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D Laude

Publications and source records attributed to D Laude.

At least 55 records · Page 3Linked to original sources
PubMed1993

[Pressure variability in the cold-pressure response test].

The effect of the immersion of the hand in ice water for 5 minutes on the short-term variability of blood pressure (BP) and heart rate (HR) was evaluated in 10 normal subjects. Indirect finger BP was measured by a non-invasive device (Finapres). Analogue-to-digital conversion of the BP was used to determine systolic, diastolic BP and HR every 0.5 second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm on 256 point time series of a stationary period. BP was increased (+28 mmHg for systolic BP and +13 mmHg for diastolic BP) and an increased overall variability of BP and HR was observed during the cold pressor test. The increased areas under the curve of the systolic, diastolic BP and HR spectra were documented with the selective analysis of the two main components of the spectra: the increase in the oscillations of BP and HR during the test predominated in the 70-140 mHz region (+30% for systolic BP, +24% for DBP and +21% for HR), corresponding to Mayer waves. The high-frequency (respiratory) component of BP and HR variability was unchanged. The significant increase in the 10 second period oscillations of BP could reflect the cold-induced sympathetic vasoconstriction.

Adaptation, Physiological↗
PubMed1992

Influence of the novel antidepressant tianeptine on neurochemical, neuroendocrinological, and behavioral effects of stress in rats.

Tianeptine is a novel tricyclic agent that activates the neuronal uptake of serotonin (5-hydroxytryptamine, 5-HT). Taking into account the antidepressant effect of tianeptine in animals and humans, we have measured the influence of a pretreatment with tianeptine (10 mg/kg IP 1 hr beforehand) on some consequences of a single 2-hr restraint stress session in male rats. Thus, we have analyzed (1) 5-HT metabolism in various brain regions and plasma glucose (an index of sympathoadrenal activity) and corticosterone levels at the end of stress, and (2) open field scores 18-19 hr after immobilization in saline- or tianeptine-pretreated rats. Tianeptine was found to leave unaltered stress-induced increases in cortical, hippocampal, hypothalamic, midbrain, and striatal serotonergic metabolism. Similarly, stress-elicited elevations in plasma glucose and corticosterone levels were not affected by tianeptine pretreatment. On the other hand, tianeptine pretreatment reversed stress-induced deficit in exploratory activity. To test whether the latter positive effect of tianeptine was associated with changes in plasma glucose and corticosterone levels during the early phase of stress, we have measured plasma glucose and corticosterone levels (at 0, 5, 15, 30, and 60 min) in resting and stressed (catheterized) rats. The results indicated that tianeptine pretreatment did not alter plasma glucose and corticosterone early responses to stress. Although this study confirmed the antidepressant effect of tianeptine, the neurochemical and neuroendocrinological mechanisms underlying this positive effect remain to be determined.

Animals↗
PubMed1991

Cardiovascular and adrenaline-releasing effects of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin in streptozotocin diabetic rats.

The 5-hydroxytryptamine1A (5-HT1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) has been reported to trigger sympathoinhibition, as evidenced by its cardiovascular effects, and adrenal catecholamine secretion. The purpose of this study was to analyze the cardiovascular and adrenaline-releasing effects of 8-OH-DPAT in 1 week streptozotocin diabetic rats. 8-OH-DPAT-induced changes in mean arterial pressure (MAP) and heart rate (HR) were determined directly in anesthetized rats, whilst changes in plasma adrenaline (and plasma corticosterone and glucose) levels were analyzed in conscious rats. Resting blood pressure and heart rate were diminished in diabetics, when compared with controls. These changes were associated with a decrease in body weight and a marked increase in resting plasma glucose levels. Diabetes did not affect MAP response to 8-OH-DPAT, except for a decrease in the amplitude of MAP maximal fall, which was associated with a diminished bradycardic response to 8-OH-DPAT. Blood pressure response to prazosin (0.5 mg/kg) in 8-OH-DPAT-pretreated rats was also diminished in diabetics. Lastly, diabetes prevented the adrenaline-releasing and hyperglycemic effects of 8-OH-DPAT (250 ug/kg).

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Clonidine reduces blood pressure and heart rate oscillations in hypertensive patients.

