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Biomedical subjects

I Macquin-Mavier

Publications and source records attributed to I Macquin-Mavier.

54 records · Page 3Linked to original sources
PubMed1989

Fentanyl-induced airway hyperreactivity in the guinea pig.

The bronchopulmonary effects of fentanyl were studied in mechanically ventilated, paralyzed guinea pigs that had been anaesthetized with pentobarbitone sodium. Fentanyl did not alter the resting bronchial tone but enhanced the bronchoconstrictor effects of 5-hydroxytryptamine in a dose-related manner. The enhancement induced by 20 micrograms kg-1 fentanyl was suppressed by pretreatments with 0.5 mg kg-1 naloxone or 5 mg kg-1 propranolol, but did not change after 3 mg kg-1 atropine. The bronchoconstrictor responses to histamine were also enhanced by 20 micrograms kg-1 fentanyl. These results suggest that fentanyl-induced airway hyperreactivity is not mediated by an increase in vagal tone but is due to a reduction in the central sympathetic drive and/or in the levels of circulating catecholamines, which occurs through stimulation of opiate receptors.

Animals↗
PubMed1989

Abnormalities in myocardial segmental wall motion during lumbar epidural anesthesia.

The effect of lumbar epidural anesthesia on myocardial wall motion was compared in two groups of patients using precordial two-dimensional echocardiography (2DE). All patients were scheduled to undergo lower abdominal or peripheral surgery. Group 1 included five healthy ASA PS 1 subjects and group 2 included 10 patients with coronary artery disease (CAD). In all patients 12.5 ml of 2% lidocaine HCl was injected into the lumbar epidural space, and systolic and diastolic blood pressures, and heart rate were continuously monitored. 2DE evaluation was performed before and at 10, 20, 30, and 60 min (T10-T60) after epidural lidocaine injection. The left ventricular wall was divided into 16 segments for parasternal long-axis, short-axis and apical four-chamber views. The wall motion of each segment was graded on a scale from 1 (dyskinesia) to 6 (hyperkinesia), with 5 representing normal motion. A decrease in segmental wall motion greater than or equal to 2 grades was considered indicative of ischemia. Plasma lidocaine and catecholamine levels were measured before and 10, 20, and 60 min after epidural lidocaine injection. Peak plasma lidocaine levels in groups 1 and 2 were 2.79 +/- 1.06 micrograms/ml (mean +/- SD) and 2.58 +/- 1.48 micrograms/ml at 10 min, respectively (NS). Plasma epinephrine and norepinephrine levels were unchanged from baseline. Systolic pressures decreased significantly in group 2 from T10 to T60. Diastolic pressure decreased significantly in the same group from T20 to T60, and in group 1 only at T10. Mean arterial pressure decreased significantly in both groups at T30, without change in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Influence of body temperature on histamine-induced bronchoconstriction in guinea pigs.

The effects of body temperature on histamine-induced bronchoconstriction were investigated in anesthetized, paralyzed, and mechanically ventilated guinea pigs. Four groups of guinea pigs were studied with constant body temperatures of 40, 38, 35, and 32 degrees C, respectively. Histamine was infused for 5 min at a rate of 50 ng.kg-1.s-1. Body cooling from 40 to 32 degrees C augmented the bronchomotor responses to histamine, which eventually rose almost fourfold. The enhancement of histamine-induced bronchoconstriction induced by body cooling was not suppressed by pretreating guinea pigs with 5 mg/kg hexamethonium or 5 mg/kg hexamethonium plus 3 mg/kg atropine; neither was the enhancement of histamine-induced bronchoconstriction suppressed in pithed guinea pigs, demonstrating that the autonomic nervous system is not involved in potentiating bronchoconstriction at low body temperatures. These results suggest that, at low body temperatures, increased airway responsiveness to histamine may be because of some direct effect of temperature on bronchial airway smooth muscle.

Animals↗
PubMed1989

Nonadrenergic bronchodilation in adult and young guinea pigs.

