Narcolepsy and idiopthic hypersomnia: biogenic amines and related compounds in CSF.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J de Champlain.
Explore the source record for details and available documents.
Plasma catecholamines, heart rate, and cardiac sympathetic activity in exercising dogs. Med. Sci. Sports Exercise, Vol. 14, No. 4, pp. 291-285, 1982. The purposes of the study were, 1) to assess the respective roles of locally released norepinephrine in the sinus node and of plasma catecholamines in the control of heart rate during exercise and 2) to verify whether the heart is a source of plasma catecholamines during exercise. Plasma catecholamines (radioenzymatic assay) and heart rate were measured in the last minute of a 5-min exercise period (3.2 km . h-1, 39% slope) in six normal dogs, in six dogs treated with 5 mg . kg-1 sotalol, and in six dogs sympathectomized with 50 mg . kg-1 6-hydroxydopamine. Compared to the exercise heart rate values of the normal dogs (228 +/- 8 beats . min-1) and the sympathectomized dogs (226 +/- 9 beats . min-1), the sotalol-treated dogs had significantly lower rates (148 +/- 6 beats . min-1). However, plasma catecholamine response was higher in the sotalol-treated dogs (7380 +/- 1350 pg . ml-1) and in the sympathectomized dogs (4280 +/- 680 pg . ml-1) than in the normal dogs (1890 +/- 360 pg . ml-1). Since the action of plasma catecholamines on the sinus node is potentiated by denervation hypersensitivity, it is suggested that in exercising normal dogs, heart rate control could be ensured by locally released norepinephrine rather than by plasma catecholamines. Plasma catecholamines were assessed in six normal dogs at rest and at various exercise levels (HR = 90-200 beats . min-1) and in blood sampled simultaneously in the aorta and the coronary sinus. Plasma catecholamines in the coronary sinus and aorta were similar at rest (490 +/- 90 vs 580 +/- 80 pg . ml-1, respectively) and at the low-intensity exercise (710 +/- 140 vs 880 +/- 120 pg . ml-1, respectively). For moderate and severe work loads, plasma catecholamine concentrations in the coronary sinus (960 +/- 160 and 1570 +/- 340 pg . ml-1, respectively) were lower than in the aorta (1380 +/- 260 and 2950 +/- 100 pg . ml-1, respectively). These results suggest that in exercising dogs the heart is not a source of plasma catecholamines.
In open-chest pentothal-chloralose anesthetized dogs, plasma catecholamine and cyclic AMP levels were evaluated in the aortic and coronary sinus blood, during stimulations of the left ansa subclavia (1, 2, and 4 Hz). Basal aortic and coronary sinus catecholamine levels were respectively 0.373 +/- 0.090 and 0.259 +/- 0.048 ng/mL and cyclic AMP levels averaged 21.4 +/- 1.4 and 20.9 +/- 1.6 pmol/mL. Statistically significant increases in cyclic AMP levels were induced by sympathetic stimulations at 1 Hz (2.0 +/- 0.6 pmol/mL, 2 Hz (2.5 +/- 1.2 pmol/mL) and 4 Hz (6.5 +/- 1.5 pmol/mL), concomitantly with elevations of coronary sinus catecholamine levels. Sotalol (5 mg/kg) abolished the increases in coronary sinus cyclic AMP levels induced in coronary sinus cyclic AMP output averaged 282 +/- 30 pmol/min (1 Hz), 662 +/- 160 pmol/min (2 Hz), and 1679 +/- 242 pmol/min (4 Hz). Sympathetically induced cyclic AMP output (4Hz) was blunted by sotalol (-81 +/- 14 pmol/min). Aortic cyclic AMP levels were not significantly influenced by stellate stimulation. Intense correlations were found between increased in coronary sinus plasma catecholamines and cyclic AMP concentration levels (r = 0.81, slope - 1.45, ordinate = -1.42, n = 15) as well as between delta cyclic AMP output versus delta catecholamine output values in the coronary sinus (r = 0.93. slope output levels. Intracoronary infusion of phenylephrine (10 micrograms/min) or nitroprusside (200 micrograms/min) had no influence on cyclic AMP plasma levels whereas aortic and coronary sinus levels were respectively increased 5.5 +/- 1.9 and 7.3 +/- 1.4 pmol/mL during the administration of isoproterenol (5 micrograms/min). These data suggested that plasma cyclic AMP constitutes a sensitive index of cardiac beta-adrenergic activity elicited by the release of endogenous catecholamine during stellate stimulations.
