PubMed Health⌕ Search

Biomedical subjects

F Lhoste

Publications and source records attributed to F Lhoste.

At least 37 records · Page 2Linked to original sources
PubMed1986

Plasma renin activity, aldosterone and catecholamine levels when swimming and running.

The purpose of this study was to determine the response of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and catecholamines to two graded exercises differing by posture. Seven male subjects (19-25 years) performed successively a running rest on a treadmill and a swimming test in a 50-m swimming pool. Each exercise was increased in severity in 5-min steps with intervals of 1 min. Oxygen consumption, heart rate and blood lactate, measured every 5 min, showed a similar progression in energy expenditure until exhaustion, but there was a shorter time to exhaustion in the last step of the running test. PRA, PAC and catecholamines were increased after both types of exercise. The PRA increase was higher after the running test (20.9 ng AngI X ml-1 X h-1) than after swimming (8.66 ng AngI X ml-1 X h-1). The PAC increase was slightly greater after running (123 pg X ml-1) than swimming (102 pg X ml-1), buth the difference was not significant. Plasma catecholamine was higher after the swimming test. These results suggest that the volume shift induced by the supine position and water pressure during swimming decreased the PRA response. The association after swimming compared to running of a decreased PRA and an enhanced catecholamine response rule out a strict dependence of renin release under the effect of plasma catecholamines and is evidence of the major role of neural pathways for renin secretion during physical exercise.

Adult↗
PubMed1986

Hormone and metabolite response to weight-lifting training sessions.

Eleven weight-trained athletes (age X +/- SD = 33 +/- 5 yrs, weight = 72 +/- 10 kg) with a maximal performance in bench press at the beginning of the study (116 +/- 19 kg) were studied at rest, after a standardized submaximal training session, and after a maximal session once a month for 4 months to study the blood metabolites and hormonal changes during weight lifting. The submaximal load was six series of eight bench presses at 70% of maximal performance presses, and the maximal load was the maximal number of repetitions at the same work load. The levels of several metabolites (lactate, glycerol, triglycerides, beta-OH-butyrate) and hormones (norepinephrine and epinephrine) increased (P less than 0.05) after submaximal work and more after maximal work. Glucose, FFA, acetoacetate, insulin, testosterone, and cortisol did not change significantly or consistently. Lactate after maximal work was higher after the 4th training month (P less than 0.05). Other variables did not change much with training while the maximal number of repetitions in the last series increased slightly (P less than 0.05). In general, the changes observed were smaller than the ones reported for endurance or interval running, which use larger muscle groups. Nevertheless, weight lifting induced changes in blood metabolites which reflect a mobilization of both carbohydrates and lipids stores for energy.

Adult↗
PubMed1985

Bronchorelaxation and plasma histamine after salbutamol inhalation.

Plasma histamine in 8 normal subjects was measured before and after inhalation of carbachol to induce a 50% fall in specific airway conductance (SGaw). The measurements were repeated 5 min after inhalation of salbutamol or placebo. No significant change in plasma histamine occurred after placebo or carbachol inhalation, despite the persistent induced bronchospasm after the latter treatment. In contrast, plasma histamine was significantly increased from 0.25 to 0.43 ng/ml after salbutamol inhalation. Simultaneously, induced bronchospasm was relieved, from 51% to 103% of baseline SGaw. Thus, the relief of carbachol-induced bronchospasm by salbutamol was associated with a rise in plasma histamine. Since salbutamol itself is a potent inhibitor of mast cell degranulation and histamine release, the present findings suggest that histamine may be released and sequestered within the lungs during carbachol-induced-bronchospasm, and also that desequestration of bronchoconstrictor mediators accumulated at the point of contact of bronchial smooth muscle may contribute to the relief of bronchospasm by salbutamol.

Adult↗
PubMed1985

Naloxone therapy of human septic shock.

