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Biomedical subjects

C Landault

Publications and source records attributed to C Landault.

At least 19 recordsLinked to original sources
PubMed2001

Haemodynamic changes and vasopressin release are not consistently associated with carbon dioxide pneumoperitoneum in humans.

BACKGROUND: Conflicting haemodynamic changes, suggested to be caused by vasopressin release, have been reported during carbon dioxide (CO2) pneumoperitoneum. However, peritoneal stimulations including open surgery cause both a systemic vasopressor response and a vasopressin release, which are suppressed by opiate administration. Also, a decreased venous return of blood to the heart causes vasopressin release. Furthermore, previous haemodynamic assessments of laparoscopic surgery have been conducted using various anaesthetic regimens, which are likely to have caused various haemodynamic effects. We hypothesised that intraoperative haemodynamic and/or humoral changes would not be observed in association with laparoscopic surgery provided that, (a) normovolaemia is continuously maintained using transoesophageal echocardiographic (TEE) assessment, and (b) adequate depth of general anaesthesia is continuously maintained by bispectral index (BIS) monitoring and high plasma Ievel opiate administration. METHODS: Twenty ASA 1 women undergoing laparoscopic surgery received 10 ml. kg-1 lactated Ringer's solution and thereafter were randomly allocated to receive intraoperatively either 8 ng. ml-1 or 4 ng. ml-1 plasma remifentanil concentrations while BIS was maintained at 50+/-5 by isoflurane alteration. The group receiving 4 ng. ml-1 remifentanil was used as control. Expired CO2 was maintained within a 32-38 kPa range throughout the investigation. Complete TEE haemodynamic investigation was performed before pneumoperitoneum (PP) (T1), and during PP horizontal (T2), with a head-up tilt (T3), with a head-down tilt (T4), horizontal (T5), and PP released (T6). Plasma vasopressin, epinephrine and norepinephrine levels were measured at T1, T3, and T6. ANOVA, Student's t-test and Mann-Whitney U-test were used for statistical analysis. RESULTS: Haemodynamic indices and humoral values did not change significantly within and between remifentanil groups throughout the investigation (all P<0.05). CONCLUSION: Continuous adequate depth of anaesthesia and normovolaemia may have prevented both a humoral and a haemodynamic response, initiated in the peritoneum by the contact with CO2 in previous investigations.

Adult↗
PubMed1999

Haemodynamic changes associated with portal triad clamping are suppressed by prior hepatic pedicle infiltration with lidocaine in humans.

Portal triad clamping (PTC) reduces venous return of blood to the heart. However, the decrease in cardiac index (CI) is associated with an unexpected increase in mean arterial pressure (MAP) and the 40% increase in systemic vascular resistance is greater than anticipated in compensation for the 10% decrease in CI. We hypothesized that a reflex elicited in the peritoneum accounted for this unanticipated haemodynamic response. Twenty patients undergoing liver resection were allocated randomly to have hepatic pedicle infiltration before PTC with either lidocaine 200 mg or placebo. MAP was recorded, and plasma osmolality and plasma concentrations of vasopressin, epinephrine, norepinephrine, dopamine, renin and endothelin were measured. After PTC, MAP increased significantly in the placebo group but decreased significantly in the lidocaine group. Plasma concentrations of vasopressin, epinephrine and norepinephrine increased significantly in the placebo group. Plasma concentrations of vasopressin decreased significantly in the lidocaine group, while plasma concentrations of epinephrine and norepinephrine were unchanged. A subsequent study in eight patients found that neither haemodynamic nor hormonal changes associated with PTC in the placebo group were altered by administration of lidocaine 200 mg i.m. before PTC.

Adolescent↗
PubMed1994

Reduction of hyperglycemia after oral glucose load by the new alpha 2-adrenergic receptor antagonist SL 84.0418 in healthy subjects.

