Effect Of Beta-adrenergic Blockade Research Articles

Effect of the beta-adrenergic blockade on intestinal lactate production and glycogen concentration in dogs infused with hexoses

To investigate effect of beta adrenergic blockade on intestinal lactate production and glycogen concentration in dogs infused with hexoses. Experiments were carried out on 35 fasted male anaesthetized dogs weighing between 9 and 16kg. The animals were divided into 7 (5 dogs per group) groups. Group I dogs served as control and infused with normal saline, groups II-IV were intravenously infused with glucose (1.1mg/kg/min), fructose (1.1mg/kg/min) and galactose (1.1mg/kg/min) respectively while groups V-VII animals were pretreated with propranolol (0.5mg/kg) and were infused with glucose, fructose or galactose respectively. A vein draining the proximal segment of the jejunum was cannulated along with right and left femoral arteries and veins. Glucose uptake was calculated as the product of jejunal blood flow and the difference between arterial and venous glucose levels (A-V glucose), part of the jejunum tissue was homogenized for estimation of glycogen concentration, and plasma lactate was assayed using lactate colorimetric kit. The result showed significant increase in venous lactate production in response to glucose (78.30±4.57mg/dL), fructose (60.72±1.82mg/dL) and galactose (71.70±1.30mg/dL) when compared with the control group (51.75±1.32mg/dL) at (p<0.05) with no significant difference in animals pretreated with propranolol. There was no significant difference in glycogen concentration (p>0.05) in animals infused with hexoses only compared with propanolol pretreated group. Results suggests that one of the possible fates of the enormous amount of glucose taken up by the intestine is conversion to lactate and not glycogen and β-adrenergic receptor does not affect it.

P1821The effect of beta-adrenergic blockade on weight change and mortality in patients with chronic heart failure

P1821The effect of beta-adrenergic blockade on weight change and mortality in patients with chronic heart failure

The effect of beta-adrenergic blockade on inflammatory and cardiovascular responses to acute mental stress

Acute mental stress elicits increases in plasma cytokine concentrations in humans, but the underlying mechanisms remain poorly understood. We assessed the impact of beta-adrenergic blockade on plasma interleukin 6 (IL-6) and IL-1 receptor antagonist (IL-1Ra) responses in a parallel group, double-blind randomised placebo-controlled trial involving 64 healthy young adult volunteers. Participants were administered 80 mg slow-release propranolol or placebo daily for 7 days before the stress testing session in which responses to 3 behavioural challenges (public speaking, mirror tracing, mental arithmetic) were evaluated. Propranolol administration was associated with reduced baseline levels of heart rate and IL-1Ra, and systolic blood pressure (BP) in men. Tasks stimulated increased plasma IL-6 concentrations sampled 45 min and 75 min after challenge, but these responses were blocked by propranolol in men (p < 0.001). Propranolol did not influence IL-6 responses in women, or IL-1Ra in either sex. Blood pressure and heart rate increased markedly during the tasks, but there was no differential stress reactivity in propranolol and placebo conditions. The results of the study support a role of sympathetic nervous system activation in stimulating acute IL-6 responses to stress, but only in men. The reasons for the differences between men and women remain to be resolved.

Effect of beta-adrenergic blockade on weight changes in patients with chronic heart failure

