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Biomedical subjects

D Cousineau

Publications and source records attributed to D Cousineau.

At least 19 recordsLinked to original sources

Effects of intra-oral sucrose on crying, mouthing and hand-mouth contact in newborn and six-week-old infants.

To determine whether a single intra-oral administration of sucrose would calm infants and elicit mouthing and hand-mouth contact, crying newborn and six-week-old infants were given sucrose solution before one feed and sterile water before another in a cross-over trial. Six-week-old infants were also given sucrose and water after feeding. For the newborn infants, the calming effect was rapid, substantial and lasted for at least four minutes. Mouthing and hand-mouth contact increased, but for shorter durations. For the six-week-old infants, sucrose calmed for one minute only before feeding, but had no effects on mouthing or hand-mouth contact. The results imply that intra-oral sucrose has acute age-related effects on crying and suckling-feeding behaviour mediated by a pre-absorptive mechanism. Sucrose may tap a functional system for reducing distress related to feeding and/or regulation of infant state.

Administration, Oral↗

Constitutive nonexocytotic norepinephrine release in sympathetic curves of in situ canine heart.

Nonexocytotic norepinephrine bulk overflow from sympathetic nerves has been previously demonstrated in the perfused isolated heart only after inhibition of sympathetic nerve metabolism by hypoxia, ischemia, or metabolic inhibitors. The measurement, however, ignores simultaneous uptake of norepinephrine by sympathetic nerves. We quantitated simultaneous norepinephrine uptake and release in pentobarbital-anesthetized dogs by the use of a transient tracer approach, the multiple indicator dilution technique, combined with measurement of endogenous arterial and venous plasma norepinephrine levels. Sympathetic vesicles were previously depleted by reserpine, and desipramine was used to inhibit the neuronal membrane pump. Labeled albumin, sucrose, and norepinephrine were injected into the coronary artery, and sequential samples were collected from the coronary sinus. Reserpine pretreatment significantly depleted tissue and decreased plasma norepinephrine levels; tracer norepinephrine uptake increased slightly, and there was a substantial decrease in the rate of release of unlabeled norepinephrine. Desipramine then decreased tracer uptake and virtually eliminated norepinephrine release. We conclude that desipramine-suppressible, constitutive nonexocytotic norepinephrine release is present in cardiac sympathetic nerves.

Animals↗

[Violence and consumption of illicit drugs in Quebec adolescents. An analysis of their perceptions].

OBJECTIVE: To study adolescents' perception of the connection between violence and the consumption of illegal drugs. DESIGN: A self-administered questionnaire. SETTING: A town with 30,000 inhabitants north of Montreal. PARTICIPANTS: Almost 3300 students between the ages of 12 and 19. RESULTS: About 25% reported that they had been victims of violence by other adolescents who were, in their estimation, under the influence of an illicit drug. This rate increased significantly among adolescents who used drugs themselves, and was highest among female adolescents between the ages of 12 and 15. CONCLUSION: Students, especially young women, who consume illegal drugs are more likely to be victims of violence than those who do not. Family physicians should advise young patients of this risk.

Adolescent↗

Illicit drug use among adolescent students. A peer phenomenon?

Illicit drug use was studied in 2071 students 11 to 18 years of age. Almost all drug users had friends who consumed drugs, compared with only one third of those who did not use drugs. This suggests a bond between adolescent drug users, who form a distinct group of which most students are unaware.

Adolescent↗

Handling of tracer norepinephrine by the dog liver.