OBJECTIVE: To assess the antihyperglycemic activity of a new peripherally acting alpha 2-adrenergic receptor antagonist, SL 84.0418 in healthy volunteers METHODS: This was a randomized, double-blind crossover study. The effects of 10, 50, and 100 mg SL 84.0418 on blood glucose, plasma insulin, C-peptide, glucagon, epinephrine, and norepinephrine were investigated in comparison with placebo and 5 mg glipizide before and after an oral glucose challenge (75 gm). RESULTS: Peak blood glucose and area under the blood-glucose curve were dose-dependently reduced by SL 84.0418; the extent of this reduction was similar with 100 mg SL 84.0418 and glipizide. Glipizide but not SL 84.0418 decreased nadir blood glucose. Plasma insulin and C-peptide were increased by glipizide but not by SL 84.0418. Treatments did not modify plasma glucagon. Plasma epinephrine increased during glipizide treatment and plasma norepinephrine increased during treatment with 50 and 100 mg SL 84.0418. Systolic and diastolic blood pressure were moderately enhanced by 50 and 100 mg SL 84.0418. Adverse effects reflecting alpha 2-adrenergic receptor blockade occurred more frequently with 100 mg SL 84.0418. The adverse effect profile of 50 mg SL 84.0418 was not different from that observed with glipizide. CONCLUSION: The alpha 2-adrenergic receptor antagonist SL 84.0418 dose dependently reduced the increase in blood glucose after glucose load without modification of plasma insulin. It may represent an alternative to sulfonylureas in the treatment of non-insulin-dependent diabetes mellitus. Further studies are needed to assess its efficacy and tolerability in non-insulin-dependent patients.

Administration, Oral↗
PubMed1994

Inhaled nitric oxide reverses the increase in pulmonary vascular resistance induced by permissive hypercapnia in patients with acute respiratory distress syndrome.

BACKGROUND: The aim of this prospective study was to determine if inhaled nitric oxide (NO) would reverse the increase in pulmonary arterial pressures and in pulmonary vascular resistance induced by acute permissive hypercapnia in patients with acute respiratory distress syndrome. METHODS: In 11 critically ill patients (mean age 59 +/- 22 yr) with acute respiratory distress syndrome (Murray Score > or = 2.5), the lungs were mechanically ventilated with NO 2 ppm during both normocapnic and hypercapnic conditions. Four phases were studied: normocapnia (arterial carbon dioxide tension 38 +/- 6 mmHg, tidal volume (655 +/- 132 ml); normocapnia plus inhaled NO 2 ppm; hypercapnia (arterial carbon dioxide tension 65 +/- 15 mmHg, tidal volume 330 +/- 93 ml); and hypercapnia plus inhaled NO 2 ppm. Continuous recordings were made of heart rate, arterial pressure, pulmonary artery pressure, tracheal pressure, and tidal volume (by pneumotachograph). At the end of each condition, arterial pressure, pulmonary artery pressure, cardiac filling pressures, and cardiac output were measured. Simultaneous arterial and mixed venous blood samples were obtained to measure arterial oxygen tension, arterial carbon dioxide tension, mixed venous oxygen tension, arterial hemoglobin oxygen saturation, mixed venous hemoglobin oxygen saturation, pH, and blood hemoglobin and methemoglobin concentrations (by hemoximeter). In addition, plasma concentrations of catecholamines were measured with a radioenzymatic assay. In 5 patients, end-tidal carbon dioxide tension was measured with a nonaspirative infrared capnometer. Calculations were made of pulmonary vascular resistance index, systemic vascular resistance index, true pulmonary shunt, and alveolar dead space. RESULTS: During hypercapnia, NO decreased pulmonary vascular resistance index from 525 +/- 223 to 393 +/- 142 dyn.s.cm-5.m-2 (P < 0.01), a value similar to that measured in normocapnic conditions (391 +/- 122 dyn.s.cm-5.m-2). It also reduced mean pulmonary artery pressure from 40 +/- 9 to 35 +/- 8 mmHg (P < 0.01). NO increased arterial oxygen tension (inspired oxygen fraction 1) from 184 +/- 67 to 270 +/- 87 mmHg during normocapnia and from 189 +/- 73 to 258 +/- 101 mmHg during hypercapnia (P < 0.01). NO decreased true pulmonary shunt during normocapnia (from 34 +/- 3% to 28 +/- 4%, P < 0.001) but had no significant effect on it during hypercapnia (39 +/- 7% vs. 38 +/- 8.5%). In five patients, NO resulted in a decrease in alveolar dead space from 34 +/- 7% to 28 +/- 10% in normocapnic conditions and from 30 +/- 9% to 22 +/- 10% in hypercapnic conditions (P < 0.05). CONCLUSIONS: Inhaled NO completely reversed the increase in pulmonary vascular resistance index induced by acute permissive hypercapnia. It only partially reduced the pulmonary hypertension induced by acute permissive hypercapnia, probably because the flow component of the increase in pulmonary pressure (i.e., the increase in cardiac output) was not reduced by inhaled NO. A significant increase in arterial oxygenation after NO administration was observed during normocapnic and hypercapnic conditions. A ventilation strategy combining permissive hypercapnia and inhaled NO may reduce the potentially deleterious effects that permissive hypercapnia alone has on lung parenchyma and pulmonary circulation.

