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Biomedical subjects

D Cousineau

Publications and source records attributed to D Cousineau.

At least 37 records · Page 2Linked to original sources
PubMed1984

Acute effects of captopril on the coronary circulation of patients with hypertension and angina.

Patients with hypertension have a high incidence of coronary artery disease. Captopril, the angiotensin-converting enzyme inhibitor, was given to eight patients with hypertension and coronary artery disease; it decreased mean arterial pressure from 121 to 103 mm Hg (p less than 0.01) but had no effect on heart rate. The rate-pressure product decreased from 12.5 to 11.4 X 10(3) (p less than 0.01). The change in coronary blood flow (90 to 80 ml per minute) and myocardial oxygen consumption (965 to 852 ml per minute) tended to parallel the decrease in the rate-pressure product. Captopril did not change global myocardial lactate (20 to 34 percent) or oxygen (9.6 to 10.0 volume percent) extraction. Hence, captopril decreases the rate-pressure product and tends to decrease myocardial oxygen consumption without causing global myocardial metabolic deterioration.

Aged↗
PubMed1984

Effects of a rapid change in muscle glycogen availability on metabolic and hormonal responses during exercise.

To evaluate the metabolic and hormonal adaptations following a rapid change in muscle glycogen availability, 14 subjects had their muscle glycogen content increased in one leg (IG) and decreased in the other (DG). In group A (n = 7), subjects exercised on a bicycle ergometer at 70% maximal oxygen uptake for 20 min using the DG leg. Without resting these same subjects exercised another 20 min using the IG leg. Subjects in group B (n = 7) followed the same single-leg exercise protocol but in the reverse order. In order to get some information on the time sequence of these possible adaptations, blood samples were collected at rest and at the beginning and the end of each exercise period (min 5, 20, 25, and 40). Results indicated that 5 min after the switch from the DG leg to the IG leg, transient increases in plasma free fatty acids (1.20 to 1.39 meq X 1(-1)) and serum insulin (10.1 to 12 mu X 1(-1)) concentrations occurred. Between minute 25 and 40 of exercise, the DG to IG switch was accompanied by a decrease in free fatty acids and glycerol concentrations as well as an increase in lactate levels. An opposite response was observed in the IG to DG condition during the same time span. Plasma norepinephrine, epinephrine, glucagon, and serum cortisol concentrations were not significantly affected by the leg change. These results suggest a rapid preferential use of muscle glycogen when available and a time lag in the response of the extramuscular substrate mobilization factors.

Adult↗
PubMed1984

Effects of a 24-h CHO-poor diet on metabolic and hormonal responses during prolonged CHO-loaded leg exercise.

This study examined the effects of a pre-experimental period of arm exercise followed by a 24-h carbohydrate (CHO)-poor intake, intended to reduce initial hepatic glycogen levels, on substrate and endocrine responses during prolonged CHO-loaded leg exercise. Seven subjects pedaled a cycle ergometer for 60 min at 62% VO2 max in the two following conditions: 1) after leg CHO loading followed by a 60-min arm exercise and a 24-h CHO-poor diet (CHOL + P), and 2) after leg CHO loading only (CHOL). Greater blood concentrations of fatty acids (1.2 vs 0.9 mEq X L-1), glycerol (0.41 vs 0.20 mmol X L-1), norepinephrine (2.09 vs 1.14 ng X ml-1), and epinephrine (0.38 vs 0.19 ng X ml-1) were observed in the CHOL + P as compared to the CHOL condition at min 60 of exercise. Insulin concentration was significantly (P less than 0.05) lower in the CHOL + P condition at rest and during exercise. There were no significant differences during exercise between the two conditions in blood glucose, lactate, glucagon, and cortisol concentrations. It is concluded that changes in blood glucose concentration do not solely account for metabolic and hormonal adaptations during prolonged leg exercise and that a pre-experimental period of arm exercise and CHO-poor diet, in spite of an increase in leg muscle glycogen, may provide a stimulus for such adaptations. It is suggested that the liver glycogen content may be involved in the regulatory mechanism.

Blood Glucose↗
PubMed1984

Effect of beta-adrenergic blockade on in vivo norepinephrine release in canine heart.

The beta-adrenergic blockade-induced reduction in myocardial norepinephrine overflow during sympathetic stimulation was examined by use of the multiple indicator-dilution 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 the rate of local release of norepinephrine into the interstitial space. The model was tested by first examining the effects of two drugs that increase myocardial norepinephrine overflow during sympathetic stimulation by differing mechanisms: desmethylimipramine, a norepinephrine uptake inhibitor, and phentolamine, an alpha-adrenergic blocker. The uptake inhibitor was demonstrated to reduce interstitial uptake and the alpha-blocker to increase local neurotransmitter release, without change in blood flow. The beta-adrenergic blocker, in contrast, reduced coronary blood flow and decreased the capillary norepinephrine permeability surface product but did not change the rate of local release. The decreased norepinephrine overflow after beta-blockade was deduced to result from the decrease in transcapillary flux and secondary increase in interstitial uptake.

Adrenergic beta-Antagonists↗
PubMed1983

Metabolic and hormonal responses of elite swimmers during a regular training session.