Norepinephrine handling by the dog liver was appraised by carrying out tracer-transient, multiple-indicator-dilution studies within steady-state conditions in a basal situation, during norepinephrine infusion and after the uptake inhibitor desipramine. In controls, tracer norepinephrine extraction averaged 61%, whereas bulk norepinephrine extraction was approximately 31%; intrahepatic secretion of unlabeled norepinephrine accounted for the difference. Infusion of norepinephrine, raising arterial levels more than an order of magnitude, constricted the hepatic vascular space but did not change tracer extraction; norepinephrine secretion remained essentially unchanged, and with this, bulk extraction approached tracer extraction. A theoretical analysis of norepinephrine uptake was developed. Analysis of tracer data with this indicated that the permeability surface products for influx and efflux, expressed per gram liver, did not change. Desipramine did not affect the uptake kinetics, indicating that the uptake process was virtually completely nonneurogenic. Late efflux of tracer normetanephrine product was detected but was small prior to recirculation. The study demonstrates that norepinephrine secretion ordinarily coexists with uptake and provides an approach to quantitating both.

Animals↗

Sympathetic response to maximal bicycle exercise before and after leg strength training.

Plasma catecholamine concentrations at rest and in response to maximal exercise on the cycle ergometer (278 +/- 15 watts, 6 min duration) have been measured on seven young active male subjects (19 +/- 1 years old; 80 +/- 3 kg; 176 +/- 3 cm) prior to and after a eight week leg strength training program (5RM, squat and leg press exercise). Strength training resulted in a significant increase in performance on squat (103 +/- 3 to 140 +/- 5 kg) and leg press exercise (180 +/- 9 to 247 +/- 15 kg) associated with a small significant increase in lean body mass (64.5 +/- 2.2 to 66.3 +/- 2.1 kg) and no change in maximal oxygen consumption (47.5 +/- 1.3 to 46.9 +/- 1.2 ml X kg-1 X min-1). Plasma norepinephrine (NE) and epinephrine (E) concentrations (pg X mL-1) were not significantly different before and after training at rest (NE: 172 +/- 19 vs 187 +/- 30; E: 33 +/- 10 vs 76 +/- 16) or in response to maximal exercise (NE: 3976 +/- 660 vs 4163 +/- 1081; E: 1072 +/- 322 vs 1321 +/- 508). Plasma lactate concentrations during recovery were similar before and after training (147 +/- 5 vs 147 +/- 15 mg X dL-1). Under the assumption that the "central command" is reduced for a given absolute workload on the bicycle ergometer following leg strength training, these observations support the hypothesis that the sympathetic response to exercise is under the control of information from muscle chemoreceptors.

Adult↗

Effects of captopril and a combination of hydralazine and isosorbide dinitrate on myocardial sympathetic tone in patients with severe congestive heart failure.

Changes in circulating catecholamines and transmyocardial catecholamine balance associated with improved left ventricular function were studied in patients with chronic heart failure after treatment with captopril (10 patients) and hydralazine in combination with isosorbide dinitrate (eight patients). Cardiac performance improved in response to both captopril and hydralazine-nitrate treatment. The systemic haemodynamic effects were also qualitatively similar, but the hydralazine-nitrate combination caused a greater increase in cardiac index and heart rate. Captopril did not change arterial adrenaline concentrations (0.63 to 0.60 nmol/l), arterial noradrenaline (4.2 to 3.9 nmol/l), or net transmyocardial noradrenaline release (390 to 317 pmol/min), while hydralazine-nitrate increased arterial adrenaline (0.91 to 1.47 nmol/l) and transmyocardial noradrenaline release (225 to 554 pmol/min). Although both captopril and hydralazine-nitrate treatment improve left ventricular performance in patients with chronic heart failure, hydralazine-nitrate enhances cardiac sympathetic tone and captopril does not. The clinical relevance of these findings, however, is not known.

Aged↗

Lack of liver vascular response to carotid occlusion in mildly acidotic dogs.