Administration, Inhalation↗
PubMed1994

Suspected postprandial hypoglycemia is associated with beta-adrenergic hypersensitivity and emotional distress.

Suspected postprandial (reactive or idiopathic) hypoglycemia is characterized by predominantly adrenergic symptoms appearing after meals rich in carbohydrates and by their rare association with low blood glucose level (< 2.77 mmol/L). We studied heart rate, blood pressure, plasma insulin, C-peptide, and catecholamine responses during a 5-h oral glucose tolerance test in eight patients with suspected postprandial hypoglycemia and eight age-, sex-, and body mass index-matched healthy controls. We also evaluated beta-adrenergic sensitivity by using the isoproterenol sensitivity test. Psychological profile was assessed by the Symptom Checklist (SCL-90R) self-report symptom inventory. Patients with suspected postprandial hypoglycemia had higher beta-adrenergic sensitivity (defined as the dose of isoproterenol required to increase the resting heart rate by 25 beats/min) than controls (mean +/- SEM, 0.8 +/- 0.13 vs. 1.86 +/- 0.25 microgram isoproterenol; P = 0.002). After administration of glucose (75 g) blood glucose, plasma C-peptide, plasma epinephrine, and plasma norepinephrine responses were identical in the two groups, but plasma insulin was higher in the patients (group effect, P = 0.02; group by time interaction, P = 0.0001). Both heart rate and systolic blood pressure were significantly higher (but remained in the normal range) after glucose administration in patients with suspected postprandial hypoglycemia than in controls (group by time interactions, P = 0.004 and 0.0007, respectively). After glucose intake, seven patients had symptoms (palpitations, headache, tremor, generalized sweating, hunger, dizziness, sweating of the palms, flush, nausea, and fatigue), whereas in the control group, one subject reported flush and another palpitations, tremor, and hunger. Analysis of the SCL-90R questionnaire revealed that patients had emotional distress and significantly higher anxiety, somatization, depression, and obsessive-compulsive scores than controls. We may conclude that patients with suspected postprandial hypoglycemia have normal glucose tolerance, increased beta-adrenergic sensitivity, and emotional distress.

Adult↗
PubMed1993

Beta-adrenoceptor blockade potentiates acute exercise-induced release of atrial natriuretic peptide by increasing atrial diameter in normotensive healthy subjects.

The role of atrial distension and/or adrenergic mechanisms in the regulation of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP, norepinephrine (NE), epinephrine (E) and left atrial diameter at rest, during and after graded bicycle exercise has been studies in 8 healthy male subjects after single doses of placebo, tertatolol 5 mg (a non-selective beta-adrenoceptor blocker), prazosin 1 mg (an alpha 1-adrenoceptor antagonist) and their combination. Systolic and diastolic left atrial diameters were measured before, during and just after exercise by bidimensional echocardiography. Exercise caused an increase in plasma ANP, which was greater after tertatolol alone, and tertatolol plus prazosin, than after placebo or prazosin alone; the mean area under the plasma ANP concentration curve was increased by 35% after tertatolol alone, by 45% after tertatolol and prazosin compared to placebo, and by 82% and 94%, respectively when compared to prazosin alone. The rise in plasma ANP was more marked during the post-exercise period: 80% after tertatolol alone, 67% after tertatolol and prazosin compared to placebo, and 133% and 115%, respectively, compared to prazosin alone. The rise in plasma ANP was accompanied by an increase in both the systolic and diastolic atrial diameter, which was also significantly greater after tertatolol alone and the combination than placebo, or after prazosin alone. beta-Adrenoceptor blockade alone did not affect the plasma catecholamine concentrations, but the exercise-induced increase in plasma norepinephrine was significantly potentiated by prazosin and by prazosin plus tertatolol, and that of plasma epinephrine by the drug combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1993

[Comparison of hemodynamic effects of the laryngeal mask and the orotracheal tube].

