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Biomedical subjects

A M Dart

Publications and source records attributed to A M Dart.

At least 91 records · Page 5Linked to original sources
PubMed1995

The relationship between arterial compliance, age, blood pressure and serum lipid levels.

OBJECTIVE: To investigate the association of serum lipids with non-invasively assessed systemic arterial compliance in a group of newly diagnosed coronary artery disease patients and their matched controls. DESIGN: Systemic arterial compliance is important in maintaining diastolic blood pressure and coronary perfusion, with decreased diastolic blood pressure in the presence of significant coronary artery disease suggested as contributing to increased morbidity. Decreased systemic arterial compliance is also associated with increased morbidity through its contribution to systolic hypertension. Despite the importance of arterial compliance, its association with biochemical factors is not certain. PATIENTS AND METHODS: Twenty newly diagnosed coronary artery disease patients and disease-free controls were matched for age, sex, smoking status and total serum cholesterol level. Systemic arterial compliance was measured using applanation tonometry and Doppler velocimetry before instigation of treatment. RESULTS: There was no difference in group low-density lipoprotein or high-density lipoprotein cholesterol levels. Systemic arterial compliance was significantly less in the coronary artery disease group. For the groups combined, a significant negative correlation was demonstrated between systemic arterial compliance and low-density lipoprotein; however, on separate group analysis the correlation was confined to the coronary artery disease group. A significant difference was found in the association between systemic arterial compliance and diastolic blood pressure for the two groups. CONCLUSIONS: Increasing low-density lipoprotein cholesterol levels are associated with decreasing systemic arterial compliance; however, the identified intergroup differences suggest that, presumably because of differences in lipid-vessel wall interactions, disease-free subjects exhibit relatively less alteration in aortic mechanical properties than those who develop coronary artery disease.

Age Factors↗
PubMed1994

HBPRCA Astra Award. Therapeutic restoration of endothelial function in hypercholesterolaemic subjects: effect of fish oils.

1. Endothelial dysfunction, evidenced as an impaired response to acetylcholine, is well documented in hypercholesterolaemic subjects. We examined the ability of dietary supplementation with fish oils to restore endothelial function in forearm resistance vessels in these patients and compared this with restoration by lipid-lowering therapy. 2. Responses of forearm blood flow to acetylcholine (4.6, 9.25, 18.5 and 37 micrograms/min) and sodium nitroprusside (200, 400, 800 and 1600 ng/min) were obtained using forearm venous occlusion plethysmography in nine hypercholesterolaemic and seven age-matched control subjects. The dose-response curve to acetylcholine was significantly blunted in hypercholesterolaemic subjects when compared with controls (P < 0.001). Responses to sodium nitroprusside were not different between the two groups (P = 0.37). 3. Lipid-lowering therapy decreased total plasma cholesterol levels by 33% and significantly augmented the responses to acetylcholine (P = 0.001) but not to sodium nitroprusside in the hypercholesterolaemic subjects. 4. Dietary supplementation with fish oils had no effect on either total or low density lipoprotein-cholesterol but significantly augmented the responses to acetylcholine (P = 0.011) in hypercholesterolaemic subjects. Responses to sodium nitroprusside were not altered (P = 0.94). 5. This study shows that endothelium-dependent relaxation is impaired in subjects with high cholesterol levels and that this impairment can be reversed by lowering low density lipoproteins (LDL) cholesterol levels. In addition, we demonstrate that restoration of endothelial function can occur without changes in LDL levels, by dietary supplementation with fish oils.

Acetylcholine↗
PubMed1994

Reperfusion following myocardial ischaemia enhances inositol phosphate release in the isolated perfused rat heart.

1. Global myocardial ischaemia (MI) for periods greater than 5 min caused an inhibition of phosphatidylinositol specific phospholipase C (PtdIns-PLC) activity. 2. Two min reperfusion following a 20 min MI period, a time point associated with reperfusion-induced arrhythmias, resulted in an activation of PtdIns-PLC activity, dependent on endogenous noradrenaline and mediated via alpha 1-adrenoceptors. 3. This 2 min reperfusion response, in contrast to healthy myocardium, resulted in: (i) enhanced PtdIns-PLC activity; (ii) increased sensitivity to endogenous noradrenaline; (iii) rapid increases in inositol(1,4,5)trisphosphate (Ins(1,4,5)P3); and (iv) PLC hydrolysis primarily of PtdIns(4,5)P2, such that the majority of InsP isomers derive from Ins(1,4,5)P3. 4. Together, these data suggest a functional role for Ins(1,4,5)P3 under post-ischaemic reperfusion conditions, and provide a possible link between alpha 1-adrenoceptor stimulation of the PtdIns turnover pathway and reperfusion injury.