A 0.01 and 0.1-mg/kg dose of iv naloxone was administered to seven patients in septic shock, in order to evaluate naloxone's hemodynamic effect and possible relation to changes in plasma beta-endorphin and catecholamine levels. Naloxone failed to modify cardiac index, blood pressure, heart rate, and systemic vascular resistance. Plasma beta-endorphin, norepinephrine, and epinephrine were elevated but did not change after naloxone administration. These results suggest that beta-endorphin release is a consequence but not a cause of shock, and that the beneficial hemodynamic effects of naloxone in animal studies could be related to species differences or nociceptive stimulations.

Adult↗
PubMed1985

Effects of thyrotrophin-releasing hormone on plasma catecholamine levels in acromegalics.

Plasma catecholamines assayed by a double isotope radio enzymatic method were studied in the basal state and during a thyrotrophin-releasing hormone (TRH)-test in 7 acromegalics, divided into 2 groups: active and non-active acromegalics, according to clinical and biological criteria. Basal plasma norepinephrine levels were significantly increased in the active group 648 +/- 22 pg/ml (P less than 0.001) and were in the normal range in the non-active group 439 +/- 26 pg/ml. Basal plasma epinephrine values were not significantly different in the 2 groups 59 +/- 15 pg/ml vs 34 +/- 7 pg/ml. During a TRH-test, norepinephrine levels remained elevated (P less than 0.001) in the active group, and the difference between the 2 groups was enhanced during the test. On the other hand the 2 patients who responded to TRH demonstrated an increase of norepinephrine levels. Our results suggest that TRH may stimulate norepinephrine release in acromegalics with an active response to TRH.

Acromegaly↗
PubMed1985

[Physiological and pharmacologic studies of the adrenal medulla by the measurement of plasma catecholamine levels].

The new techniques for the assay of the plasma catecholamines: noradrenaline, dopamine and, most importantly, adrenaline, because of their sensitivity and precision, have provided new information about the physiology and the pharmacology of the adrenal medulla in animals and in man. The most effective of these new techniques are the radioenzymatic techniques. The activation of the adrenal medulla in the dog or the rat appears to be frequency-dependent by maintaining a fixed concentration ratio in the systemic circulation of 4/1. In this way, it is possible to quantify the pharmacological effects of various substances for a given frequency and to evaluate their impact on the neuro-neuronal or neuro-humoral sympathetic system. In this context, the use of pithed rats, with or without adrenalectomy, is particularly useful. This model can be used to demonstrate that the global electrical activation of the sympathetic system results in a preferential stimulation of adrenaline secretion (1,000%) compared with 150% for noradrenaline secretion. Such a global activation never occurs in clinical or experimental pathology, except for activation of a baro-reflex, acidosis or hypoglycaemia. Thus it is possible that there is a separate physiological regulation of the neuro-neuronal sympathetic axis and the neuro-adrenal sympathetic axis. Neuro-neuronal regulation is sensitive to central manipulations, but especially to peripheral presynaptic stimulations and inhibitions. Neuro-adrenal regulation is particularly sensitive to inhibition by centrally acting alpha 2 type drugs, such as clonidine, but also, unlike the sympathetic neurones, to substances with a direct peripheral effect such as calcium antagonists.

Adrenal Medulla↗
PubMed1985

Pharmacological, hemodynamic and biochemical mechanisms involved in the blood pressure lowering effects of pergolide, in normotensive and hypertensive dogs.

