- 22 pg/ml). Exercise under beta-blockade is associated with an increased preload of the heart. These results further support the hypothesis that atriopeptin release during exercise is under the control of atrial stretch. The higher plasma atriopeptin concentration observed during exercise under beta-blockade may contribute to the reduction of the response of plasma renin activity (1.0 +/- 0.1 vs. 3.0 +/- 0.6 ng.ml-1.h-1) and aldosterone concentration (87 +/- 36 vs. 138 +/- 25 pg/ml). Vasopressin concentration was lower at rest and during exercise under propranolol (3.5 +/- 1.3 vs. 4.9 +/- 0.9 and 6.1 +/- 2.2 vs. 9.9 +/- 1.5 pg/ml, respectively), which might reflect a dissociation between activity of the renin-angiotensin system and vasopressin release.

Adrenergic beta-Antagonists↗