The effect of mild acidosis on the reduction in liver vascular volume provoked by reflex sympathetic activation was ascertained in dogs by use of the multiple indicator-dilution technique. Portal vein-hepatic vein dilution patterns were obtained following injection of a mixture containing 51Cr-labeled red blood cells (a vascular reference), 14C-labeled sucrose (an interstitial reference), and 3H-labeled water (a cellular reference). Liver vascular, interstitial, and cellular water spaces were measured in normal and mildly acidotic dogs under basal conditions and during bilateral carotid artery occlusion. Carotid occlusion resulted in a large increase in arterial blood pressure in normal and a lesser increase in acidotic dogs, but the increase in portal and hepatic vein norepinephrine and decrease in liver vascular and interstitial volumes observed in normal dogs did not occur in the acidotic animals; no change in labeled water accessible liver cellular spaces was perceptible. The data indicate that mild acidosis abolishes the ordinarily expected reduction in liver vascular volumes on sympathetic activation in the intact dog but not the arterial pressor response.

Acidosis↗

Plasma expansion effect on cardiac capillary and adrenergic exchange in intact dogs.

The effect of plasma volume expansion on transcapillary exchange and norepinephrine release in the heart was examined in pentobarbital sodium-anesthetized dogs by use of the multiple indicator-dilution technique. Animals were studied under basal conditions and following infusion of the plasma expander, dextran. Catheters were placed in coronary artery and coronary sinus in a closed-chest preparation. Labeled albumin, sucrose, and norepinephrine were injected into the coronary artery and outflow-dilution curves were secured. Analysis of these provided parameters reflecting coronary flow and permeability-surface product, and a norepinephrine tracer kinetic-bulk model provided simultaneous estimates of the rate of norepinephrine release into the myocardial interstitial space. The infusion of dextran resulted in a large increase in coronary flow without significant changes in myocardial norepinephrine release; at the same time the permeability-surface product values increased, amplifying the capacity of the higher flow to deliver substrates to sarcolemmal cells. The findings indicate that plasma volume expansion increases transcapillary exchange in the heart without activating the cardiac sympathetic system.

Animals↗

Decreased basal cardiac interstitial norepinephrine release after neuronal uptake inhibition in dogs.

The effect of neuronal uptake inhibition on basal interstitial release of norepinephrine in the canine heart was examined by use of the multiple tracer dilution-bulk balance technique. A kinetic model incorporating the effects of flow, capillary permeability-surface product for norepinephrine, the interstitial uptake rate constant for neurotransmitter, and plasma norepinephrine input and output values was used to estimate rates of uptake from and release of norepinephrine into the interstitial space. The intravenous injection of the neuronal uptake inhibitor desipramine in anesthetized dogs under basal conditions reduced interstitial uptake of tracer norepinephrine in the heart, without significant changes in plasma concentration of norepinephrine in aorta and coronary sinus. The lack of change in the arteriovenous balance for norepinephrine across the heart, in the face of the lowered uptake for this amine, suggested that the liberation of norepinephrine by cardiac sympathetic fibers was reduced. Analysis of the data with the norepinephrine tracer kinetic-bulk model showed that, after desipramine, the interstitial release of norepinephrine was reduced to the same extent as uptake was diminished. As a result, the concentration of norepinephrine in the extracellular space of the heart did not increase significantly. The findings indicate the presence of a presynaptic neuronal feedback inhibition of release, which serves to fine tune the myocardial interstitial concentration of norepinephrine in the basal state; with this, after desipramine, both norepinephrine uptake and release are correspondingly diminished.

Animals↗

Effects of a 24-h carbohydrate-poor diet on metabolic and hormonal responses during prolonged glucose-infused leg exercise.