Short-term fluctuations in blood pressure (BP) and heart rate (HR) were analyzed in a group of eight men with essential hypertension. Indirect finger BP was measured by a Finapres device. Analog-to-digital conversion of the BP was used to determine systolic (SAP), diastolic (DAP), and mean arterial pressure (MAP) and HR every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. The effects of an oral dose of clonidine (150 micrograms) were studied in a double-blind, crossover, placebo-controlled study. Clonidine markedly reduced the variability of BP and HR after 90 min as indicated by a reduction in the standard deviations of BP by 36.7% for SAP, 21.0% for DAP, 22.1% for MAP, and 26.0% for HR. At this time clonidine reduced the average BP by 19.7 mm Hg for SAP, 10.6 mm Hg for DAP, 16.0 mm Hg for MAP, and 1.0 beat/min for HR. Spectral profiles of BP and HR illustrated the alterations in the spontaneous oscillations underlying the standard deviation changes. Clonidine dramatically reduced the amplitude of BP and HR oscillations in the mid-frequency region 66-129 mHz, which depends on the activity of the autonomic nervous system. We suggest that an increased sensitivity of the baroreflex is responsible for the apparent better control of BP and HR with clonidine.

Adult↗
PubMed1991

Effects of respiration on blood pressure and heart rate variability in humans.

1. Non-invasive continuous finger blood pressure (BP) measurement and a spectral technique based on the Fourier transform (FT) were recently combined to quantify short-term fluctuations in haemodynamic variables. 2. Systolic BP (SBP) recording combined low frequency (LF, Mayer waves) plus high frequency (HF, respiratory) oscillations. The presence of HF oscillations of SBP probably reflects fluctuations in cardiac output. Heart rate (HR) also exhibited a combination of low and HF (respiratory) oscillations. The vagus nerve mediates the efferent control of the respiratory sinus arrhythmia (RSA). 3. During controlled breathing in a supine position, a change in SBP is associated with an opposite consequent change in HR. Respiratory sinus arrhythmia could therefore depend on the baroreceptor-HR response to underlying SBP oscillations. 4. The fast regulation of R-R interval by SBP through the baroreceptor-HR reflex may explain why the respiratory variations in the diastolic BP are small.

Blood Pressure↗
PubMed1991

[Short-term variability in arterial pressure and heart rate in man].

Short-term fluctuations in blood pressure (BP) and heart rate (HR) were analysed in a group of seventeen males with essential hypertension (n = 8) or with normotension (n = 9). Indirect finger BP was measured by a Finapres device. Analog-to-digital conversion of the BP was used to determine systolic, diastolic, and mean arterial pressure and HR every s. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. BP recordings combined low frequency plus high frequency oscillations. The presence of high frequency oscillations of SBP probably reflects fluctuations in cardiac output. HR exhibited a combination of low and high frequency oscillations, such as systolic pressure. The corresponding spectra illustrate these observations. The high frequency (respiratory) oscillation corresponded to one peak easily detected on the spectrum of SBP and/or HR. Slow waves were detected in a 4-129 mHz range and divided into a 4-66 mHz low frequency region and a 66-129 mHz mid frequency region (Mayer waves). The sum of the values of consecutive bands was calculated to represent an integrated spectrum of each series of treatment. Controlled respiration produced at rest a marked increase in the high frequency component. HR variability increased with the level of HR. This study illustrates the applicability of a spectral procedures combined to an indirect BP measurement to study short-term oscillations of BP and HR.

Adult↗
PubMed1990

Effects of the 5-HT1C/5-5-HT2 receptor agonists DOI and alpha-methyl-5-HT on plasma glucose and insulin levels in the rat.

