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Biomedical subjects

J de Champlain

Publications and source records attributed to J de Champlain.

At least 127 records · Page 7Linked to original sources
PubMed1986

Increased sympatho-adrenal tone and adrenal medulla reactivity in DOCA-salt hypertensive rats.

Sympatho-adrenal tone and reactivity were evaluated in anaesthetized normotensive and DOCA-salt hypertensive rats, by measuring arterial plasma concentrations of norepinephrine and epinephrine under basal conditions and following bilateral carotid occlusion. Baseline norepinephrine levels were significantly higher in DOCA-salt hypertensive animals than in their respective normotensive controls, whether they were studied with intact vagi or following bilateral vagotomy. The possibility of a relationship between the increased basal sympathetic fibres and the maintenance of DOCA-salt hypertension is strongly suggested by the finding of a significant correlation between mean arterial pressure (MAP) and basal circulating norepinephrine values in those animals. Furthermore, the epinephrine increase following carotid occlusion was found to be markedly potentiated in hypertensive animals (intact or vagotomized), suggesting adrenal medullary hyperreactivity to baroreflex activation in this model of hypertension. In normotensive rats the epinephrine increase induced by the carotid occlusion was greatly potentiated by the administration of an alpha 2-antagonist (yohimbine), and completely abolished by administration of an alpha 2-agonist (clonidine). In contrast, the epinephrine response to carotid occlusion, which is already enhanced in hypertensive animals, was unaffected by the same treatments. These results therefore suggest that adrenal medullary hyperreactivity observed in DOCA-salt hypertensive rats may be due to a dysfunction of an alpha 2-adrenergic mechanism modulating adrenal medullary secretion.

Adrenal Medulla↗
PubMed1986

Presynaptic inhibitory effects of sotalol, propranolol, and acebutolol on noradrenaline release upon cardiac sympathetic nerve stimulation in anesthetized dogs.

Effect of sotalol (STL) was compared with that of (+/-)-propranolol, (+)-propranolol (PPL), and acebutolol (ABL) on noradrenaline (NA) release as measured in coronary sinus (CS) blood during postganglionic stimulation (2 Hz, 30 s) of the left cardiac sympathetic nerves in anesthetized dogs. In control dogs receiving saline, increasing responses of CS-NA concentration, mean CS blood flow, and CS-NA output to repetitive stimulation were relatively stable throughout a given experimental period. Both STL (1,2.5, and 5 mg/kg, i.v.) and (+/-)-PPL (0.5 and 2.5 mg/kg, i.v.) diminished the increased CS-NA concentration by approximately 35 (P less than 0.05) to 60% (P less than 0.01) in a dose-dependent fashion. However, (+)-PPL (0.02-2.5 mg/kg, i.v.) and ABL (0.5-5 mg/kg, i.v.) did not significantly alter the increasing response of CS-NA concentration upon stimulation. STL, (+/-)-PPL, and ABL markedly inhibited the CS blood flow response to stimulation at all doses tested, while (+)-PPL did not significantly diminish the flow response even at the highest dose tested. Consequently, CS-NA output decreased significantly (p less than 0.01) in the presence of STL, (+/-)-PPL, and ABL at all doses tested but not with (+)-PPL at any dose tested. The inhibitory effect of STL and (+/-)-PPL on the increasing response of CS-NA concentration upon stimulation could be related to their beta-blocking effect, which exerts presumably on postulated presynaptic beta-adrenoceptors, as (+)-PPL did not at all diminish the response.(ABSTRACT TRUNCATED AT 250 WORDS)

Acebutolol↗
PubMed1986

Effects of acute and chronic administration of sotalol on the blood pressure and the sympathoadrenal activity of anesthetized deoxycorticosterone acetate-salt hypertensive rats.