In pentobarbital-anesthetized normotensive dogs, clonidine (20.0 micrograms/kg i.v.), in contrast to pergolide (30.0 micrograms/kg i.v.), reduced significantly both aortic blood pressure and plasma concentration of norepinephrine. However, in dogs that had been made hypertensive by sectioning the vagi and carotid sinus nerves, pergolide, like clonidine, lowered the blood pressure and plasma concentrations of epinephrine and norepinephrine that were enhanced markedly by deafferentation. Furthermore, in this preparation pergolide decreased the calculated resistance in vascular regions supplied by the upper abdominal aorta and the innervated femoral and renal arteries, but it increased vascular resistance in the denervated hind leg. Pergolide (1.0 microgram/kg) injected intracisternally (i.c.m.) induced a fall in blood pressure of comparable magnitude to that produced by a 30 times higher i.v. dose. Intravenously and i.c.m. administered pergolide lowered blood pressure by acting at distinct anatomical sites inasmuch as i.v. sulpiride blocked the effects of i.v. but not i.c.m. pergolide. The combination of sulpiride plus yohimbine injected i.c.m. was necessary to abolish the decrease in blood pressure evoked by i.c.m. pergolide. In atropinized spinal dogs, i.v. pergolide inhibited the vasoconstriction elicited by electrical stimulation of the lumbar sympathetic chain, an effect which was antagonized by sulpiride. Similarly, pergolide (30.0 micrograms/kg i.v.) like clonidine, reduced the heart rate and coronary venous plasma norepinephrine concentration raised by sustained electrical stimulation of the cardioaccelerator nerve. Sulpiride, but not phentolamine, antagonized this pergolide-induced inhibition of sympathetic nerve function. In chlorisondamine-pretreated dogs, pergolide produced a transient pressor response due to stimulation of postsynaptic vascular alpha-2 adrenoceptors. In conclusion, the failure of i.v. pergolide to decrease aortic blood pressure in pentobarbital-anesthetized normotensive dogs is presumably due to the inability of pergolide to produce a significant inhibition of the vascular sympathetic tone in this preparation. However, in neurogenic hypertensive dogs which are characterized by an elevated level of sympathetic drive, i.v. pergolide reduced blood pressure and aortic plasma norepinephrine concentration. These effects of pergolide are compatible with a DA-2 dopamine receptor stimulation on peripheral sympathetic nerve fibers. In contrast, the antihypertensive effects of i.c.m. pergolide would appear to be mediated by both alpha-2 adrenoceptors and DA-2 dopamine receptors located within the central nervous system.

Anesthesia↗
PubMed1985

[Role of the adrenal medulla in the effect of antihypertensive drugs].

Recent studies have suggested a role for adrenaline in the pathogenesis of essential hypertension. In the present study, the effects of several anti-hypertensive agents were compared in normal (plasma adrenaline concentration: 0.267 + 0.040 ng/ml) and adrenomedullectomised (plasma adrenaline concentration: 0.063 + 0.011 ng/ml; p less than 0.01) dogs. The hypotensive and tachycardic effects of phentolamine (1.5 mg/kg i.v.) or dihydralazine (1 mg/kg i.v.) were the same in the two groups of dogs. Verapamil (0.2 mg/kg i.v.)-induced hypotension was less pronounced in dogs without adrenal medulla. In these adrenomedullectomised dogs, clonidine (10 micrograms/kg i.v. or 1 microgram/kg i.c.) elicited tachycardia and its hypotensive properties were delayed. In dogs with neurogenic hypertension, the antihypertensive properties of propranolol (1 mg/kg i.v.) remained unchanged. These results show the importance of adrenal medulla in the antihypertensive action of clonidine, or verapamil. These agents (but not dihydralazine, propranolol or phentolamine) could reduce adrenaline secretion from the adrenal medulla.

Adrenal Medulla↗
PubMed1985

Studies on the cardiovascular actions of apomorphine in dogs: central versus peripheral mechanisms and role of the adrenal medulla.

The effects of apomorphine on blood pressure and heart rate were studied in normotensive chloralose anaesthetized dogs. Intravenous apomorphine (200 micrograms/kg) induced both a marked decrease of blood pressure and an increase in heart rate. These two cardiovascular responses to intravenous apomorphine were suppressed by haloperidol (1 mg/kg i.v.) or phentolamine (1 mg/kg i.v.). In contrast, pretreatment with atropine (1 mg/kg i.v.) only abolished the chronotropic (but not the hypotensive) response to apomorphine. Intravenous (500 micrograms/kg) but not intracisternal (50 micrograms/kg) domperidone suppressed the hypotensive responses elicited by intravenous or intracisternal apomorphine. In contrast, domperidone, injected either by intravenous or intracisternal route, abolished apomorphine-induced tachycardia. In adrenal demedullated dogs, the hypotensive response to apomorphine was abolished. These results suggest that the hypotensive response to apomorphine in normotensive dogs is mainly mediated by activation of peripheral dopaminergic mechanisms. The drug decreases blood pressure through stimulation of dopaminergic receptors located on sympathetic nerve terminals and on the adrenal medulla leading to a decrease of the release of catecholamines.