BackgroundWeight loss is common in patients with chronic heart failure (CHF) and is associated with adverse outcome. Activation of the sympathetic nervous system has been implicated in weight loss, wasting and cachexia. However, the effect of sympathetic antagonism on weight change in patients with CHF is not well defined. MethodsWe evaluated changes in body weight, the incidence of cachexia (weight loss >6%) and significant weight gain (>5%) in unselected patients with CHF due to left ventricular systolic dysfunction (LVSD) (LV ejection fraction (LVEF) <40%) and studied the effect of beta-blockade on weight change. ResultsOf the 1480 patients enrolled (median NTproBNP:1651 ng/L, median LVEF:31%), 86% received beta-blocker, 11% never had beta-blocker and 3% discontinued beta-blocker between baseline and 1 year.Patients who did not have or tolerate beta-blocker were more likely to develop cachexia (23% vs 10%, p < 0.001) and less likely to have significant weight gain (22% vs 24%, p < 0.001) than patient who had beta-blocker.During a median follow up of 1876 days (IQR: 993–3052 days), 894 (60%) patients died. Higher body mass index (BMI) at baseline, weight gain and beta-blocker therapy were associated with better outcome. Patients who had all 3 features: beta-blocker therapy, baseline BMI ≥ 25 and significant weight gain had the best outcome (22% mortality at 5 years). ConclusionPatients with CHF due to LVSD who receive beta-blocker were less likely to develop cachexia and more likely to have significant weight gain and better outcome compared to patients who did not receive or tolerate beta-blocker.

Correction to: Effects of Beta-Adrenergic Blockade on Diabetes-Induced Neurobehavioral Alterations in Mice

Correction to: Effects of Beta-Adrenergic Blockade on Diabetes-Induced Neurobehavioral Alterations in Mice

Effects of Beta-Adrenergic Blockade on Diabetes-Induced Neurobehavioral Alterations in Mice

Neurobehavioral activities were estimated in three groups of male albino mice using the open field, elevated plus maze, light/dark board, and hole-board tests. The control group included intact animals, while alloxan-induced diabetes was evoked in the other two groups (single i.p. injection of 120 mg/kg alloxan). In the third group, a nonspecific beta-adrenoreceptor antagonist, propranolol, was i.p. injected (40 mg/kg) before the induction of diabetes. In diabetic mice, all neurobehavioral indices tested in the four above-mentioned tests were significantly (P< 0.05) smaller than those in the control group. The frequencies of rearings and grooming episodes in the open field, number of entries into the open arms and time spent in these arms in the elevated plus maze test, and number of head dips in the hole-board test demonstrated the most intense drops (more than twofold). Pretreatment with propranolol provided significant (P < 0.05) normalization of all neurobehavioral indices in diabetic mice; such normalization with respect to the locomotion intensity, frequency of grooming, time spent in the open arms, and both indices in the light/dark board was nearly complete. Thus, diabetes in the animal model used is accompanied by the development of the state of abnormally high anxiety. The activity of the betaadrenergic system is noticeably involved in the formation of this state; pharmacological blocking of beta-adrenoreceptors provides significant anxiolytic effects.

Gene‐Specific Effect of Beta‐Adrenergic Blockade on Corrected QT Interval in the Long QT Syndrome

In the long QT syndrome (LQTS) the effects of beta-blocker treatment on prevention of cardiac events differs according to the genotype. We aimed to assess the effect of beta-blocker treatment on QT/QTc duration in Type 1 LQTS (LQT1) and Type 2 LQTS (LQT2) patients. 24-hour digital Holter ECG were recorded before and after beta-blocking therapy initiation in LQT1 (n = 30) and LQT2 patients (n = 16). QT duration was measured on consecutive 1-minute averaged QRS-T complexes leading to up to 1440 edited QT-RR pairs for each recording. We computed subject- and treatment-specific log/log QT/RR relationships which were used to correct the QT intervals. The QT duration was also evaluated at predefined heart rates and after correction using Bazett and Fridericia coefficients. At baseline, individual QT/RR coefficients were higher in LQT2 than in LQT1 patients (0.53 ± 0.10 vs. 0.40 ± 0.11, P < 0.001) and QT1000 was longer in LQT2 than in LQT1 patients (521 ± 38 vs. 481 ± 39 ms, P < 0.01). Beta-blockers significantly prolonged the mean RR interval (from 827 ± 161 to 939 ± 197 ms, P < 0.0001). The individual QT/RR coefficients were not significantly modified by beta-blockers. Beta-blocker treatment was associated with a prolongation of the QT1000 interval (from 481 ± 39 to 498 ± 43 ms, P < 0.01) in LQT1 patients but with a shortening in LQT2 patients (from 521 ± 38 to 503 ± 32 ms, P < 0.01). The effect of beta-adrenergic blockade on QTc duration is different in LQT1 and LQT2 patients. Our data suggest that, in LQT1 patients, the well-known positive effect of beta-blockade might be associated with a prolongation of QTc duration. The mechanisms of beta-blockade protection may be different in LQT1 and in LQT2 patients.