Using plasma catecholamine (CA) levels as an index of the sympathoadrenal activity, the effects of chronic and acute beta-blockade on the blood pressure and sympathetic activity were evaluated in deoxycorticosterone acetate (DOCA) - salt hypertensive (HT) rats. The acute administration of one beta-blocker (sotalol, 5 mg/kg) to intact of vagotomized anesthetized HT animals induced a significant decrease in plasma norepinephrine (NE) concentrations and mean arterial pressure (MAP). The amplitude of the decrease of the MAP or NE levels were linearly correlated with the basal NE levels, suggesting that sotalol reduced the blood pressure and sympathetic NE release more efficiently in rats with increased sympathetic activity. Similarly, chronic infusion of sotalol (1.5 mg X day-1 X rat-1) through an osmotic pump for 12 days in DOCA-salt HT rats significantly reduced NE and epinephrine (E) plasma levels compared with those observed in untreated DOCA-salt HT rats. Moreover, the chronic treatment with sotalol significantly reduced the plasma E elevation induced by bilateral carotid occlusion (CO) in vagotomized normotensive (NT) and HT rats. It therefore appears that acute administration of sotalol to HT rats causes a significant reduction in the sympathetic activity which is associated to a decrease in MAP. Although chronic sotalol treatment causes a significant reduction in the sympathoadrenal basal activity and in the adrenal reactivity, this treatment did not prevent the development of DOCA-salt hypertension.

Adrenal Glands↗
PubMed1986

Sodium and water excretion abnormalities in congestive heart failure. Determinant factors and clinical implications.

The renal hemodynamic and neurohumoral determinants of sodium and water excretion abnormalities were studied in 66 patients with severe chronic congestive heart failure. Abnormalities were not closely related to any one variable but were the result of the convergence of a number of determinants. The most important determinants for sodium excretion were activation of the renin-angiotensin system and ventricular function; and the most important for water excretion were plasma vasopressin, plasma norepinephrine, and renal and ventricular functions. In a subgroup of patients, neurohumoral overactivation led to severe sodium and water excretion abnormalities and to increased furosemide requirements. A 17-month follow-up of all 66 patients showed a less favorable clinical course for this subgroup even when compared with hemodynamically matched patients.

Aged↗
PubMed1986

Atrial natriuretic factor: a possible link between left atrium, plasma volume, adrenergic control and renin-aldosterone in the mitral valve prolapse syndrome.

The immunoreactive atrial natriuretic factor (ANF) was measured by radioimmunoassay after extraction with SEP-PAK cartridges in 16 hyperadrenergic patients with the mitral valve prolapse (MVP) syndrome. Plasma renin activity and plasma aldosterone were concomitantly measured by radio-immunoassay. Plasma and blood volumes were obtained indirectly after measurement of red cell volume. Norepinephrine and epinephrine were measured by a radio-enzymatic microtechnique. Seven out of 16 patients (44%) had high values of immunoreactive ANF. Blood volume was uniformly decreased in MVP patients, but this was more marked in patients with high ANF. There was a significant correlation between ANF and the reduction in blood volume. Plasma norepinephrine was not significantly different in patients with high ANF and low or normal ANF. Thus, some patients with the MVP syndrome may have both an increased adrenergic state and abnormal values of ANF. The interplay between these two neuro-endocrine disorders may account for some of the symptoms of these patients. The data confirm that this syndrome may be associated with a complex 'neuro-endocrine cardiovascular process'.

Aldosterone↗
PubMed1985

Sympathetic indices during psychological and physical stimuli before and after training.

The effects of psychological and physical stimuli on cardiovascular and catecholamine changes were studied before and after physical training. These functions were investigated in eight labile hypertensive men in response to the mild psychological stimulus of playing a video game and the mild physical stimuli of sitting and standing. The results show that plasma norepinephrine concentration rises with sitting and standing but plasma epinephrine concentration increases only with the psychological stimulus. Physical training was associated with smaller increases in blood pressure during psychological and physical stimuli and with a lower heart rate at rest. On the other hand, plasma catecholamines at rest as well as in response to the different stimuli were unchanged following moderate training. These observations suggest that the adrenal medulla is selectively activated during a period of mild psychological stress, while the activity of the sympathetic fibers is preferentially increased during mild physical stimuli. Furthermore, the results of this study show that plasma catecholamine levels at rest and their increase during various stimuli are unchanged following training.

Adult↗
PubMed1985

Catecholamine release and ventricular arrhythmias during coronary occlusion and reperfusion in the dog.