Adrenal Medulla↗
PubMed1984

Attenuation by diltiazem of arterial baroreflex sensitivity in man.

The effect of oral diltiazem 120 mg, on the responses to baroreflex activation and deactivation by phenylephrine and nitroglycerin, respectively, were investigated in normotensive subjects, with simultaneous measurement of plasma catecholamine levels. Diltiazem significantly reduced the tachycardia induced by bolus injections of nitroglycerin and abolished the concomitant increase in plasma noradrenaline. It also significantly decreased the bradycardiac response to phenylephrine infusion. Diltiazem reduced, although not significantly so, the bradycardia induced by boluses of phenylephrine. The overall reduction in baroreflex sensitivity, which might contribute to the limited tachycardiac effect of diltiazem in man, is consistent with the drug-induced attenuation of the sympathetic and also of the parasympathetic components of the baroreceptor reflex.

Adolescent↗
PubMed1984

Decreased plasma epinephrine concentrations after glucose ingestion in humans.

Plasma levels of norepinephrine (NE), epinephrine (E), immunoreactive insulin (IRI), and glucose were measured in six healthy volunteers after glucose consumption and in six volunteers after a water solution. Ingestion of the glucose (100 g) solution significantly decreased E levels from 46.7 +/- 8.0 to 20.8 +/- 1.9 pg/mL (P less than 0.01). Three hours after the glucose ingestion, plasma E levels nearly returned to basal values. Plasma IRI and glucose levels peaked at 45 minutes after glucose consumption (P less than 0.01), then declined toward basal values. Plasma NE levels were unaffected by glucose consumption. There were no changes in glucose, IRI, NE, or E levels in the control group. These results suggest that E behaves as a counter-regulatory hormone to insulin under stimulation by glucose.

Adult↗
PubMed1984

Plasma histamine and catecholamines during carbachol-induced bronchoconstriction in normal subjects.

To determine (1) whether changes in plasma histamine occurred during provoked bronchospasm and (2) if so, whether such changes could be related to variations in plasma catecholamines, venous plasma histamine and catecholamines were measured during a dose-response carbachol challenge in eight healthy volunteers. A significant rise in plasma histamine was observed, whereas induced bronchoconstriction was small, 80% +/- 4% of initial specific airway conductance. There was no further increase in plasma histamine, whereas induced bronchoconstriction became more marked (70%, 60%, and 50% of specific airway conductance initial value). Plasma catecholamines did not change throughout the study. We conclude that mast cell degranulation occurs during a carbachol challenge, and that the variations in plasma histamine are not related to changes in plasma catecholamines.

Adult↗
PubMed1984

Sympathetic nervous system activation in postextrasystolic potentiation: role of catecholamine release in enhancement of ventricular function.

The role of catecholamines in postextrasystolic potentiation was assessed in 30 patients during continuous coupled right ventricular pacing. Hemodynamic data were recorded in 15 patients (group 1); in the other 15 patients (group 2), coronary blood flow and metabolic variables, including catecholamines, were measured. Data were recorded in the control state and after 10 minutes of coupled pacing. Both groups had similar control pulse rates and mean aortic pressures: these variables decreased abruptly by 32 beats/min and 12 mm Hg, respectively, (p less than 0.001 for each) after the initiation of coupled pacing. In group 1, all indexes of left ventricular function and contractility increased during coupled pacing (p less than 0.001 for each), thus confirming postextrasystolic potentiation. In group 2, coupled pacing increased coronary blood flow, myocardial oxygen consumption and free fatty acid uptake (p less than 0.001 for each) but not lactate extraction. Plasma epinephrine was unchanged, but norepinephrine levels increased in arterial (421 +/- 27 to 576 +/- 41 ng/liter) and coronary sinus plasma (611 +/- 46 to 836 +/- 46 ng/liter) (p less than 0.001 for both). Indirectly calculated norepinephrine release within the myocardium increased from 25.6 +/- 2.8 to 39.7 +/- 5.2 ng/min (SEM) (p less than 0.05), suggesting a sympathetic nervous system activation. It is argued that coupled pacing acutely lowered mean aortic pressure, leading to baroreflex sympathetic activation which may contribute to augmented cardiac contractility in postextrasystolic potentiation.