Metabolic and hormonal measures of eight elite swimmers were taken at rest and during a regular training session after a prolonged bout of swimming (4560 +/- 68 m) at moderate intensity (MI) and after medium duration-high intensity (HI) swimming exercise (1471 +/- 157 m). MI and HI swims were respectively associated with significant increases in free fatty acids (0.4 at rest to 0.8 and 0.67 microeq . ml-1) glycerol (0.1 to 0.26 and 0.25 mmol . l-1), growth hormone (14 to 65 and 51 ng . ml-1) and norepinephrine (0.5 to 3.9 and 4.1 ng . ml-1). HI contrary to MI swimming was also associated with a significant (p less than 0.01) increase in blood lactate (1.5 to 8.8 mmol . l-1) and epinephrine (0.13 to 0.71 ng . ml-1) concentrations. Glucose, insulin, glucagon, and cortisol concentrations were not changed during the training session. It is concluded that a regular training session in elite swimmers is associated with an increase in lipid utilization, and a modest change in some of the hormones directly involved in the regulation of blood glucose level.

Adolescent↗
PubMed1983

Blood flow and norepinephrine effects on liver vascular and extravascular volumes.

The relative effects of changes in hepatic blood flow and in levels of sympathetic activity on liver volumes were ascertained by use of multiple-indicator dilution studies. Portal vein-hepatic vein dilution patterns were obtained following injection of a mixture containing 51Cr-labeled red blood cells (a vascular reference) and 14C-labeled sucrose (a reference extracellular substance). Hepatic blood volume was calculated as the product of liver blood flow and red cell transit times, and interstitial space as the product of plasma flow and the difference between labeled sucrose and red cell transit times. Concentrations of norepinephrine and epinephrine were measured in aorta, portal vein, and hepatic vein. Hepatic blood volume and interstitial space increased with increased blood flow; and elevated plasma norepinephrine levels, especially in portal vein (following either exogenous infusion or activation of peripheral sympathetic fibers) selectively reduced the distending effect of hepatic inflow on the vascular volume. The data provide a description of the in vivo variation in canine liver vascular and interstitial volumes with blood flow and sympathetic activation.

Animals↗
PubMed1983

Reduced aortocoronary sinus extraction of epinephrine in patients with left ventricular failure secondary to long-term pressure or volume overload.

Heart failure is associated with a reduction in tissue norepinephrine concentration, catecholamine fluorescence, and tyrosine hydroxylase activity. We hypothesized that this attrition of sympathetic nerve function might also be associated with a reduction in the ability of the neuronal membrane to sequester catecholamines. Since the heart does not release epinephrine, the cardiac extraction of epinephrine should be an index of the membrane uptake system. In 12 patients with documented left ventricular failure (pulmonary edema) secondary to mechanical overload and in 10 patients with no history of heart failure, we measured simultaneous plasma catecholamine concentrations in the aorta, coronary sinus, and femoral vein. The aortocoronary sinus extraction of epinephrine was 43 +/- 17% in the group with no evidence of heart failure but 0 +/- 14% in the group with failure. Net norepinephrine outflow (release minus extraction) was significantly higher in the group with failure, possibly because of reduced extraction. There was neither a reduction in the ability of the lower limb to extract epinephrine nor an increased norepinephrine outflow from the limb. These findings suggest that the sympathetic neuronal membrane uptake system is also depressed in the failing heart and that if the mechanism of catecholamine sequestration in the heart is related to that in the lower limb, the ablation of sympathetic nerve function is specific to the heart and is not a result of a generalized depression of the peripheral sympathetic nervous system.

Aorta↗
PubMed1983

Changes in cardiac transcapillary exchange with metabolic coronary vasodilation in the intact dog.

The effects of metabolic coronary vasodilation on transcapillary exchange in the heart were examined in anesthetized dogs by use of the multiple indicator dilution technique. Animals were studied under basal conditions and during coronary sinus pacing. To obviate adrenal medullary stimulation, catheters were placed in coronary artery and coronary sinus in a closed chest preparation. Plasma catecholamine concentrations were determined to provide an index of the level of sympathetic tone. Labeled albumin and sucrose were injected into the coronary artery, and outflow dilution curves were secured. Analysis of these, with a model incorporating throughput and returning components, and heterogeneity of capillary transit times, provided parameters reflecting flow, permeability-surface product for sucrose, and capillary heterogeneity. Coronary sinus pacing increased both heart rate and plasma norepinephrine values; in response, myocardial oxygen consumption increased, metabolic vasodilation occurred, and coronary flow increased. The capillary permeability-surface product for sucrose increased with the flow but tended to plateau at higher values, showing a saturation phenomenon. Capillary heterogeneity, present in control animals with low sympathetic tone, was grossly decreased during cardiac metabolic activation. The Crone-Renkin approximation formula for the permeability-surface product yielded values that were too low at low flows and values approaching those from the complete model at high flows. The findings indicate an integrated pattern of circulatory response to cardiac metabolic activation characterized by decreased resistance, increased flow, increased permeability-surface product, and reduced heterogeneity. The last two effects amplify the capacity of increased flow to deliver substrates to heart muscle cells.