The effects of beta-adrenergic blockade on the hypothalamic and neurohypophysial vasopressin and oxytocin content in pinealectomized male rats.

Pinealectomized (PX), sham-operated and non operated control rats were injected intraperitoneally (i.p.), once daily at 8.00 over five days, with: (a) 0.9% sodium chloride, (b) propranolol hydrochloride in a dose of 10 mg/kg (= 0.1 ml solution per 100 g b.w.). Three hours following the last injection the animals were decapitated and the content of vasopressin and oxytocin was bioassayed in the hypothalamus and neurointermediate lobe. PX was followed by known decrease of both vasopressin and oxytocin in the hypothalamus and neurohypophysis. In rats not-PX propranolol did not change the vasopressin and oxytocin content in the hypothalamus and neurointermediate lobe. In PX-rats, treatment with propranolol resulted in a distinct increase of the vasopressin in the neurohypophysis. It may be therefore supposed that the beta-adrenergic transmission is in some way involved in the regulatory mechanisms of pineal-neurohypophysial functional relationship.

Afterload Reduction May Halt and Beta-Adrenergic Blockade May Worsen Progression of Left Ventricular Dysfunction in Patients With Chronic Compensated Mitral Regurgitation: A Retrospective Cohort Study

Severe chronic mitral regurgitation (MR) is associated with progressive left ventricular (LV) systolic dysfunction. Both afterload reduction and beta-adrenergic blockade have been suggested as methods for preventing LV dysfunction in asymptomatic patients with MR and normal LV function, who are therefore not yet candidates for surgical intervention. The objective of this study was to determine if afterload reduction reduces progression of LV dysfunction in patients with severe MR. The reports of echocardiographic studies performed 20 +/-14 months apart were compared in a retrospective cohort of 134 asymptomatic patients with moderate-severe chronic MR and baseline ejection fraction (LVEF) >50%. Groups were defined by exposure to any afterload-reducing drug: Group 0, no exposure; Group 1, exposure beginning after the first echocardiogram; and Group 2, drug exposure beginning before the baseline echocardiogram. The groups differed importantly only in treatment duration. In 72 patients not exposed to beta-adrenergic blockade, LVEF decreased by a relative -3.2% in Group 0, while Group 1 increased by 3.4% and Group 2 increased by 5.1%, p <0.01. Among 62 patients exposed to beta-adrenergic blockade, LVEF consistently worsened (Group 0, 4.8%; Group 1, -3.3%; Group 2, -1.7%; p = 0.71) compared to the 72 patients without beta-adrenergic blockade. In a multivariate model that included treatment duration and exposure to other medications, the beneficial effect of afterload reduction (p <0.03) and the deleterious effect of beta-adrenergic blockade (p < 0.02) were significant. Afterload reduction halted or reversed the progressive worsening of left ventricular function while beta-adrenergic blockade had a deleterious effect.

1114-202 Effects of beta-adrenergic blockade in pediatric marfan syndrome

1114-202 Effects of beta-adrenergic blockade in pediatric marfan syndrome

Effects of cold exposure on submaximal exercise performance and adrenergic activation in patients with congestive heart failure and the effects of beta-adrenergic blockade ( carvedilol or metoprolol)