The plasma norepinephrine concentration (NE, ng . ml-1) in the pulmonary artery of dogs increased above resting values (0.22 +/- 0.04) for moderate (0.53 +/- 0.06) and severe exercise (1.45 +/- 0.23) and during prolonged exercise of moderate intensity (2.06 +/- 0.14). The plasma epinephrine concentration (E) increased above resting values (0.14 +/- 0.04) for severe exercise only (0.76 +/- 0.10) or when moderate exercise was prolonged (1.81 +/- 0.24). The E response, which appeared greater than that found in humans, is probably related to the species difference in the vasomotor response to exercise between humans and dogs, the latter not being subjected to compensatory vasoconstriction in nonworking areas. The activity of the adrenal medulla is confirmed by the plasma catecholamine (CA) gradient between proximal and distal posterior vena cava at rest (0.20 +/- 0.09) and during short- (0.35 +/- 0.08) and long-duration exercise (1.37 +/- 0.23). On the contrary, the heart is not a source of plasma CA in dogs: coronary sinus CA did not exceed aortic CA at rest and for moderate exercise and was lower than aortic CA for severe exercise (4.80 +/- 0.25 vs. 6.55 +/- 0.76 ng . ml-1).. The sources of plasma NE remain unclear in exercising dogs. Significant amounts of NE may be released by the adrenal medulla.
Plasma norepinephrine (NE) concentration was measured by means of a sensitive radioenzymatic assay in blood collected from an antecubital vein in 10 healthy male subjects (37 +/- 2 yr, mean +/- SE). The subjects were evaluated at rest and during exercise before and after a 20-wk training program on bicycle ergometer (three 30-min sessions per week at 80% of maximal heart rate). Following the training program, maximal oxygen uptake increased significantly from 33 +/- 2 to 42 +/- 1 ml . kg-1 . min-1. Resting plasma NE remained unchanged after training (167 +/- 38 before and 185 +/- 29 pg . ml-1 after training). For a given absolute work load (735 +/- 51 kg . m. min-1) the sympathetic nervous response was lower after training as reflected by the decrease in NE concentration (1,371 +/- 286 vs. 687 +/- 64 pg . ml-1). At the same relative work load (heart rate: 158 +/- 5 before and 157 +/- 5 beats . min-1 after training) plasma NE concentration was unchanged after training (1,371 +/- 286 vs. 1,729 +/0 371 pg . ml-1). Results from the present study show that the sympathetic nervous activity is closely linked to the exercise demands and confirm earlier suggestions that it remains constant in relation to the relative work load.
Explore the source record for details and available documents.
1. A reduced noradrenaline turnover rate has been previously demonstrated in the brain stem of deoxycorticosterone acetate (DOCA)-sodium hypertensive rats. In the present study, the turnover rate was measured in smaller brain regions and the effect of sodium depletion was studied on the turnover rate of these regions. 2. Catecholamine turnover rate was significantly reduced only in the pons, was slightly but not significantly reduced in the thoracic spinal cord and was normal in the upper and lower medulla oblongata, in the mesencephalon, in the hypothalamus and in the telencephalon. 3. The administration of a sodium-free diet for 3 weeks lowered significantly the blood pressure and concomitantly accelerated the turnover rate in the pons area of DOCA hypertensive rats. 4. It is concluded that pontine catecholaminergic fibres, sensitive to sodium balance, might be involved in the maintenance of DOCA-sodium hypertension in the rat.
Explore the source record for details and available documents.
Several experimental evidences have shown that, under standarized conditions, circulating catecholamines (CA) or norepinephrine (NE) levels can be used as a valid index of the sympatho-adrenal activity in animal and man. This approach in the study of hypertensive patients has permitted to uncover that about 50% of patients with labile hypertension and about 30% of patients with stable hypertension had elevated CA levels at rest for 20 minutes in the supine position. The increased CA levels were mainly due to a rise in NE in stable hypertension and to a rise in epinephrine (E) in labile hypertension. On the basis of circulating CA levels, the hypertensive patients were divided into hyperadrenergic (CA levels above normal range) and normoadrenergic (CA levels within the normal range) subgroups. The hyperadrenergic labile or stable hypertensive subgroups were found to be also characterized by an enhanced CA or NE increase in response to change in position from supine to standing, by a faster heart rate and by an increased myocardial contractility, while these parameters were normal in the normoadrenergic subgroups. These findings support therefore the existence of an increased sympathetic tone and reactivity in association with hyperkinetic cardiac functions in an important population of hypertensive patients. In response to two weeks treatment with beta-blockers (either propranolol or metoprolol) hyperadrenergic stable hypertensive patients were found to be more responsive to this therapy than normoadrenergic patients although both groups had the same initial blood pressure. Moreover, this treatment lowered basal NE or CA levels and restored the enhanced CA or NE response to change in position toward normal in hyperadrenergic patients while it did not modify significantly circulating supine or standing CA and NE in normoadrenergic patients. These findings strongly support a participation of the sympathetic system in the maintenance of an elevated blood pressure in hyperadrenergic patients and raise the possibility of using a more rational approach in the therapy of hypertension.
Explore the source record for details and available documents.