Administration of the 5-HT1C/5-HT2 receptor agonist 1-(2,5-dimethoxy-4- iodophenyl)-2-aminopropane (DOI, 0.125-2.0 mg/kg i.v.) triggered dose-dependent increases in plasma glucose; plasma insulin levels remained unchanged. Pretreatment with the 5-HT1C/5-HT2 receptor antagonists LY 53857, ritanserin, or the mixed 5-HT2/alpha 1-adrenoceptor antagonist ketanserin either diminished or prevented the hyperglycemic effect of DOI (0.5 mg/kg). Administration of the mixed 5-HT1C receptor agonists/5-HT2 receptor antagonists 1-(3-chlorophenyl)-piperazine (mCPP) or 1-(3-trifluoromethyl)phenyl)piperazine level (TFMPP) did not affect plasma glucose levels. However, pretreatment with mCPP or TFMPP decreased DOI-induced hyperglycemia in a dose-dependent manner. The alpha 2-adrenoceptor antagonist idazoxan and the ganglionic blocker hexamethonium both decreased DOI-induced hyperglycemia, Whilst the alpha 1-adrenoceptor antagonist prazosin amplified the rise in plasma glucose elicited by DOI. The peripherally acting 5-HT1C/5-HT2 receptor agonist alpha-methyl-5-HT (0.5-1.0 mg/kg i.v.) triggered a rise in plasma glucose levels that was associated with an increase in plasma insulin levels. Pretreatment with LY 53857 diminished alpha-methyl-5-HT-induced hyperglycemia. These data indicate that 5-HT2 receptors, but not 5-HT1C receptors, and catecholaminergic systems, mediate DOI-induced hyperglycemia. Moreover, it is suggested that the inhibition of insulin release by DOI is centrally mediated, and that activation of peripheral 5-HT2 receptors may affect glycemia.

Amphetamines↗
PubMed1990

Ganglionic transmission is a prerequisite for the adrenaline-releasing and hyperglycemic effects of 8-OH-DPAT.

The present study concerned the influence of ganglionic nicotinic blockade (by hexamethonium, 5 mg/kg and 10 mg/kg) of the 8-OH-DPAT-induced elevations in plasma adrenaline, corticosterone and glucose levels in conscious rats. Prior treatment with hexamethonium dose dependently decreased the basal glucose levels and increased the basal corticosterone levels but did not significantly affect the basal adrenaline levels. Hexamethonium decreased in a dose-dependent manner the elevations in plasma adrenaline, corticosterone and glucose levels that were elicited by the 5-HT1A receptor agonist, 8-OH-DPAT (0.25 mg/kg). These results indicate that acetylcholine release is a prerequisite for both the adrenaline-releasing and hyperglycemic effects of 8-OH-DPAT. The data also point to the possibility that adrenaline release participates in the elevation in plasma corticosterone levels that is elicited by 5-HT1A receptor activation.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1990

In vivo evidence that insulin does not inhibit hepatic tryptophan pyrrolase activity in rats.

Previous reports have indicated that insulin administration triggers an early increase in plasma tryptophan (TRP) levels in fasted rats. Then, the present study was undertaken to investigate the putative role of liver tryptophan pyrrolase (TPO) in this short-term effect of insulin. In 24 hr fasted rats, doses of insulin that triggered an increase in plasma TRP levels (i.e., 2-3 I.U./kg, 1 hr) did not alter either holoenzyme or total enzyme activity. In another series of experiments, the administration of insulin (2 I.U./kg) to 24 hr fasted rats promoted biphasic time effects on plasma TRP levels and liver TPO activity. Thus, insulin initially triggered a rise in plasma TRP (without any change in liver TPO activity) and then increased liver TPO activity whilst plasma TRP returned toward control levels. In addition, hypercorticosteronemia was evidenced throughout the first phasis. Lastly, the influence of insulin administration (2 I.U./kg) on fasting-induced TPO induction was analysed. Whereas fasting increased liver TPO activity in a time-dependent manner, insulin administration (2 I.U./kg, 30 min) did not modify either plasma TRP or liver TPO activity. The data reported herein bring evidence that the effect of insulin administration on circulating TRP is not mediated by an inhibition of hepatic TPO.

Animals↗
PubMed1990

Pentobarbital anaesthesia prevents the adrenaline-releasing effect of the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino) tetralin.

Administration of the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.25 mg/kg i.v.), to conscious rats increased plasma adrenaline and glucose levels for 30 and 60 min, respectively. Both 8-OH-DPAT-induced changes in plasma adrenaline and glucose levels were totally abolished in pentobarbital-anaesthetized rats. The present data indicate that pentobarbital anaesthesia, a procedure that is commonly used in pharmacological studies, prevents the release of adrenaline evoked by 5-HT1A receptor activation.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1990

Evidence that the 5-HT1A receptor agonists buspirone and ipsapirone activate adrenaline release in the conscious rat.