Animals↗
PubMed1994

Sex differences in the parasympathetic nerve control of rat heart.

1. As it has been shown that oestrogen enhances the cholinergic muscarinic activity in the central nervous system, we studied sex differences in the response to parasympathetic nervous stimulation in the rat heart using in vivo and in vitro preparations. 2. In in situ perfused, innervated hearts, stimulation of bilateral vagus nerves (15 Hz with 1 mumol/L physostigmine) inhibited sympathetic nerve stimulation (5 Hz) induced noradrenaline release to a greater extent in female than in male rats (54 +/- 5 vs 72 +/- 5% of control). Similarly, vagus nerve stimulation at 1-20 Hz reduced heart rate (HR) more in females than males, and this sex difference became more marked in the presence of physostigmine. The chronotropic effect of vagal stimulation was attenuated after ovariectomy but potentiated after castration when compared with sham-operated controls. In contrast, the muscarinic agonist methacholine reduced neural NA release and HR equally well in both sexes. 3. In anaesthetized rats, reduction in HR and mean arterial pressure by vagus nerve stimulation (1-20 Hz) was more pronounced in females than in males after inhibition of acetylcholinesterase with physostigmine. 4. The results indicate that activation of parasympathetic nerve leads to greater presynaptic and postsynaptic effects in female than in male rat hearts, presumably due to a higher level of acetylcholine release following nerve activation.

Anesthesia↗
PubMed1994

Low cholesterol and impaired cardiac function following heart transplantation.

1. During follow-up of 59 cardiac transplant recipients over 2 or more years, a small group of subjects was observed who displayed an unpredictable, relatively marked, reduction in plasma cholesterol. 2. A significant proportion of these subjects were subsequently observed as having experienced a marked decline in left ventricular function at the time of routine radionuclide ventriculography. 3. While the mechanism for this fall in cholesterol is unclear, the observation of such an unexpected reduction in total cholesterol, late after heart transplantation should be considered significant and prompt further investigation including an assessment of allograft function.

Cholesterol↗
PubMed1994

Effects of dietary marine oil supplementation on reactivity of human buttock subcutaneous arteries and forearm veins in vitro.

1. The vascular reactivity of resistance arteries isolated from gluteal skin biopsies and veins isolated from forearms of subjects fed marine oils were examined. 2. Twenty seven healthy adult males were randomly allocated to one of two different treatment groups. The first group received maxEPA (eicosapentaenoic acid 0.178 g g-1; docosahexaenoic acid 0.116 g g-1) capsules 10 g per day for 28 days while the second group received an equivalent amount of mixed oil placebo capsules. Biopsies were performed on day 29 (13 for gluteal sections; 14 for forearm vein biopsies). Subcutaneous arteries and veins were mounted in myographs and standard organ baths, respectively. 3. The internal diameter of the subcutaneous arteries at a calculated transmural pressure of 100 mmHg averaged 183.7 +/- 10.3 microns in the maxEPA group and 182.6 +/- 19.8 microns in the placebo controls. Arteries from subjects on maxEPA demonstrated increased sensitivity to angiotensin II (maxEPA vs placebo: -log EC50 (M) -8.36 +/- 0.18 vs -7.91 +/- 0.14) but not to noradrenaline or 5-hydroxytryptamine. Concentration-response curves to acetylcholine, substance P and sodium nitroprusside obtained for noradrenaline precontracted vessels were unaltered with marine oil treatment as was the concentration-response curve to calcium in K(+)-depolarized vessels. 4. Vein internal diameter at a calculated transmural pressure of 20 mmHg averaged 3.06 +/- 0.23 mm in the maxEPA group and 2.96 +/- 0.89 in the placebo group. Responses to noradrenaline, 5-hydroxytryptamine, angiotensin II and endothelin-1 were obtained in the absence and presence of indomethacin (1 microM) in veins from both maxEPA and placebo-treated subjects. Neither dietary supplementation with marine oils nor indomethacin had any effect on the responses obtained to these agonists.5. The major finding of the present study was that in general, maxEPA supplementation did not affect responses to various vasoactive substances on isolated subcutaneous arteries or forearm veins. An exception was the observation of an enhanced response to angiotensin II in subcutaneous resistance arteries studied in vitro. This effect was selective for angiotensin II and was not apparent in veins isolated from the forearm.