The contribution of the nonadrenergic inhibitory system to airway responses to infusion of 5-hydroxytryptamine (5-HT) was evaluated in anesthetized, tracheotomized, and paralyzed young (13 days) and adult (82 days) guinea pigs. Animals were mechanically ventilated by a constant flow ventilator. Compliance (C) and conductance (G) of the respiratory system were continuously monitored. Three series of experiments were performed involving intravenous pretreatment with 1) atropine (3 mg/kg) and propranolol (1 mg/kg); 2) atropine (3 mg/kg), propranolol (1 mg/kg), and phentolamine (2 mg/kg); and 3) atropine (3 mg/kg) and hexamethonium (2 mg/kg). 5-HT was then intravenously infused for 5 min at a rate of 40 ng.kg-1.s-1 in adults and 60 ng.kg-1.s-1 in young guinea pigs to obtain the same degree of bronchoconstriction in both groups. At the 3rd min of the infusion, bilateral cervical vagotomy was performed and C and G were measured at the maximal response, 1-2 min thereafter. Vagotomy increased bronchoconstriction (P less than 0.01) in both young animals and adults. Phentolamine did not modify this increase, but hexamethonium completely inhibited it. These results indicate that, in adult and young guinea pigs, 5-HT infusion induces reflex activation of the nonadrenergic inhibitory system, which in turn modulates the bronchoconstrictor responses to 5-HT. This neural modulation is not mediated by an alpha-adrenergic pathway.

Animals↗
PubMed1989

Mechanisms of endothelin-mediated bronchoconstriction in the guinea pig.

Intravenous injection of anesthetized ventilated guinea pigs with doses of endothelin ranging from 0.25 to 2.50 micrograms/kg caused dose-dependent decreases in respiratory system conductance and compliance. These effects were maximal 1 min after injection and had disappeared 15 min thereafter. When guinea pigs were pretreated with 3 mg/kg of propranolol or 5 mg/kg of hexamethonium, endothelin-induced bronchoconstriction rose significantly, but when they were pretreated with 3 mg/kg of propranolol plus 3 mg/kg of atropine it remained unchanged. The bronchoconstrictor effects of endothelin were suppressed in guinea pigs pretreated with 0.5 or 2 mg/kg of meclofenamate but remained unchanged in those pretreated with 30 micrograms/kg of nicardipine. Endothelin did not increase either lung permeability, as assessed by 99m technetium diethylenetriamine pentaacetic acid clearance, or airway responsiveness to histamine or 5-hydroxy-tryptamine. Histological studies showed that endothelin induced reversible contraction of airway and pulmonary artery smooth muscles but no inflammatory reactions. These results demonstrate that, in guinea pigs, endothelin 1) induces airway smooth muscle contraction mediated by cyclooxygenase metabolites and modulated by the autonomic nervous system and 2) does not induce airway hyperreactivity or inflammation.

Animals↗
PubMed1989

[Current data on the pharmacology of rilmenidine].

Oral rilmenidine (1 mg/kg/day for 2 weeks) significantly reduces the blood pressure and heart rate of conscious barodenervated dogs. A dose-dependent decrease in blood pressure and heart rate has been demonstrated with intraveinous rilmenidine (0.1 to 1 mg/kg) in pentobarbitone anaesthetised spontaneously hypertensive rats (SHR). Chronic subcutaneous administration of rilmenidine (5 to 15 mg/kg/day) also produces a dose-dependent decrease of these two parameters in conscious SHR. In addition, rilmenidine reduces plasma noradrenaline and the liberation of catecholamines from the adrenal medulla; these actions could contribute to its antihypertensive effect. The hypotensive effect of rilmenidine, clonidine and related molecules, is due to a reduction in sympathetic tone of central or peripheral origin. Although rilmenidine binds to alpha-2 adrenergic receptors, it does not cause sedation in animal models: it does not prolong barbiturate-induced sleep in the mouse and rat at doses of up to 10 mg/kg and does not affect spontaneous locomotor activity in the rat at doses of up to 2.5 mg/kg. The results show a dissociation of the sedative and antihypertensive effects of rilmenadine. The almost complete absence of sedation in animal models may be explained by: as yet unknown properties inhibiting sedation, a preferential peripheral site of action and/or the presence of separate central receptors accounting for the sedative or hypotensive effects. The precise mechanism of the hypotensive effects of rilmenidine is currently under study. The binding of rilmenidine at central "imidazoline receptor" sites responsible for the regulation of the blood pressure could explain its mode of action and why its pharmacological profile is different to that of other centrally acting hypotensive agents.

Animals↗
PubMed1988

Effects of rilmenidine on bronchomotor responses in the guinea pig.