The aim of this study was to investigate the effects of the 5-HT1A receptor agonists buspirone and ipsapirone (1-10 mg/kg) on plasma adrenaline (A) levels and on glycemia in the conscious rat. The results indicate that buspirone was able, within 5 min, to increase plasma A and glucose levels in a dose-dependent manner. Ipsapirone administration triggered similar patterns, except that the highest dose used (10 mg/kg) promoted a time-dependent increase in plasma A and glucose levels that was maximal at the end of analysis.

Animals↗
PubMed1990

Effects of the 5-HT1 receptor agonists DP-5-CT, CGS 12066B, and RU 24969 on plasma adrenaline and glucose levels in the rat.

Recent results have indicated that the 5-HT1A receptor subtype mediates the adrenaline-releasing and hyperglycemic effects of 8-hydroxy-2-(di-n-propylamino)tetralin in the rat. The aim of this study was to analyse, by means of the peripherally acting 5-HT1A receptor agonist, N,N-dipropyl-5-carboxamidotryptamine (DP-5-CT), whether these 5-HT1A receptors are peripherally or centrally localised. In view of the appreciable affinity of DP-5-CT for the 5-HT1D receptor subtype, the effects of the mixed 5-HT1B/5-HT1D receptor agonist 7-trifluoromethyl-4-(4-methyl-1-piperazinyl)-pyrrolo(1,2-a)quinoxaline (CGS 12066B), and the mixed 5-HT1A/5-HT1B/5-HT1D receptor agonist 5-methoxy-3(1,2,3,6-tetrahydropyridine-4-yl)1H-indole (RU 24969) were also investigated. Administration of DP-5-CT (0.3 and 1 mg/kg i.v.) increased plasma glucose levels dose-dependently, whereas only the 1 mg/kg dose of DP-5-CT elicited a rise in plasma adrenaline levels. In contrast, CGS 12066B (1.5 and 4.5 mg/kg i.v.) did not affect either plasma adrenaline or plasma glucose levels. Administration of RU 24969 (0.5-4.5 mg/kg i.v.) increased dose-dependently both plasma adrenaline and glucose levels. The data suggest that central 5-HT1A receptors, but neither 5-HT1B nor 5-HT1D receptors, regulate plasma adrenaline and glucose levels.

Animals↗
PubMed1990

Evidence that 5-HT1A receptors are involved in the adrenaline-releasing effects of 8-OH-DPAT in the conscious rat.

8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) is a 5-HT1A receptor-selective agonist that has recently been reported to trigger adrenal catecholamine release and hyperglycemia. The aim of this study was to analyze in the conscious rat whether the 5-HT1A receptor subtype is involved in these effects. 8-OH-DPAT (0.1-1 mg/kg, i.v.) evoked dose-dependent increases in plasma adrenaline and glucose concentrations. Increases in plasma adrenaline levels peaked 5 min after administration of 8-OH-DPAT; in contrast, plasma glucose levels rose throughout the 20 min period of analysis. Prior administration of (-)pindolol, a beta-adrenoceptor antagonist that blocks 5-HT1A receptors, markedly diminished the rise in plasma adrenaline levels and abolished the hyperglycemia triggered by 8-OH-DPAT. On the other hand, neither the selective beta 1-adrenoceptor antagonist, betaxolol, the selective beta 2-adrenoceptor antagonist, ICI 118.551, nor the 5-HT2 receptor antagonist, ketanserin, affected 8-OH-DPAT-induced increases in plasma adrenaline levels. In addition, except for ICI 118.551 pretreatment, which delayed the hyperglycemic effect of 8-OH-DPAT, none of these antagonists affected the rise in glycaemia evoked by 8-OH-DPAT. The data suggest that the adrenaline-releasing and a major part of the hyperglycemic effects of 8-OH-DPAT are mediated by activation of 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1990

Spectral analysis of blood pressure and heart rate in conscious rats: effects of autonomic blockers.