In anesthetized dogs, 60-min occlusions of either the proximal (n = 14), distal (n = 8) left circumflex (LCX), or left anterior descending (LAD, n = 10) arteries were followed by reperfusion. Coronary sinus and aortic norepinephrine and epinephrine plasma concentrations were measured. The ventricular arrhythmias were ventricular premature depolarizations (VPDs), unsustained ventricular tachycardia (VT) (greater than or equal to 3 and less than 20 VPDs), sustained VT (greater than or equal to 20 VPDs), and ventricular fibrillation (VF). A gradual twofold increase (p less than 0.05) in myocardial norepinephrine overflow followed occlusion in all three groups. The increases in the amounts of norepinephrine released in the coronary sinus blood during reperfusion were significant and proportional to the size of the occluded area: proximal LCX, from 0.236 +/- 0.038 to 1.528 +/- 0.490 ng/mL of plasma (p less than 0.001); LAD, from 0.180 +/- 0.027 to 0.795 +/- 0.286 ng/mL (p less than 0.05); distal LCX, from 0.215 +/- 0.039 to 0.404 +/- 0.110 ng/mL (p less than 0.05). Aortic epinephrine concentrations were significantly increased only by LAD occlusion; at 15 min, the value had increased to 0.187 +/- 0.053 ng/mL from an initial value of 0.069 +/- 0.029 ng/mL (p less than 0.001). Two phases of ventricular arrhythmias followed both occlusion and reperfusion. Phase 1 postocclusion was characterized by VPDs and phase 2 by VPDs and unsustained VT. Sustained VT was seen only in phase 1 postreperfusion, whereas unsustained VT was seen in phase 2. VF was seen in 50, 35, and 25% of the dogs with proximal LCX, LAD, and distal LCX occlusion and reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Plasma norepinephrine, epinephrine, and dopamine beta-hydroxylase activity during exercise in man.

Many experimental studies have utilized the activity of dopamine-beta-hydroxylase (DBH) as an index of sympathetic activity, since this enzyme is not submitted to uptake mechanisms or to enzymatic metabolism as are the circulating catecholamines norepinephrine (NE) and epinephrine (E). However, large discrepancies have been found between the results of these studies. The hypothesis which is examined in this study is that these discrepancies might arise from the different intensities in the stimuli utilized. In order to examine this possibility, plasma DBH activity was measured in seven subjects at rest and in three different conditions known to increase sympathetic activity to varying degrees, i.e., during hand-grip, standing, and supra-maximal bicycle exercise. Plasma NE and E concentrations were also measured during these stimuli. The results of this study show that DBH activity increases above resting levels only during supramaximal dynamic exercise, while plasma NE and E concentrations increase during each experimental condition. Furthermore, the increases in NE and E are related to each other and are also related to heart rate when all experimental conditions are considered. On the contrary, the variations in plasma DBH (expressed as a percentage of the resting value) are not related to other sympathetic indices or to heart rate. Since NE and E vary little from subject to subject at rest and increase discretely in response to the various stimuli, these plasma catecholamine concentrations therefore appear to represent the most accurate indices of sympathetic activity.

Dopamine beta-Hydroxylase↗
PubMed1985

Increased apparent norepinephrine release rate in anesthetized DOCA-salt hypertensive rats.

Using a technique developed by Esler et al in man, we determined the NE spillover rate in plasma, the NE clearance and plasma NE concentrations in chloralose anesthetized control and DOCA-salt hypertensive rats. The study was undertaken with the infusion of tracer concentrations of high specific activity tritiated norepinephrine. Determination of the steady state of circulating NE specific activity provided an estimate of NE clearance and release rate. As previously reported endogenous plasma NE levels were greatly increased in DOCA-salt hypertensive rats. The NE clearance was only slightly decreased while the spillover rate was significantly increased in those animals. It can thus be concluded that the increased plasma NE levels observed in DOCA-salt animals cannot be attributed primarily to a diminished NE clearance rate but mainly to an increased diffusion from the sympathetic synaptic cleft to the plasma. Moreover, a significant linear correlation was found between the apparent release rate and the mean arterial levels whereas no correlation was found between the NE clearance and the blood pressure. Since the spillover rate is closely related to the NE release rate from sympathetic endings, this study supports the hypothesis that DOCA-salt hypertension is clearly associated with an enhanced basal sympathetic fibers activity.

Animals↗
PubMed1985

Free and conjugated catecholamines in plasma and erythrocytes of normotensive and labile hypertensive subjects during exercise and recovery.