Animals↗
PubMed1981

Plasma norepinephrine response to exercise before and after training in humans.

Plasma norepinephrine (NE) concentration was measured by means of a sensitive radioenzymatic assay in blood collected from an antecubital vein in 10 healthy male subjects (37 +/- 2 yr, mean +/- SE). The subjects were evaluated at rest and during exercise before and after a 20-wk training program on bicycle ergometer (three 30-min sessions per week at 80% of maximal heart rate). Following the training program, maximal oxygen uptake increased significantly from 33 +/- 2 to 42 +/- 1 ml . kg-1 . min-1. Resting plasma NE remained unchanged after training (167 +/- 38 before and 185 +/- 29 pg . ml-1 after training). For a given absolute work load (735 +/- 51 kg . m. min-1) the sympathetic nervous response was lower after training as reflected by the decrease in NE concentration (1,371 +/- 286 vs. 687 +/- 64 pg . ml-1). At the same relative work load (heart rate: 158 +/- 5 before and 157 +/- 5 beats . min-1 after training) plasma NE concentration was unchanged after training (1,371 +/- 286 vs. 1,729 +/0 371 pg . ml-1). Results from the present study show that the sympathetic nervous activity is closely linked to the exercise demands and confirm earlier suggestions that it remains constant in relation to the relative work load.

Adult↗
PubMed1980

Electro- and echocardiographic study of the left ventricle in man after training.

Fourteen sedentary middle-aged men underwent a chest X-ray, a 12 lead ECG, a VCG, and an echocardiographic examination prior to and following 5 months of training a moderately severe intensity, on a cycle ergometer. No modification in the X-ray cardiac profile was observed following training. Some electrocardiographic (R wave amplitude in V5 and V6 and Sokolow index: SV1 + RV5 or V6) and vectorcardiographic (maximal QRS vector amplitude, maximal spatial QRS vector, and R wave amplitude) indices of left ventricular hypertrophy were slightly but significantly increased following training. The echocardiographic measurements in diastole (septal and posterior wall thickness, left ventricular internal diameter, and left ventricular mass) were unchanged after training. Results suggest that electrical changes may not provide adequate indications of left ventricular morphological modifications. The lack of echocardiographic evidences of left ventricular hypertrophy suggest that: (1) training does not necessarily induce left ventricular hypertrophy; (2) the large heart sometimes observed in athletes may be the result of a genetic factor or of a prolonged and very intensive training pursued since a very young age, over a number of years; and (3) left ventricular enlargement probably plays a minor role in the increase in aerobic capacity following training.

Echocardiography↗
PubMed1980

Evidences supporting an increased sympathetic tone and reactivity in a subgroup of patients with essential hypertension.

Several experimental evidences have shown that, under standarized conditions, circulating catecholamines (CA) or norepinephrine (NE) levels can be used as a valid index of the sympatho-adrenal activity in animal and man. This approach in the study of hypertensive patients has permitted to uncover that about 50% of patients with labile hypertension and about 30% of patients with stable hypertension had elevated CA levels at rest for 20 minutes in the supine position. The increased CA levels were mainly due to a rise in NE in stable hypertension and to a rise in epinephrine (E) in labile hypertension. On the basis of circulating CA levels, the hypertensive patients were divided into hyperadrenergic (CA levels above normal range) and normoadrenergic (CA levels within the normal range) subgroups. The hyperadrenergic labile or stable hypertensive subgroups were found to be also characterized by an enhanced CA or NE increase in response to change in position from supine to standing, by a faster heart rate and by an increased myocardial contractility, while these parameters were normal in the normoadrenergic subgroups. These findings support therefore the existence of an increased sympathetic tone and reactivity in association with hyperkinetic cardiac functions in an important population of hypertensive patients. In response to two weeks treatment with beta-blockers (either propranolol or metoprolol) hyperadrenergic stable hypertensive patients were found to be more responsive to this therapy than normoadrenergic patients although both groups had the same initial blood pressure. Moreover, this treatment lowered basal NE or CA levels and restored the enhanced CA or NE response to change in position toward normal in hyperadrenergic patients while it did not modify significantly circulating supine or standing CA and NE in normoadrenergic patients. These findings strongly support a participation of the sympathetic system in the maintenance of an elevated blood pressure in hyperadrenergic patients and raise the possibility of using a more rational approach in the therapy of hypertension.

Adult↗
PubMed1978

Circulating catecholamines and systolic time intervals in labile and sustained hypertension.

1. Average supine circulating total catecholamine concentrations were found to be higher than the normal range in about 50% of patients with labile hypertension and in about 30% of patients with sustained essential hypertension. 2. These higher resting concentrations were mainly due to an increase in adrenaline in labile hypertension and to an increase in noradrenaline in sustained hypertension. 3. Patients with elevated catecholamine concentrations were also characterized by a higher heart rate, by an increased myocardial contractility and by greater hypotensive response after treatment with beta-adrenoreceptor blocking agents. 4. These studies suggest the existence of sub-groups of hypertensive patients with increased sympathetic tone.

Catecholamines↗