Extant literature dealing with metabolic and hormonal adaptations to exercise following carbohydrate (CHO) reduced diets is not sufficiently precise to allow researchers to partial out the effects of reduced blood glucose levels from other general effects produced by low CHO diets. In order to shed light on this issue, a study was conducted to examine the effects of a 24-h CHO-poor diet on substrate and endocrine responses during prolonged (75 min; 60% Vo2max) glucose-infused leg exercise. Eight subjects exercised on a cycle ergometer in the two following conditions: 1) after a normal diet (CHON), and 2) after a 24-h low CHO diet (CHOL). In both conditions, glucose was constantly infused intravenously (2.2 mg . kg-1 . min-1) from the 10th to the 75th min of exercise in relatively small amounts (10.4 +/- 0.8 g). No significant differences in blood glucose concentrations were found between the two conditions at rest and during exercise although a significant increase (p less than 0.01) in glucose level was observed in both conditions after 40 min of exercise. The CHOL as compared to the CHON condition, was associated with significantly (p less than 0.05) lower resting concentrations of insulin, muscle glycogen (8.7 vs 10.6 g . kg-1), and triacylglycerol, and greater concentrations of beta-hydroxybutyrate (0.5 vs 0.2 mmol . L-1), and free fatty acids. During exercise, the CHOL condition as compared to the CHON condition, was associated with significantly (p less than 0.05) lower insulin and R values, as well as greater free fatty acid (from min 20 to 60) and epinephrine (min 60 to 75) concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗

Effects of muscle CHO-loading manipulations on hormonal responses during prolonged exercise.

This study examined the effects of a pre-experimental period of muscle carbohydrate (CHO)-loading manipulations followed by a 24-h CHO-poor diet, intended to increase muscle glycogen content and reduce hepatic glycogen levels, on substrate and endocrine responses during a period of prolonged exercise. Seven subjects pedaled a cycle ergometer for 70 min at 64% leg VO2max (1) after normal CHO intake (CHON) and (2) after leg muscle CHO loading (CHOL), both of these procedures being followed by a period of arm exercise (70 min; 70% arm VO2max) and 24 h CHO-poor intake. CHON, as compared to CHOL condition, resulted in greater blood concentrations of free fatty acids (1.8 vs 1.3 mmol X L-1), glycerol (0.41 vs 0.28 mmol X L-1), norepinephrine (2.2 vs 1.5 ng X ml-1), epinephrine (0.90 vs 0.27 ng X ml-1), and cortisol (47 vs 23 g X dl-1) at min 70 of exercise. Insulin concentrations during exercise showed a strong tendency to be lower in CHON than in CHOL condition, although the differences were not significant. There were no significant differences between the two conditions in blood glucose, lactate, and glucagon concentrations. These data indicate that muscle CHO-loading manipulations intended to specifically increase the muscle glycogen content are associated with the difference in metabolic adaptation and hormonal changes during exercise.

Adult↗

Reflex sympathetic effects on liver vascular space and liver perfusion in dogs.

The effects of sympathetic fiber activation on liver vascular volume and on the perfusion of the liver were ascertained in dogs by use of the multiple indicator-dilution technique. Portal vein-hepatic vein dilution patterns were obtained following injection of a mixture containing 51Cr-labeled red blood cells (a vascular reference), 14C-labeled sucrose (an interstitial reference), and 3H-labeled water (a cellular reference). Liver vascular, interstitial, and cellular water spaces were measured from the dilution data under control conditions and following activation of the sympathetic system by bilateral occlusion of carotid arteries. Carotid occlusion significantly increased plasma norepinephrine values without changing plasma epinephrine concentration, indicating that the resulting reflex sympathetic activation was selective for peripheral fibers. Although average blood flow did not change, liver vascular volume decreased by 40% during the sympathetic activation, and sucrose interstitial space and accessible cellular water space were unchanged. These findings indicate that there were no areas of no flow in the liver during the sympathetic activation, despite the observed large diminution in vascular blood content.

Animals↗

Lack of reflex increase in myocardial sympathetic tone after captopril: potential antianginal effect.