Adolescent↗
PubMed1994

Exercise training increases total systemic arterial compliance in humans.

Using a noninvasive technique we have investigated the effect of 4 wk of exercise training on total systemic arterial compliance (SAC) in 13 previously sedentary young males. SAC is assessed from simultaneous measurements of ascending aortic blood velocity using Doppler velocimetry and surrogate estimates of aortic root pressure obtained by applanation tonometry of the right carotid artery. Subsequent calibration of the pressure waveform is by linear interpolation against brachial arterial pressures measured sphygmomanometrically. Exercise training increased the overall mean maximum oxygen consumption (VO2 max) by 5.1 ml.min-1 x kg-1 (95% confidence limits 1.30-8.80, P < 0.01) and decreased mean systolic blood pressure by 8.4 mmHg [95% confidence interval (CI) 2.9-13.9, P < 0.01]. Mean SAC increased by 0.26 units (95% CI 0.10-0.43, P < 0.01) with the regional stiffness of the aortic arch (measured echocardiographically using the beta-index) showing a complementary decrease of 1.03 (95% CI -2.25-0.19, P < 0.05). Assuming a logarithmic arterial volume-pressure relationship, we were able to dissociate the change in SAC due to the exercise training-induced decrease in blood pressure from that due to change in the intrinsic compliance of the systemic arteries. Our results indicate that 1) exercise training increases SAC; 2) that the increase in SAC is greater than that due to changes in blood pressure and is likely to include a component due to change in intrinsic arterial compliance; and 3) that the induced change in SAC is linearly related to change in VO2 max.

Adolescent↗
PubMed1994

Interactions between the effects of exercise and weight loss on risk factors, cardiovascular haemodynamics and left ventricular structure in overweight subjects.

OBJECTIVE: To assess the individual and combined effects of exercise and weight loss on the cardiovascular risk factors and cardiac left ventricular structure and function in overweight individuals. METHODS: A randomized, parallel-group, crossover study design was adopted. The following treatments were employed: exercise three times a week at 70% maximum work capacity for 30 min; dietary modification to achieve weight loss involving 4200 kj/day dietary restriction; and a combination of both exercise and dietary modification weight-loss programmes. Each subject was randomly assigned to one group only and was studied after a 12-week treatment and 12-week control period, performed in a random order. Thirty subjects entered the trial, 23 completing both treatment and control phases. RESULTS: Body weight remained unchanged with exercise alone and fell significantly both with weight loss and with the combination. The corresponding effects on blood pressure were also significant. Exercising groups also showed a significant increase in maximal oxygen consumption and a reduction in heart rate. Serum cholesterol and triglycerides fell significantly only after the combination, whereas high-density lipoprotein-cholesterol increased with exercise, decreased with weight loss and did not change with the combination. Interventricular septum and posterior wall thickness measurements remained unchanged after 12 weeks' treatment in all groups. No significant changes occurred in left ventricular internal diastolic diameter, wall thickness:radius ratio or the heart rate corrected ratio of peak early diastolic filling velocity:peak late diastolic filling velocity. Left ventricular mass and mass indexed to body surface area were not changed in any group. CONCLUSIONS: The results indicate that the effects of exercise and weight reduction on blood pressure are additive, although a positive interaction may exist with respect to lipids. Despite lowering blood pressure, exercise and weight loss had no effect on cardiac left ventricular structure or function in these overweight individuals.

Adult↗
PubMed1993

Mechanisms of noradrenaline release in the anoxic heart of the rat.