Several lines of investigation suggest an abnormal sympathetic nervous activity (SNA) in hypertension. In an attempt to better evaluate SNA in a subgroup of hypertensive patients, free and sulpho-conjugated (conjugated) catecholamines (CA) [norepine-phrine (NE) and epinephrine (E)] were measured in plasma and red blood cells (RBC) of 10 labile hypertensive subjects at rest, during dynamic exercise and during recovery. Results were compared with the levels observed in seven normotensive subjects. At a given heart rate during the first 15 min of exercise, free plasma CA and diastolic blood pressure were significantly greater in labile hypertensives. Throughout the 1 h of exercise, conjugated plasma CA increased only in labile hypertensives, while free RBC NE increased only in normotensives. During recovery, free plasma CA decreased more slowly and blood pressure remained higher in labile hypertensives. These observations indicate that the mechanisms regulating sulphoconjugation may be altered in labile hypertensives and also suggest a defect in RBC CA transport mechanisms in these subjects. It is possible that these defects could contribute to the higher CA levels observed in labile hypertensives during exercise and recovery, and that they could be linked with the slower cardiovascular recovery observed in these subjects.

Adult↗
PubMed1984

Free and conjugated catecholamines in plasma and red blood cells of normotensive and hypertensive patients.

Plasma free and conjugated norepinephrine levels were found to be significantly increased in patients with labile and sustained hypertension whereas epinephrine levels were normal in these patients. While free NE and E levels increased significantly during postural change, conjugated NE and E levels were not altered by this stimulus suggesting that conjugated NE levels could be an index of chronic rather than acute changes in the sympathetic tone. In hypertensive patients, plasma free dopamine levels increased during postural change and conjugated DA levels tended to be higher suggesting a dysfunction in the dopamine metabolism. Red blood cells were also found to contain free and conjugated CA. While conjugated CA levels in red blood cells (RBC) were equal or lower than in the plasma, free CA were found in larger concentrations than in the plasma. In hypertensive patients conjugated CA levels in RBC were similar to those found in normotensive subjects but free NE and E levels were significantly higher in hypertensive patients. These studies demonstrate various abnormalities in the metabolism of CA in hypertensive patients. Each of these could contribute to the maintenance of hypertension by an alteration of the biological expression of the sympathetic tone at the cellular level of these patients.

Catecholamines↗
PubMed1983

QT interval prolongation and increased plasma catecholamine levels in patients with mitral valve prolapse.

The heart rate corrected QT interval (QTc) and plasma catecholamine (CA) and norepinephrine (NE) levels were measured in 15 symptomatic patients with idiopathic mitral valve prolapse (MVP) and in 19 control subjects. MVP patients showed longer mean QTc and were divided into two groups: group A normal QTc (greater than 440 msec) and group B prolonged QTc (less than 440 msec). In supine resting conditions CA levels were as follows: group A 0.420 +/- 0.035 ng/ml and group B 0.619 +/- 0.104 ng/ml (p less than 0.05); both were greater than control values (0.348 +/- 0.017 ng/ml, p less than 0.005). NE levels were as follows: group A 0.350 +/- 0.031 ng/ml and group B 0.376 +/- 0.052 ng/ml (NS); both were greater than control values (0.242 +/- 0.025 ng/ml, (p less than 0.05). When a standing position was assumed, CA and NE levels increased significantly in all groups but this was most marked in group B as compared to control levels (CA: 1.039 +/- 0.123 ng/ml versus 0.625 +/- 0.037 ng/ml; NE: 0.737 +/- 0.076 ng/ml versus 0.504 +/- 0.031 ng/ml) (p less than 0.001 and p less than 0.05, respectively). Thus the longest QTc was observed in patients with MVP who had the highest levels of CA and NE, in both supine and standing positions. These data may account, in part, for the occurrence of severe ventricular arrhythmias in some patients with MVP and may offer a rationale for adrenergic blockade in that subset of patients with MVP and markedly prolonged QTc.

Adrenergic beta-Antagonists↗
PubMed1983

Selective activation of the adrenal medulla during acute bilateral carotid occlusion and its modulation by alpha-adrenergic receptors in the rat.