Many vasodilators have been tried as antianginal agents, but the reflex increase in sympathetic tone produced by these drugs necessitate their use with caution in patients with angina. In the first part of this study, captopril was given to 14 patients with angina and systolic arterial pressures of greater than 120 mm Hg. Over the short term, captopril decreased arterial blood pressure (from 110 +/- 18 to 98 +/- 18 mm Hg, p less than .01) without increasing heart rate (75 +/- 15 vs 74 +/- 15 beats/min), arterial concentrations of epinephrine (0.38 +/- 0.28 vs 0.34 +/- 0.25 nM) or norepinephrine (2.7 +/- 2.1 vs 2.8 +/- 2.1 nM), or transmyocardial norepinephrine balance (216 +/- 254 vs 146 +/- 170 p mol/min). Captopril decreased average myocardial oxygen consumption (9.7 +/- 4.1 to 8.2 +/- 2.7 ml/min, p less than .01). Given over the long term (mean 5.5 months), captopril decreased the severity of angina from NYHA classification 3.0 +/- 0.8 to 1.6 +/- 0.8. In the second part of this study, captopril was given in a prospective, randomized, double-blind, placebo-controlled study to 21 patients with stable exercise-induced angina and systolic arterial pressures greater than 120 mm Hg. Captopril increased exercise time (309 +/- 137 vs 374 +/- 142 sec, p less than .05) without changing anginal threshold (rate-pressure product 17.0 +/- 6.0 vs 17.1 +/- 5.6 X 10(-3)). We conclude that captopril decreases mean arterial pressure without causing a reflex increase in myocardial sympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Tracer norepinephrine kinetics in coronary circulation of patients with heart failure secondary to chronic pressure and volume overload.

Controversy exists over the nature of the abnormality in cardiac sympathetic nerves in heart failure. In the cardiomyopathy of the Syrian hamster, reduction in tissue stores and increased turnover of norepinephrine is clearly associated with excessive sympathetic stimulation but in animal models and humans with heart failure secondary to mechanical overload there is evidence for depression of neuronal uptake. Because norepinephrine is both released and taken up by sympathetic fibers it is impossible to assess norepinephrine kinetics in an intact heart without separating these two functions. A technique for doing so has recently been developed in normal dogs and we therefore acquired similar data in humans with heart failure secondary to chronic pressure and volume overload. The technique involves the combination of transient norepinephrine tracer coronary sinus outflow in relation to intravascular and interstitial references after simultaneous injection into the left coronary artery and the measurement of endogenous norepinephrine concentrations in artery and coronary sinus. We found a marked reduction in cardiac norepinephrine release and uptake in a group of patients with clinical left ventricular failure secondary to mechanical overload, relative to a group of patients with no failure. Norepinephrine balance and overflow across the heart were not significantly different. We conclude that there is hypofunction of the cardiac sympathetic nerves in heart failure secondary to mechanical overload and that traditional methods are inadequate in assessing cardiac norepinephrine kinetics when there are simultaneous changes in neuronal uptake and release.

Adult↗

Plasma norepinephrine, epinephrine, and dopamine beta-hydroxylase activity during exercise in man.

Many experimental studies have utilized the activity of dopamine-beta-hydroxylase (DBH) as an index of sympathetic activity, since this enzyme is not submitted to uptake mechanisms or to enzymatic metabolism as are the circulating catecholamines norepinephrine (NE) and epinephrine (E). However, large discrepancies have been found between the results of these studies. The hypothesis which is examined in this study is that these discrepancies might arise from the different intensities in the stimuli utilized. In order to examine this possibility, plasma DBH activity was measured in seven subjects at rest and in three different conditions known to increase sympathetic activity to varying degrees, i.e., during hand-grip, standing, and supra-maximal bicycle exercise. Plasma NE and E concentrations were also measured during these stimuli. The results of this study show that DBH activity increases above resting levels only during supramaximal dynamic exercise, while plasma NE and E concentrations increase during each experimental condition. Furthermore, the increases in NE and E are related to each other and are also related to heart rate when all experimental conditions are considered. On the contrary, the variations in plasma DBH (expressed as a percentage of the resting value) are not related to other sympathetic indices or to heart rate. Since NE and E vary little from subject to subject at rest and increase discretely in response to the various stimuli, these plasma catecholamine concentrations therefore appear to represent the most accurate indices of sympathetic activity.

Dopamine beta-Hydroxylase↗