This study compares the effects of 2 alpha 2-adrenergic agonists, rilmenidine (S 3341) and clonidine, on histamine-induced bronchoconstriction (HIB) in guinea pigs. Clonidine has previously been shown to potentiate HIB in guinea pigs. The study was conducted in anesthetized, paralyzed and ventilated guinea pigs. Six groups of at least 6 guinea pigs were pretreated with saline, rilmenidine (0.1, 0.3 and 1 mg/kg intravenously) or clonidine (0.01 and 0.03 mg/kg intravenously), respectively. Conductance, dynamic compliance and static compliance of the respiratory system were measured before and during histamine infusion (80 ng/kg/s) and expressed as percent variation. Clonidine potentiated HIB as previously reported. In contrast, rilmenidine potentiated HIB only at the dose of 1 mg/kg. As it is well known that HIB is influenced by adrenergic outflow, these results suggest that rilmenidine has less inhibitory effect than clonidine on adrenal secretion.

Adrenergic alpha-Agonists↗
PubMed1988

Respiratory mechanics for assessment of histamine bronchopulmonary reactivity in guinea pigs.

In the course of bronchial challenge, bronchopulmonary response assessment requires pleural pressure measurement. This measurement, mostly obtained in guinea pigs by a pleural catheter, is difficult to perform in anaesthetized paralysed ventilated animals needing periodical large inflations. The aim of this study was to demonstrate that the pulmonary response to intravenous histamine can be correctly appreciated from the respiratory response. In twelve anaesthetized paralysed mechanically ventilated guinea pigs, pulmonary and respiratory compliances (CL and Crs), were measured together with pulmonary and respiratory conductances (GL and Grs), using the method proposed by Rossi et al. (J. Appl. Physiol. 58: 1849-1858, 1985). Pulmonary and total respiratory mechanics were compared in the basal state, and at the end of a 5 min histamine infusion (100 ng.kg-1.sec-1). Pulmonary and respiratory compliances under histamine (HCL and HCrs), as well as pulmonary and respiratory conductances under histamine (HGL and HGrs), were expressed as a percentage of the corresponding basal values. Highly significant correlations were found between HCL and HCrs on the one hand (r = 0.98, P less than 0.001), and HGL and HGrs on the other (r = 0.97, P less than 0.001). We conclude that, in guinea pigs, the response of the total respiratory system to histamine infusion provides a simple and accurate assessment of the pulmonary response.

Animals↗
PubMed1988

Acute left ventricular dysfunction during unsuccessful weaning from mechanical ventilation.

The authors studied the hemodynamic effects of rapidly weaning from mechanical ventilation (MV) 15 patients with severe chronic obstructive pulmonary disease (COPD) and cardiovascular disease who were recovering from acute cardiopulmonary decompensation. In each patient, 10 min of spontaneous ventilation (SV) with supplemental oxygen resulted in reducing the mean esophageal pressure (X +/- SD, + 5 +/- 3 to -2 +/- 2.5 mmHg, P less than .01) and increasing cardiac index (CI) 3.2 +/- 0.9 to 4.3 +/- 1.3 1/min/M2, P less than .001), systemic blood pressure (BP 77 +/- 12 to 90 +/- 11 mmHg, P less than .001), heart rate (HR 97 +/- 12 to 112 +/- 16 beats/min, P less than .001), and, most importantly, transmural pulmonary artery occlusion pressure markedly increased (PAOPtm 8 +/- 5 to 25 +/- 13 mmHg, P less than .001), mandating a reinstitution of MV. In four patients with left ventricular (LV) catheters, the PAOP correlated with the LV end-diastolic pressure during both MV and SV. Gated blood pool imaging showed SV increased the LV end-diastolic volume index (65 +/- 24 to 83 +/- 32/M2, P less than .002) with LV ejection fraction unchanged. Patients were treated for a mean of 10 days with diuretics, resulting in a reduction of blood volume (4.55 +/- 0.9 1 to 3.56 +/- 0.55 1) and body weight (-5 kg, P less than .001). Subsequently, nine of the 15 patients were weaned successfully from mechanical ventilation with unchanged PAOP.

Adult↗
PubMed1988

Comparative effects of bisoprolol and acebutolol in smokers with airway obstruction.

1. The effects of single oral doses of 10 mg bisoprolol and 400 mg acebutolol on respiratory function were studied in nine smokers with airway obstruction in a double-blind, placebo-controlled experiment. 2. The effects of the drugs were assessed by measuring specific airway conductance (sGaw) for 3 h after their administration and by studying their interaction with the bronchodilator response to inhaled salbutamol. 3. sGaw did not change for 3 h after bisoprolol or acebutolol administration. The bronchodilator response to inhaled salbutamol was not affected by bisoprolol but significantly reduced by acebutolol (P less than 0.05 vs placebo). 4. Under these conditions, bisoprolol behaves like a selective beta 1-adrenoceptor antagonist but acebutolol exhibits less beta 1-adrenoceptor selectivity.