This prospective study was designed to compare the haemodynamic response to insertion of either a laryngeal mask or an orotracheal tube. Twenty patients scheduled for orthopaedic surgery were randomly assigned to two groups : laryngeal mask group (n = 10) and orotracheal tube group (n = 10). Patients were premedicated with flunitrazepam (1 mg i.m.) and anaesthesia was induced with propofol (bolus of 2.5 mg.kg-1, followed by a continuous infusion of 10 mg.kg-1.h-1) and vecuronium (0.1 mg.kg-1). Heart rate and mean arterial pressure were assessed non-invasively before and after induction of anaesthesia and immediately after tube or laryngeal mask insertion. Orotracheal intubation elicited a significant increase in heart rate (92 +/- 16 vs 77 +/- 19 b.min-1, p < 0.05) and in mean arterial pressure (117 +/- 21 vs 85 +/- 16 mmHg, p < 0.05), whereas there was significant increase in heart rate (74 +/- 11 vs 72 +/- 12 b.min-1) and mean arterial pressure (86 +/- 8 vs 81 +/- 10 mmHg) after insertion of the laryngeal mask. In both groups, plasma catecholamine concentrations were not significantly modified after tube or laryngeal mask insertion. It is concluded that, under propofol anaesthesia, laryngeal mask insertion does not induce any significant haemodynamic response in ASA 1 patients. In the opposite, orotracheal intubation increases both heart rate and mean arterial pressure.

Adult↗
PubMed1993

Tertatolol potentiates exercise-induced atrial natriuretic peptide release by increasing atrial diameter in healthy subjects.

To evaluate the contribution of atrial distension and/or adrenergic mechanisms in the regulation of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP, norepinephrine (NE), epinephrine (E), and left atrial diameter were measured at rest, during, and after graded upright standardised bicycle exercise in 8 healthy male subjects after single-dose administration of placebo, tertatolol (5 mg), prazosin (1 mg), or combination of tertatolol (5 mg) and prazosin (1 mg). Systolic and diastolic left atrial diameters were measured before, during, and just after exercise by bidimensional echocardiography. Exercise raised plasma ANP concentrations. This rise was greater on tertatolol alone and tertatolol and prazosin than on placebo or prazosin alone: mean area under the plasma ANP concentration curve increased by 35% on tertatolol alone, 45% on tertatolol and prazosin when compared with placebo (p < 0.01), and by 82 and 94%, respectively, when compared with prazosin alone (p < 0.01). The rise in plasma ANP was greater during the postexercise period: 80% for tertatolol alone, 67% for tertatolol and prazosin when compared with placebo (p < 0.01) and 133 and 115%, respectively, when compared with prazosin alone (p < 0.01). The rise in plasma ANP was accompanied by an increase in both systolic and diastolic atrial diameters which was significantly greater on tertatolol alone and on the tertatolol and prazosin combination than on placebo or prazosin alone (p < 0.001). Beta-blockade alone did not affect plasma catecholamine concentrations but exercise-induced increase in plasma NE was significantly potentiated by prazosin and the prazosin and tertatolol combination, and that of plasma E by the prazosin and tertatolol combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

Plasma calcitonin gene-related peptide decreases in chronic congestive heart failure.

To investigate the role of calcitonin gene-related peptide (CGRP) in cardiac failure, a sensitive and specific radioimmunoassay was developed to study plasma levels of CGRP in 37 normal subjects and 41 patients with heart failure (HF). The mean plasma levels of CGRP were 294.3 pg.ml-1 (SEM: 41.4) in normal subjects and 121.2 pg.ml-1 (SEM: 21.2) in HF patients. The significant decrease observed in HF patients suggests that CGRP is involved in the pathogenesis of heart failure via a direct effect or via modulation of sympathetic nervous activity.

Calcitonin Gene-Related Peptide↗
PubMed1992

[Laparoscopic surgery versus laparotomy. Comparative analysis of stress markers].

The place of laparoscopic surgery continues to increase in the field of surgery in our specialty. Although the advantages would seem to be obvious, it seemed to us interesting to quantify, if possible, the parameters of operative stress and compare laparoscopic surgery with conventional surgery. Markers studied are Prolactin, Cortisol, Adrenaline, Nor-Adrenaline, Dopamine and the Beta-Endorphins. The only marker that shows any difference in the two procedures in our study is Beta-Endorphin which is significantly less raised in laparoscopic surgery directly after the operation (p less than 0.01). This was very specific for pain, which is one of the benefits of this technique and shown in this parameter which confirms the clinical impression. The curves of the changes in the different markers have been analysed and discussed.