The sympathoadrenal activity was studied during baroreflex stimulation in chloralose anesthetized rats. Circulating norepinephrine (NE) and epinephrine (E) levels were used as indices of sympathetic fiber and adrenal medulla activities, respectively, under basal conditions and during a 1-min bilateral carotid occlusion (CO). In vagotomized rats, the CO induced a significant increase in mean arterial pressure (MAP) associated with an increase in circulating E levels, while this procedure did not alter blood pressure or circulating NE or E levels in intact animals. Following vagotomy, the baroreflex stimulation activated specifically the adrenal medulla, without alteration of the sympathetic fiber activity since the NE levels were not modified by the occlusion. Moreover, in support of that hypothesis, chemical sympathectomy did not decrease the pressure response to CO while bilateral adrenalectomy almost completely abolished this response. The elevation of circulating E induced by the CO was greatly potentiated by pretreatment with Yohimbine, a selective alpha 2-antagonist, and was completely abolished by administration of Clonidine, an alpha 2-agonist, while phenoxybenzamine, which is mainly an alpha 1-antagonist, did not potentiate significantly the E response to CO. These results therefore suggest that the baroreflex activation of the adrenal medulla induced by CO may be modulated in vivo via alpha 2-adrenergic receptors that could be localized on chromaffin cells.

Adrenal Medulla↗
PubMed1982

Increased plasma catecholamine levels in patients with symptomatic mitral valve prolapse.

Total plasma catecholamine levels, plasma norepinephrine levels, heart rate, and systolic and diastolic pressures were measured in 15 symptomatic patients with mitral valve prolapse and in 19 normal subjects in supine baseline conditions and in a standing position. In the 15 symptomatic patients, total plasma catecholamine levels and plasma norepinephrine levels were significantly elevated in both positions, and heart rate was lower than in normal subjects in the supine position but returned to normal in the upright position. Thus, symptomatic patients with mitral valve prolapse demonstrate increased resting sympathetic tone. In addition, the associated supine bradycardia suggested that increased vagal tone might also be present at rest. These observations support the hypothesis of a dual autonomic dysfunction in these patients and could account for some of the clinical manifestations of the mitral valve prolapse syndrome.

Agoraphobia↗
PubMed1982

Increased plasma catecholamines in patients with Friedreich's ataxia.

We studied free plasma catecholamines in 23 patients with Friedreich's ataxia, having a mean age of 22 +/- 9.6 (SD) years. Conjugated catecholamines were also studied in 10 patients. Mean plasma norepinephrine and epinephrine were significantly higher than controls both in the supine and standing positions. In total 15 out of 23 patients (65%) had increase free and/or conjugated plasma catecholamines. The increased in plasma catecholamines was more marked in patients with severe neuromotor impairment. Among the patients with left ventricular concentric hypertrophy (wall thickness greater than 12 mm), only 3 had no demonstrable sympathetic hyperfunction. Since the high local concentrations of norepinephrine at the site of release from sympathetic nerve terminals may serve as a trigger for the hypertrophic response of the myocardial cell, it is suggested that early pharmacological intervention could prevent or limit the cardiomyopathic process or its clinical consequences.

Adolescent↗
PubMed1982

Plasma catecholamines and response to exercise in 6-hydroxydopamine-treated dogs.

Plasma catecholamine (CA; picograms per millilitre) concentrations were measured simultaneously with heart rate (HR, beats per minute) during short-duration exercise, and with plasma glucose, lactate, and free fatty acid (FFA) concentrations (millimoles per litre) during long-duration exercise, in control dogs (N-dogs) and in sympathectomized dogs (S-dogs) with 6-hydroxydopamine (50 mg X kg-1). At rest, higher plasma CA in S-dogs (690 +/- 90 vs. 320 +/- 60) was associated with higher HR (126 +/- 3 vs. 90 +/- 5), plasma glucose (6.4 +/- 0.2 vs. 5.1 +/- 0.2), lactate (2.9 +/- 0.2 vs. 1.6 +/- 0.2), and FFA concentrations (1.08 +/- 0.11 vs. 0.81 +/- 0.11). During short-duration exercise a normal HR response in S-dogs (226 +/- 9 vs. 228 +/- 8) was dependent upon larger than normal plasma CA values (4280 +/- 680 vs. 1990 +/- 360). Metabolic adjustments to long-duration exercise were impaired in S-dogs as evidenced by the higher plasma glucose and lactate concentrations (8.2 +/- 0.5 and 5.5 +/- 0.3 vs. 6.4 +/- 0.4 and 4.6 +/- 0.3) and the lower plasma FFA concentration (0.66 +/- 0.16 vs. 1.20 +/- 0.09). These occurred despite a normal plasma CA response in S-dogs (6850 +/- 1450 vs. 8740 +/- 1680). Following chemical sympathectomy the adrenal medulla can compensate to ensure an adequate heart rate response to short-duration exercise, but not to ensure adequate metabolic adjustments to prolonged exercise.

Adrenal Medulla↗