Acebutolol↗
PubMed1988

Impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension.

It has been suggested that stimulation of adrenoreceptors could be responsible for some of the haemodynamic effects of isoflurane. But there are no solid data demonstrating the role of sympatho-adrenal stimulation induced by pain during isoflurane administration. The impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension has been investigated in 28 patients (47-76 years), scheduled for total hip arthroplasty. After premedication with morphine hydrochloride (0.1 mg/kg), patients were randomly assigned to receive either no fentanyl (control group) or fentanyl (5 micrograms/kg before tracheal intubation, 5 micrograms/kg before skin incision, and 2 micrograms/kg each 15 min during the 1st hour). Isoflurane was given to maintain mean arterial blood pressure in the range 6.7-8 kPa in both groups. Haemodynamic data and blood samples for determination of plasma renin activity (PRA) and epinephrine (E) and norepinephrine (NE) levels were collected before and during hypotension. The fentanyl group and the control group differed significantly during hypotension: heart rate, cardiac index, oxygen consumption and E, NE and PRA were lower (P less than 0.01) in the fentanyl group than in control group. Fentanyl lowered the required concentration of isoflurane to achieve the same degree of hypotension (end-tidal concentration: 0.8 +/- 0.2% in the fentanyl group and 1.4 +/- 0.15% in the control group; P less than 0.001). Our results demonstrate that the cardiovascular effects of higher isoflurane concentrations in the absence of narcotic analgesia are counterbalanced by adrenergic stress stimulation of released epinephrine and norepinephrine. Among the likely reasons for catecholamine release during isoflurane administration, inadequate analgesia may be considered.

Aged↗
PubMed1988

Effects of cardioselective beta blockade on the peripheral lung in guinea pigs.

Impairment of lung function with selective beta-1 blocking drugs has been repeatedly demonstrated in guinea pigs, normal subjects and asthmatic patients. The effects of several beta blockers, propranolol (non-selective), atenolol (beta-1 selective), IPS 339 (beta-2 selective) on histamine-induced bronchoconstriction have been investigated in 30 anaesthetized and mechanically ventilated guinea pigs, measuring changes in conductance and dynamic compliance. Their effects on peripheral lung, where only beta-2 adrenoceptors are present, were more specifically assessed using changes in lung distensibility by means of static pressure-volume curves. Atenolol (1 mg.kg-1), IPS 339 (2 mg.kg-1) and propranolol (2 mg.kg-1) enhanced histamine-induced decrease in lung distensibility, conductance and dynamic compliance. The decrease was of the same order of magnitude for all three parameters. Atenolol (1 mg.kg-1) and propranolol (2 mg.kg-1) decreased lung distensibility to the same extent. By contrast low dose atenolol (0.1 mg.kg-1) did not potentiate histamine-induced bronchoconstriction although this dose did produce a significant cardiac beta blockade. These results demonstrate that 1) beta blockers have a clear effect on the peripheral lung, 2) beta-1 adrenoceptors are not involved in pulmonary effects of cardioselective drugs. They suggest that dose dependent loss of selectivity is the major mechanism behind impairment of lung function following such drugs.

Adrenergic beta-Antagonists↗
PubMed1988

Mechanism of histamine-induced epinephrine release in guinea pig.

The aims of this study were to provide direct evidence that in anesthetized guinea pigs i.v. administration of histamine induces sympathoadrenal activation and to identify the source and mechanism of histamine-induced epinephrine release. Plasma epinephrine measurements were used as the index of sympathoadrenal activity. In intact guinea pigs, histamine infusion caused a 3-fold rise in plasma epinephrine levels. In guinea pigs pretreated with 6-hydroxydopamine to obtain chemical sympathectomy, the rise in plasma epinephrine induced by histamine was distinctly smaller than in controls. This rise was completely inhibited in guinea pigs pretreated with the ganglion blocking agent hexamethonium and in pithed guinea pigs. Pretreatment with the H2-receptor antagonist cimetidine or the H1-receptor antagonist mepyramine reduced the rise in plasma epinephrine. These results demonstrate that in guinea pigs, epinephrine is released not only from the adrenal medulla but also from nerve endings and that histamine releases epinephrine by indirect action through central reflex pathways.