OBJECTIVE: The aim was to examine the time course of exocytotic and "spontaneous" noradrenaline overflow and the influence of an Uptake1 inhibitor, desipramine, in rat hearts subjected to anoxic and substrate-free perfusion. METHODS: Hearts were perfused with a constant flow and exocytotic noradrenaline overflow was elicited either by electrical stimulation of the left stellate ganglion or by K+ depolarisation. Noradrenaline overflow was measured by HPLC. RESULTS: Energy depletion for a period of 30 min resulted in an enhanced spontaneous noradrenaline overflow and a progressive decline in the nerve stimulation induced noradrenaline overflow. However, noradrenaline overflow induced by 40 mM K+ was enhanced by three- to fourfold in the energy depleted conditions. During anoxia, desipramine (0.3 microM) inhibited the spontaneous noradrenaline overflow and partly increased, in the early phase of anoxia, noradrenaline overflow by nerve stimulation, but showed no effect on K+ induced overflow. Further experiments showed that K+ at 10 mM failed to evoke noradrenaline overflow in normoxic hearts but induced a significant overflow in energy depleted hearts, either in the presence or absence of desipramine; quantities of noradrenaline overflow in response to 10-40 mM K+ were substantially higher in anoxia. This difference in noradrenaline overflow caused by K+ during normoxia and anoxia was partly narrowed by desipramine which enhanced overflow in normoxia. CONCLUSIONS: "Spontaneous" and exocytotic noradrenaline release coexist within the 30 min period of anoxia but their responses to Uptake1 inhibitor differ. K(+)-induced noradrenaline overflow was markedly augmented by energy depletion due to a combination of failed neuronal reuptake and enhanced exocytosis.

Animals↗
PubMed1993

Sympathetic activation and increased extracellular potassium: synergistic effects on cardiac potassium uptake and arrhythmias.

During acute myocardial ischemia, a combination of increased extracellular K+ concentration and sympathetic nerve activation exists. Using a perfused innervated rat heart model, we studied the influence of increased extracellular K+ concentrations on neural norepinephrine (NE) release, adrenergic stimulation-induced K+ uptake by the heart, and the occurrence of ventricular arrhythmias. Hearts were globally perfused with control (4 mM) or increased concentrations of K+ (7-16 mM). Sympathetic nerve stimulation-induced NE release was analyzed by radioenzymatic assay. Cardiac K+ uptake was assessed by the reduction in K+ concentration in the coronary venous effluent induced by nerve stimulation. Neural NE release was not influenced by increasing K+ from 4 mM to 7, 10, and 13 mM, but was suppressed by 16 mM K+ (-40 +/- 10%). Nerve stimulation induced cardiac uptake of K+, which was blocked by the beta-adrenoceptor antagonist timolol. This stimulated K+ uptake was substantially enhanced by increasing extracellular K+ and was also dependent on the intensity of sympathetic stimulation at 10 mM K+. Sympathetic nerve stimulation, together with a high K+ of 10 mM, was potent in initiating ventricular tachyarrhythmias, and quantitative NE release was well correlated with the frequency of ventricular arrhythmias. Our results demonstrate the synergistic effects of increased extracellular K+ and sympathetic activation, which may be involved in the genesis of ventricular arrhythmias.

Animals↗
PubMed1993

Inhibition of prostaglandin synthesis does not affect contractile responses to noradrenaline, serotonin, angiotensin II nor endothelin-1 in human forearm isolated veins.

1. The functional role of endogenous cyclo-oxygenase products was examined in the human forearm isolated vein. 2. Six healthy normal adult males (age > 18 years old) were recruited. Forearm veins were biopsied and ring segments mounted in standard organ baths for recording of isometric force. 3. Noradrenaline (-log molar EC50: 7.75 +/- 0.19; -log molar threshold concentration: 8.80 +/- 0.20), 5-hydroxytryptamine (-log molar EC50: 7.52 +/- 0.17; -log molar threshold concentration: 9.50 +/- 0.64), angiotensin II (-log molar threshold concentration: 9.00 +/- 0.28) and endothelin-1 (-log molar threshold concentration: 9.13 +/- 0.47) were equipotent in this preparation. Indomethacin (10 microM) had no effect on either the threshold concentration or EC50 of noradrenaline, 5-hydroxytryptamine nor the threshold concentration of angiotensin II nor endothelin-1. 4. Sodium nitroprusside (1 nM-10 microM) relaxed noradrenaline-precontracted preparations. Evidence of minimal endothelial influence was confirmed by the lack of relaxant response to acetylcholine (1 nM-10 microM). Histology using silver staining confirmed that endothelial cells were absent over greater than 90% of the lumen surface. 5. We conclude that endogenous prostanoids derived from smooth muscle cells, either released basally or agonist-stimulated, do not play a role in the regulation of vascular tone in the human forearm isolated vein.