Adult↗
PubMed1991

Low molecular weight hydroxyethyl starch 6% compared to albumin 4% during intentional hemodilution.

Intentional normovolemic hemodilution was chosen as the model to compare a 6% low molecular weight hydroxyethyl starch (LMW HES) to 4% albumin. The study ran over the plasma exchange period for 24 h. Nine patients, scheduled for abdominal aortic surgery, were included in each group. After basal measurements, blood was withdrawn and simultaneously replaced by either 4% albumin (Group 1) or 6% LMW HES (Group 2) to achieve a final hematocrit of approximately 30%. Hemodynamic blood oxygen gas and hormonal plasma levels were determined before hemodilution then at 30 min, 1, 2, 3, and 24 h after the end of hemodilution. Basal value for total blood volume was 4377 +/- 162 ml in group 1 and 4138 +/- 315 ml in group 2. As in both groups the decrease in blood cell volume was exactly compensated by the increase in plasma volume, no significant change in total blood volume (respectively 4432 +/- 159 and 4305 +/- 267 ml) was observed. Throughout the study, in both groups, no significant change in mean arterial and right atrial pressures was observed. In group 2 (LMW HES), a significant increase of pulmonary capillary wedge pressure was noted 120 min after hemodilution. After hemodilution, despite a significant decrease in arterial oxygen O2 content, systemic oxygen transport did not significantly vary until 24 h in relation to the increased cardiac index. An increase in O2 extraction was observed after the exchange but no further increase was observed until the 24 h. No significant changes either in global O2 consumption or in lactate concentration were detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

The alpha 2-adrenergic receptor antagonist yohimbine inhibits epinephrine-induced platelet aggregation in healthy subjects.

Onset of sudden death, myocardial infarction, and stroke occurs more likely in the morning hours. Similarly, a morning increase in epinephrine-induced platelet aggregation was observed accompanied by an increase in plasma catecholamines. Inhibition of the morning increase in platelet aggregation would be of therapeutic benefit. In this study the effect of the selective alpha 2-adrenergic receptor antagonist yohimbine on platelet aggregation was evaluated in healthy subjects. Yohimbine administered orally selectively antagonized epinephrine but not collagen, arachidonic acid, or adenosine diphosphate-induced ex vivo platelet aggregation. The lowest dose of yohimbine that significantly inhibited epinephrine-induced platelet aggregation was 8 mg. The inhibitory effect of yohimbine on platelet aggregation lasted 10 hours with the 12 mg dose. At the doses studied (4, 8, and 12 mg), yohimbine did not modify blood pressure, standing heart rate, or plasma catecholamine or glucose concentrations. Twelve milligrams of yohimbine moderately but significantly accelerated supine heart rate (mean maximal increase, 7 +/- 3 beats/min). Further clinical studies are needed to evaluate whether bedtime administration of 12 mg yohimbine may block the morning increase in epinephrine-induced platelet aggregation.

Administration, Oral↗
PubMed1991

Peripheral vascular effects of thiopental and propofol in humans with artificial hearts.

The peripheral vascular effects of thiopental 5 mg/kg and propofol 2.5 mg/kg were compared in five patients whose lungs were being ventilated and in whom a Jarvik-7 artificial heart had been implanted. The patients were monitored, using catheters that had been surgically inserted into the radial artery, the right and left atria, and the pulmonary artery. The Jarvik-7 settings were modified to render the artificial heart "preload independent" and to maintain cardiac output constant. Each patient received both drugs, with the interval between each drug ranging from 16 to 28 h. Hemodynamic parameters and catecholamine and atrial natriuretic peptide plasma concentrations were measured before drug administration and 5, 10, 15, 30, and 45 min later. Both drugs significantly decreased arterial pressure, systemic vascular resistance index, pulmonary arterial pressure (PAP), and right and left atrial pressures (RAP and LAP, respectively). However, propofol 2.5 mg/kg induced a significantly greater and more prolonged decrease in arterial pressure, systemic vascular resistance index, and RAP than that after administration of thiopental 5 mg/kg (P less than 0.05). Five minutes after drug injection, mean arterial pressure decreased by 21% after thiopental and by 39% after propofol (P less than 0.01); systemic vascular resistance index decreased by 21% after thiopental and by 44% after propofol (P less than 0.05); RAP decreased by 20% after thiopental and by 50% after propofol (P less than 0.05); mean PAP decreased by 18% after thiopental and by 32% after propofol (P less than 0.09); and LAP decreased by 40% after thiopental and by 46% after propofol (P less than 0.2). With both drugs, atrial natriuretic peptide, norepinephrine, and epinephrine plasma concentrations remained stable throughout the study period. Because cardiac output was maintained constant throughout the study, these results suggest that propofol 2.5 mg/kg is a more potent vasodilator of venous and arterial beds than is thiopental 5 mg/kg.