Adolescent↗
PubMed1984

Nicardipine: pharmacokinetics and effects on carotid and brachial blood flows in normal volunteers.

The effects of nicardipine, 20 mg, three times daily, nicardipine slow release, 30 mg, twice daily and a placebo on brachial and carotid arteries diameters and flows have been investigated by the pulsed Doppler technique during a single blind and cross-over study performed in six healthy volunteers. Simultaneously, nicardipine plasma levels and relative bioavailability were determined. Nicardipine significantly increased brachial and carotid arteries diameters (by 16 and 10% respectively) and flows (by 60 and 35% respectively). These effects peaked after 4 h and lasted no longer than 6 h. Forearm vascular resistance was significantly decreased. Hence nicardipine dilated both large and small arteries. Nicardipine slow release elicited the same effects on brachial and carotid arteries diameters and flows as nicardipine. These effects peaked at 6 h and lasted up to 10 h. Although the profiles of the pharmacodynamic effects and of the kinetics of nicardipine were almost parallel in each individual after administration of both nicardipine formulations, there was no correlation between the nicardipine plasma relative bioavailability and its effects on brachial and carotid arteries blood flows when considering all subjects together.

Adult↗
PubMed1984

Pharmacological, hemodynamic and autonomic nervous system mechanisms responsible for the blood pressure and heart rate lowering effects of pergolide in rats.

In conscious spontaneously hypertensive rats, pergolide (50.0 micrograms/kg s.c.) produced a sustained decrease in tail artery pressure which was blocked by haloperidol (1.0 mg/kg s.c.) pretreatment. In anesthetized spontaneously hypertensive rats this effect was accompanied by a fall in total peripheral resistance inasmuch as pergolide did not significantly change cardiac output. In anesthetized normotensive rats, pergolide (30.0 micrograms/kg i.v.) also lowered blood pressure. This effect was not significantly modified by adrenalectomy, methysergide, idazoxan (alpha-2 adrenoceptor antagonist), vagotomy alone or plus ligation of carotid arteries or plus atenolol, but was entirely prevented by domperidone or sulpiride pretreatment and was reverted to a pressor response (due to stimulation of alpha adrenoceptors and 5-hydroxytryptamine receptors) by blockade of ganglionic transmission with chlorisondamine. Pergolide given either i.v. or into the cisterna magna or the lateral cerebral ventricle produced changes in blood pressure of the same magnitude. In intact or adrenalectomized rats, i.v. pergolide significantly lowered plasma norepinephrine concentration. Furthermore, in saline but not sulpiride-pretreated pithed rats, pergolide reduced the pressor responses and the accompanying increases in plasma norepinephrine evoked by electrical stimulation of the spinal cord. However, pergolide failed to modify the vascular reactivity to several pressor agents and lacked beta-2 and DA-1 dopamine receptor agonist properties. These results indicate that the decrease in blood pressure produced by pergolide can be accounted for by an inhibition of sympathetic tone resulting from stimulation of peripheral neuronal dopamine receptors. A possible central contribution remains to be substantiated. The pronounced bradycardia produced by pergolide (30.0 micrograms/kg i.v.) in anesthetized intact rats was partly reduced by vagotomy, methylatropine, domperidone, sulpiride, idazoxan, phentolamine or atenolol. The effects of pergolide in vagotomized rats were further diminished by domperidone but they were blocked by the combination of phentolamine or idazoxan plus domperidone. In rats pretreated with atenolol or in rats with the cervical section of spinal cord and the low level of heart rate increased with an isoprenaline infusion, the decrease in heart rate produced by pergolide was abolished by domperidone, methylatropine or idazoxan. In pithed rats, pergolide changed neither the base-line heart rate nor the tachycardia to exogenous norepinephrine nor the bradycardia evoked by carbachol or electrical stimulation of the peripheral cervical vagus.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