The intracortical distribution of the biogenic amines (BA), norepinephrine (NE), dopamine (DA) and serotonin (5-HT), was determined for the parietal and occipital cortical areas of the cat. Under microscopic control, slices of each region were dissected out into 4 fractions: (1) an upper gray fraction (G1); (2) a medium gray fraction (G2); (3) a lower gray fraction (G3) and (4) a white-matter fraction (W). The BA were assayed by means of specific and sensitive radioenzymatic techniques; using catechol-O-methyltransferase (COMT) for the catecholamines (CA), and N-acetyltransferase (NAT) and hydroxyindole-O-methyltransferase (HIOMT) for the 5-HT. In the two cortical regions studied, NE and DA were found to be distributed in an orderly laminar fashion. The highest levels of endogenous CA were measured in the superficial layers (fractions G1 and G2) while the white matter (fraction W) exhibited the lowest content of both NE and DA. DA represented 32--38% of the total CA content of the parietal cortex and 32--41% of the total CA content in the occipital cortex. In the parietal cortex, the distribution of 5-HT was similar in pattern to that of the CA, i.e., a decreasing concentration gradient with the highest endogenous levels in the G1 fraction and the lowest content in the W fraction. In the occipital cortex, the distribution was also found to be laminar for the gray matter but the W fraction showed a higher endogenous content than the lower gray fraction (G3). The release of NE, DA and 5-HT was studied by means of cortical superfusion in an in vivo preparation. The concentrations of BA measured in 30 min interval superfusates was fairly constant in a given experiment under basal conditions but varied widely from experiment to experiment. Variations in the basal overflow of NE were often independent of those found for DA and the basal overflow of 5-HT seemed independent of those of CA. The laminar intracortical distribution of endogenous NE, DA and 5-HT in cerebral cortex demonstrated by microdissection and biochemical assay techniques suggests a definite and structured pattern of aminergic innervation. Furthermore, the fact that these BA are released and a basal overflow can be detected and measured appears compatible with significant roles of NE, DA and 5-HT in synaptic transmission in the cerebral cortex.
Plasma catecholamine levels were determined in 26 cases of uncomplicated myocardial infarction within 24 hours of onset of acute chest pain. Blood samples were collected at time of entry and at 4-hour intervals during the 48 hours following admission. Average values of plasma catecholamines within 1 hour of onset of pain were 0.87 ng./ml +/- 0.21 and remained elevated during the first 24 hours period. A gradual fall in catecholamine values was observed during the second 24-hour period. Catecholamines were higher in patients with sinus tachycardia and lower in patients with sinus bradycardia, and were higher in patients with anterior or anterolateral infarction. Catecholamine values were significantly higher when determined while patients presented ventricular ectopic beats or ventricular tachycardia. Sinus tachycardia, ventricular arrhythmias, and elevated plasma catecholamine values may be considered indicators of pain, anxiety, and/or left ventricular dysfunction without necessarily being causally related between themselves.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Several experimental observations accumulated during recent years have suggested an active participation of the sympathetic system in the pathogenesis and maintenance of hypertension in various experimental models of hypertension. The evaluation of sympathetic tone by various indirect means in human hypertension has also revealed that the sympathetic system plays an important role in the maintenance of hypertension in a subgroup of the human hypertensive population. The study of circulating catecholamines, which appears to be the best and most reliable indirect means to evaluate the sympathetic activity in the human, at present, has indicated that 25 to 40 per cent of patients with essential hypertension are characterized by higher basal circulating catecholamines and by a higher sympathetic reactivity in response to postural changes. These hyperadrenergic patients are also characterized by a higher heart rate, heart contractility, cardiac index and probably by higher plasma renin activity. The identification of these patients as a separate entity is desirable since it is possible that the evolution of the hypertensive disease and the response to therapy differ in this group of patients. The study of these patients could lead to a better understanding of the mechanisms underlying the pathogenesis of cardiovascular complications and to the development of more rational and efficient therapeutic approaches.
The effect of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) on blood volume was studied in unanesthetized splenectomized and nonsplenectomized dogs. A significant increase in total blood volume essentially accounted for by a marked plasma volume expansion was found in both groups after 6-OHDA treatment (50 mg/kg). The red cell volume in the nonsplenectomized dogs was significantly reduced 3 and 7 days after sympathectomy but returned to normal after 15 days. In contrast, the red cell volume was unchanged in the splenectomized dogs after sympathectomy. The blood volume changes were accompanied in both groups by significant decreases in hematocrit in plasma sodium and potassium and in serum protein concentrations while serum calcium concentrations were only slightly increased. These results confirm that the inhibition of adrenergic tone directly influences blood volume. They also indicate that an increase in blood volume constitutes an important compensatory mechanism for the long-term maintenance of adequate blood pressure levels after chemical sympathectomy by 6-OHDA.