Adult↗
PubMed1993

Lack of modulation by dietary unsaturated fats on sympathetic neurotransmission in rat hearts.

We examined the effect of dietary polyunsaturated fatty acids (PUFA) on cardiac sympathetic neurotransmission. Rats were fed semisynthetic diets (18.5% fat wt/wt) high in saturated fatty acids (control diet), high in n-6 PUFA (corn oil), or enriched with n-3 PUFA (Maxepa). A perfused innervated heart model was used to examine different aspects of sympathetic neurotransmission 10 wk after the feeding. Dietary PUFA increased the content of n-6 or n-3 PUFA in myocardial phospholipids compared with animals fed control diets. Myocardial norepinephrine content, sympathetic nerve stimulation-induced norepinephrine release, neural reuptake, presynaptic alpha-adrenergic inhibition of norepinephrine release, and postsynaptic inotropic response (+/- dP/dt) to sympathetic nerve stimulation or to a beta-agonist were essentially not influenced by dietary PUFA. Neural norepinephrine release during prolonged ischemia (60 min) was also similar in hearts from rats fed n-6 PUFA and control diets. Thus a modification of sympathetic neurotransmission was not achieved by feeding PUFA-enriched diets for 10 wk.

Animals↗
PubMed1993

Propranolol and lidocaine inhibit neural norepinephrine release in hearts with increased extracellular potassium and ischemia.

BACKGROUND: Propranolol and lidocaine are effective antiarrhythmic drugs in myocardial ischemia and infarction. As sympathetic nerve activation and norepinephrine release in ischemic hearts are arrhythmogenic, we tested the possibility that both agents inhibit neural norepinephrine release following sympathetic activation in the ischemic environment. METHODS AND RESULTS: The model used was an in situ perfused innervated rat heart. Norepinephrine release was induced by electrical stimulation of the left cervicothoracic stellate ganglion and analyzed using radioenzymatic assay or high-performance liquid chromatography. In normoxically perfused hearts, evoked norepinephrine release was not affected by either of the two agents at doses of 1 to 10 mumol/L when extracellular K+ concentration was 4 mmol/L but dose-dependently reduced at 10 mmol/L K+ (D,L-propranolol: -53 +/- 4% at 1 mumol/L and -64 +/- 6% at 10 mumol/L K+, lidocaine: -37 +/- 11% at 0.1 mumol/L, -67 +/- 5% at 1 mumol/L, and -75 +/- 6% at 10 mumol/L). At 10 mmol/L K+, norepinephrine release was not affected by timolol or atenolol (both 10 mumol/L but was equally inhibited by D- or L-propranolol at 10 mumol/L (-56 +/- 5% and -53 +/- 9%, respectively), indicating a beta-blocking-independent mechanism. In hearts with metabolic acidosis (pH 6.85) at K+ of 4 mmol/L, neural norepinephrine release was also reduced by propranolol at 10 mumol/L (-37%). Finally, in hearts perfused with 4 mmol/L K+ and subjected to 6-minute periods of ischemia, neural norepinephrine release was similarly suppressed by D,L-propranolol (-38 +/- 6% at 0.1 mumol/L, -44 +/- 5% at 1 mumol/L, and -78 +/- 3% at 10 mumol/L) or lidocaine (-39 +/- 7% at 0.1 mumol/L, -58 +/- 9% at 1 mumol/L, and -91 +/- 3% at 10 mumol/L). CONCLUSIONS: These data indicate that propranolol and lidocaine inhibit neural norepinephrine release via a Na+ channel-blocking mechanism that is synergistic with changes induced by ischemia, primarily raised extracellular K+. This mechanism may contribute to the anti-ischemic and antiarrhythmic properties of both agents in acute myocardial ischemia, which induces increased extracellular K+ and sympathetic activation.

Animals↗
PubMed1993

Marine oils dose-dependently inhibit vasoconstriction of forearm resistance vessels in humans.