We investigated the fluctuations which underly the spontaneous variability of blood pressure and heart rate in conscious rats. Intrafemoral blood pressure was computed to generate evenly spaced signals (systolic, diastolic, mean blood pressure, heart rate) at 200 ms intervals. This equidistant sampling allowed a direct spectral analysis using a Fast Fourier Transform algorithm. Systolic blood pressure and heart rate exhibited low-frequency oscillations (Mayer waves, 20-605 mHz) and a high- frequency oscillation related to respiration (1855 mHz). The respiratory fluctuations in heart rate were almost abolished by vagal blockade (atropine). Heart rate fluctuations in the low-frequency regime were diminished by vagal blockade or cardiac sympathetic blockade (atenolol). The respiratory frequency fluctuations in systolic blood pressure were markedly increased by alpha-sympathetic blockade (prazosin). In contrast, the low-frequency oscillations in systolic blood pressure were reduced by alpha-sympathetic blockade. These data indicate that in conscious rats: (1) the heart rate oscillation with respiration is vagally mediated; (2) the heart rate fluctuation in the low-frequency range is jointly mediated by beta-sympathetic and parasympathetic activities; (3) the respiratory oscillation in systolic blood pressure depends on fluctuations in cardiac output and is normally counteracted by the sympathetic tone; (4) the low-frequency oscillations in systolic blood pressure reflect the sympathetic activity to the resistance vessels.

Animals↗
PubMed1989

PHysical exercise: evidence for differential consequences of tryptophan on 5-HT synthesis and metabolism in central serotonergic cell bodies and terminals.

The aim of the present study was to investigate the effects of physical exercise (running) on serotonin (5-hydroxytryptamine, 5-HT) synthesis and metabolism in midbrain on the one hand, and in striatum and hippocampus on the other hand. To address such a question, tryptophan (TRP) and 5-hydroxytryptophan (5-HTP) were measured in running rats pretreated with an inhibitor of aromatic amino acid decarboxylase, namely NSD 1015. In another series of experiments, the consequences of a TRP load on TRP, 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels were compared in resting and running rats. Although running triggered a 30% increase in TRP levels in the three brain regions examined, inhibition of 5-HT synthesis by NSD 1015 was found to promote increased (midbrain), unchanged (striatum) or decreased (hippocampus) 5-HTP accumulation in the running situation, respectively compared to that measured in the resting situation. Inasmuch as running-induced elevation in TRP was not associated with an increased 5-HTP accumulation in the striatum and the hippocampus, the consequences of running on regional TRP, 5-HT and 5-HIAA levels were analyzed in saline- and TRP-injected rats. Indeed, running, per se, was found to increase central TRP, 5-HT and 5-HIAA levels. On the other hand, a TRP load that promoted identical increases in central TRP levels in running and resting rats revealed that running, according to the region examined, differentially affected TRP utilization in the 5-HT synthesis pathway. Thus, in the midbrains of the resting and running rats, respective 210-250% increases in TRP led to identical 25% increases in 5-HT and 90% increases in 5-HIAA levels. Conversely, in hippocampus, TRP loads triggered marked increases in TRP levels that were similar in the controls and the runners, but the rise in 5-HIAA promoted by such a precursor load was found to be significantly minored in the runners, compared to the resting rats. Moreover, such a running-induced impairment in 5-HT synthesis and metabolism was even more observable in the striatum; thus, TRP loads which promoted identical increases in striatal TRP levels in the resting and the running rats respectively triggered a 50% and a 32% increase in 5-HT levels and a 76% and a 47% increase in 5-HIAA levels. The results presented herein indicate that under certain pharmacological conditions, TRP utilization into the 5-HT synthesis pathway is altered in serotonergic nerve terminals, but not in the cell bodies of the running rat.

Animals↗
PubMed1989

Plasma 5-hydroxyindoleacetic acid as an endogenous index of renal plasma flow.

5-Hydroxyindoleacetic acid (5-HIAA), the major serotonin metabolite, was measured in human plasma and urine using liquid chromatography and electrochemical detection. The renal extraction of 5-HIAA was 78%, a value compatible with an almost complete extraction during a single passage of the blood through the kidney. In addition, plasma levels of 5-HIAA measured in patients with a wide range of renal function was inversely correlated (r = 0.85) with the clearance of para-aminohippuric acid (PAH). The results indicate that 5-HIAA determinations can be used as an alternative procedure to the PAH clearance method for the estimation of renal plasma flow in clinical practice.

Adult↗