Adult↗
PubMed1990

Alterations in beta-adrenergic sensitivity and platelet alpha 2-adrenoceptors in obese women: effect of exercise and caloric restriction.

1. Peripheral adrenergic responses were studied in eight obese women before and after 15 days of caloric restriction (2500 kJ/day) and in eight sex- and age-matched lean controls. 2. beta-Adrenergic sensitivity (defined as the dose of isoprenaline required to increase resting heart rate by 25 beats/min) was evaluated before and after the diet. Density and affinity (determined as the apparent dissociation constant) of platelet alpha 2-adrenergic receptors, and plasma adrenaline and noradrenaline levels, were measured after overnight bed-rest and after 9 min of standardized exercise performed before and after the low caloric diet. 3. Before the diet basal antecubital venous plasma noradrenaline concentrations were lower in obese women when compared with lean women (0.94 +/- 0.06 vs 1.27 +/- 0.17 nmol/l, P less than 0.02). Isoprenaline sensitivity did not differ between lean and obese women. 4. At rest, platelet alpha 2-adrenoceptor density was lower in overweight than in lean women (129 +/- 21 vs 168 +/- 16 fmol/mg of protein, P less than 0.02). Exercise significantly increased platelet alpha 2-adrenoceptor density and decreased affinity in lean women. This decrease correlated with the rise in plasma noradrenaline. 5. In obese women exercise did not modify platelet alpha 2-adrenoceptor density or affinity, despite a significant increase in plasma catecholamines. However, the increase in plasma noradrenaline during exercise was lower in obese women. 6. The low caloric diet produced a beta-adrenergic supersensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Unawareness of hypoglycemia by insulin-dependent diabetics.

After several years of insulin therapy, about 20% of insulin-dependent diabetics have little or no perception of hypoglycaemia because of a loss of the adrenergic warning symptoms. This defect, poorly correlated with the presence of autonomic neuropathy, has been classically explained by a defect in the catecholamine secretion. We compared the hormonal counterregulation during hypoglycaemia induced by subcutaneous injection of insulin in 7 insulin-dependent diabetics with poor perception of hypoglycaemia and experiencing repeated episodes of severe hypoglycaemia (group A) and 7 insulin-treated diabetics with very good perception of hypoglycaemia and not experiencing severe hypoglycaemia (group B). Groups A and B were similar in terms of age, duration of diabetes, HbA1c level and degenerative complications. The glucagon levels were identical and non-reactive in the two groups. The basal levels and secretion peaks of adrenaline, noradrenaline, growth hormone and cortisol were similar between the two groups, but there was a significant delay in secretion in group A with a blood glucose threshold of adrenergic secretion of between 3.1 +/- 0.5 and 1.6 +/- 0.2 mmoles/l in group A and between 4.6 +/- 0.3 and 3.2 +/- 0.2 mmoles/l in group B (P less than 0.05). This delayed secretion could be explained by desensitisation of the hypothalamic glucostat and could be due to the frequency and/or severity of hypoglycaemic episodes.

Adult↗
PubMed1990

[Noninvasive evaluation of partial beta adrenergic agonist properties of xamoterol in cardiac insufficiency].

The effects of an intravenous injection of 0.15 mg/Kg of xamoterol were studied non-invasively under basal conditions and during beta-1-adrenergic stimulation with dobutamine in 16 patients with dilated cardiomyopathy and severe cardiac failure. Xamoterol did not cause any detectable agonist effect but was well tolerated under basal conditions. Its potential antagonist effect was only detected during the dobutamine infusion: xamoterol significantly reduced the increase in heart rate (p less than 0.001), the systolic blood pressure (p less than 0.01), the rate-pressure product (p less than 0.001) and the cardiac index (p less than 0.001) produced by the administration of dobutamine.

Adrenergic beta-Agonists↗