The effects of dietary supplementation with marine oils on vascular reactivity in human forearm resistance arteries were studied. Healthy male adults (six to nine subjects per group) were given either maxEPA capsules (content: eicosapentaenoic acid, 0.178 g/g; docosahexaenoic acid, 0.116 g/g) at doses of 20, 10, or 5 g/day or placebo capsules at 20 g/day for 28 days. Capsule compliance was confirmed by measurement of platelet membrane incorporation of n-3 fatty acids. Blood pressure was not affected by either maxEPA or placebo. The influence of treatment interventions on forearm vasoconstrictive responses to local infusions of angiotensin II and norepinephrine was examined using venous occlusion plethysmography before and after treatment. Responses to both agonists were significantly suppressed by 20 g/day maxEPA (slopes before and after maxEPA, respectively: angiotensin II, 3.34 and 0.89; norepinephrine, 0.91 and 0.41). When analyzed as difference in area under the dose-response curves, the suppressive effects of maxEPA were clearly dose dependent (angiotensin II: 20 g area reduced by 72%, 10 g by 67%, 5 g by 33%). Similarly, responses to norepinephrine were dose-dependently suppressed by maxEPA (20 g area reduced by 61%, 10 g by 63%, and 5 g by 33%). Placebo had no effect on the responses to either constrictor. The responses to both agonists returned to preoil levels after 2 months' discontinuation of 20 g/day maxEPA. We conclude that the suppressive effects of marine oils on vascular reactivity may, in part, contribute to their cardioprotective influence in humans.

Adolescent↗
PubMed1993

Indomethacin inhibits the effects of dietary supplementation with marine oils on vasoconstriction of human forearm resistance vessels in vivo.

OBJECTIVE: Dietary supplementation with marine oils attenuates the responses to noradrenaline and angiotensin II in human forearm resistance arteries. The mechanisms underlying these effects were the subject of the present study. METHODS: Twenty-two normal male adults were allocated to one of three groups. The first group (n = 11) received 10 g/day marine oil capsules (maxEPA) for 28 days. The second group (n = 7) received maxEPA plus 25 mg indomethacin three times a day on days 28 and 29. The third group (n = 4) received 10 g/day mixed-oil placebo capsules for 28 days, plus indomethacin on days 28 and 29 as in group 2. Forearm venous occlusion plethysmography was performed before and immediately after each treatment period. RESULTS: Responses to acetylcholine, sodium nitroprusside or reactive hyperaemia (area under the time-response curve: pre-maxEPA 14,850 +/- 3502, post-maxEPA 17,118 +/- 4576 units) were unaffected by maxEPA. The suppressive effect of maxEPA on responses to noradrenaline and angiotensin II (from group 1) was no longer apparent in the group receiving indomethacin in addition to maxEPA. Indomethacin, in subjects on placebo capsules, had no effect on the responses to either agonist. CONCLUSION: We conclude that the suppressive effects of maxEPA result from alterations to in vivo prostanoid profiles.

Adolescent↗
PubMed1992

Exercise training reduces the sympathetic component of the blood pressure-heart rate baroreflex in man.

1. Exercise training reduces resting sympathetic activity, but the effects on sympathetic activation or withdrawal during baroreflex responses to blood pressure perturbations are controversial. The purpose of this study was to investigate the effects of training on both the vagal and sympathetic reflex heart rate responses to blood pressure changes. 2. Using 10 healthy males in a randomized cross-over design, we examined the effects of three 30 min cycling sessions at 70% of maximal capacity for 4 weeks on the steady-state reflex heart rate responses to perturbations in mean arterial pressure induced with injections of nitroprusside and phenylephrine. The method provides a sigmoidal relationship between changes in heart rate and blood pressure. The upper plateau (maximum tachycardia in response to blood pressure reduction) and lower plateau (maximum bradycardia in response to blood pressure elevation) are mainly mediated by the cardiac sympathetics and vagus, respectively. The slope of the relationship is a measure of reflex gain. 3. Training, which increased maximal oxygen consumption by 13 +/- 2% (mean +/- standard error of the difference), reduced supine and standing blood pressures by 3 +/- 1/3 +/- 1 mmHg (P less than 0.05) and 4 +/- 1/2 +/- 2 mmHg (P less than 0.05 for systolic), respectively, whereas resting heart rate was lowered by 6 +/- 1 beats/min (P less than 0.05). Reflex sensitivity in the presence of functioning vagus and sympathetics was not altered with training, but the vagal component of sensitivity, as assessed after sympathetic blockade with propranolol, was significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