Animals↗
PubMed1988

Comparison of the dose-response curves obtained by forced oscillation and plethysmography during carbachol inhalation.

We compared the cumulative dose-response curves obtained during carbachol inhalation by simultaneous measurements of airway specific conductance (sGaw) and respiratory conductance, in 23 subjects with or without bronchial hyperresponsiveness. The sGaw was measured by a body plethysmograph, whilst the random noise forced oscillation technique (FOT) was used to determine respiratory conductance. The sGaw was compared to respiratory conductance extrapolated to zero frequency (Grs0). Bronchial sensitivity was assessed by the threshold dose of carbachol (TD) that induced a decrease in sGaw and Grs0 of twice the baseline coefficient of variation. Bronchial responsiveness was assessed by the slopes (S) of the individual dose-response curves. The TD and S values obtained by FOT and by plethysmography were closely correlated (p less than 0.001). The carbachol doses inducing a 50% reduction in sGaw were equivalent to those causing a 42% reduction in Grs0 (r = 0.90; p less than 0.001). During bronchial challenge testing, FOT provides comparable information in terms of bronchial sensitivity and responsiveness to that supplied by plethysmography.

Adult↗
PubMed1987

Failure of enhancement by labetalol of bronchopulmonary effects of histamine in guinea-pigs: independence of alpha-adrenoceptor antagonism.

The effect of labetalol on histamine-induced bronchoconstriction was studied in anaesthetized guinea-pigs. Unlike propranolol (1 mg kg-1), the same dose of labetalol did not enhance histamine-induced bronchoconstriction. To determine whether the absence of enhancement of the respiratory effects of histamine by labetalol was due to its alpha 1-blocking properties or to its partial agonist activity at beta 2-adrenoceptors, the effects of propranolol plus prazosin and of propranolol plus labetalol on histamine-induced bronchoconstriction were examined. In both cases, the bronchoconstrictor effects of histamine were enhanced to the same extent as with propranolol alone. These data support the hypothesis that the non impairment of respiratory mechanics by labetalol is not due to antagonism at alpha-adrenoceptors and may be mediated by its partial agonist activity at beta 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Effects of 17beta-estradiol on peripheral and coronary vasomotor function in postmenopausal women].

Women appear to be protected, until the menopause, from the development of coronary artery syndromes. This protective effect seems to be due to the beneficial effect of ovarian hormones, in particular oestrogens. A number of potential mechanisms for the protective effect of oestrogens have been proposed. An important postulated mechanism could be by improving the function of vascular endothelium. In this review, we present the currently published studies that have evaluated the effects of 17 beta-estradiol, the only oestrogen used in France for hormone replacement therapy, on peripheral and coronary vasomotor function in postmenopausal women.

Blood Circulation↗
PubMedDate not supplied

[Cutaneous microvascular flow studied by laser-Doppler. A study of 100 healthy volunteers].

Cutaneous capillary flow (tip of the 3rd right finger) was measured with a laser Doppler (Periflux, Perimed), in 100 healthy volunteers without any history of hypertensive or vasospatic diseases, 15 females smoke and were taking contraceptive drugs. Smokers (n = 16 M, 25 F) stopped smoking 3 hours before the study. Basal laser Doppler flux (BLDF), amplitude of vasomotion waves (AV), post-occlusive reactive hyperthermia peakflow (F Max), difference between BLDF and F Max (delta F Max), time to reach 50 percent of the initial value (t1/2 r) and total recovery (tr), t Max (peak of over-shoot) and t/2 over shoot were measured. F Max after heating stimulus (40 degrees) (f Max H), delta F Max H (difference between BLDF and F Max H) and t Max H time (mn) to reach F Max H were measured before a cold stimulus was applied. Results were expressed in arbitrary units (cvolts), BLDF showed inter-individual variation but was reproducible over months in the same subject. The basal flux was statistically different between males (352.7 +/- 21.7) and females (249.6 +/- 22.4). Spontaneous vasomotion waves and different times (in sec.) to reach the peak after three minutes of arterial occlusion could be measured with this technique. These normal range of values can allow comparison and assessment of variations in pathological conditions, mainly Raynaud's phenomenon, high blood pressure, diabetes, smokers, sickle-cell anemia. Acute pharmacological tests can be carried out with drugs showing specific action on microcirculation and spontaneous vasomotion.

Adult↗