Patients with congestive heart failure (CHF) exhibit a decrease in maximal exercise capacity in response to a cold environment. The aim of this study was to further investigate the impact of cold exposure on submaximal exercise capacity, systemic adrenergic drive, and the effects of long-term β-adrenergic blockade on these parameters. Thirty-three patients with CHF, with exercise limited by dyspnea and left ventricular ejection fraction of 26 ± 4%, were randomized to receive metoprolol or carvedilol for 6 months. The observations were compared with 12 age-matched healthy volunteers. Maximal exercise performance with gas exchange analyses were assessed using a ramp protocol, and endurance capacity was measured using 2 constant-load exercise tests performed randomly at 20°C and −8°C. Healthy volunteers increased their submaximal exercise time by 20% (1,353 ± 455 [20°C] vs 1,635 ± 475 seconds [−8°C]; p <0.05), whereas patients with CHF exhibited a 21% decrease in exercise time (1,182 ± 549 [20°C] vs 931 ± 524 seconds [−8°C]; p <0.05) at −8°C. Beta blockers increased submaximal exercise duration at 20°C (+261 ± 617 seconds; p <0.05) and −8°C (+374 ± 729 seconds; p <0.05). Norepinephrine increased to a greater extent at 4 minutes and at the time of exhaustion (at −8°C) only in patients with CHF. Beta-adrenergic blockade caused no significant decrease in plasma norepinephrine levels. Patients with symptomatic CHF exhibited a significant decrease in submaximal exercise time in response to moderate cold exposure. Beta-blocker therapy with either metoprolol or carvedilol significantly increases submaximal exercise time and attenuates the impact of cold exposure on functional capacity.

Minimally invasive direct coronary artery bypass (MIDCAB) versus coronary artery stenting for elective revascularization of the left anterior descending artery

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The effect of beta-adrenergic blockade after encoding on memory of an emotional event

Animal and human studies lend support to the hypothesis that enhanced memory associated with emotional experiences involves activation of the beta-adrenergic system. Evidence for the role of noradrenaline in emotional memory in humans has been gathered from experimental studies where blockade of the beta-adrenergic system with a beta-blocker selectively impaired long-term memory for an emotionally arousing story (a slide show), when the beta-blocker was given before subjects were confronted with the emotional stimuli. The purpose of this study was to test whether effective beta-adrenergic blockade occurring only after the stage of encoding has a similar impairing effect on memory. In a double blind experimental design, 60 healthy adult subjects received randomly one tablet of either propranolol (Inderal, 40 mg) or placebo. Drugs were administered just before the slide show begun and (in view of its pharmacokinetics) propranolol reaches peak levels 1 h after drug intake. Physiological arousal was monitored by heart rate and blood pressure. Half of the beta-blocker and placebo groups watched either a neutral or an arousal version of an 11-slide presentation. Memory performance was tested with a surprise free recall and recognition test 1 week later. Memory performance, specifically for the second phase in which emotional elements were introduced, was better in subjects who viewed the arousal version than subjects who saw the neutral version of the slide show. However, no effect of the beta-blocker condition was found. This experiment does not support a role for noradrenaline in the post-encoding phase and on the later processes of consolidation and retrieval. Although it remains possible that with a different dosage or timing protocol a post-treatment effect of noradrenaline in humans can be found, this experiment could not find support for it.

Potential Use of β3‐Adrenoceptor Antagonists in Heart Failure Therapy

Recently, a functional, negatively inotropic, beta(3)-adrenoceptor was characterized in the human heart. Several studies now suggest that this receptor might play an important role in the pathophysiology of heart failure, by counterbalancing the effects of a beta(1)- and beta(2)-stimulation. Therefore, this review summarizes the rationale and effects of beta-adrenergic blockade in chronic heart failure and specifically addresses the question of the potential use of beta(3)-adrenoceptor antagonists in the treatment of heart failure and other pathophysiological conditions associated with a decreased cardiac contractility.

Effect of beta-adrenergic blockade on elevated arterial compliance and low systemic vascular resistance in cirrhosis.

Patients with cirrhosis exhibit a characteristic hyperdynamic circulation with increased cardiac output and heart rate and reduced systemic vascular resistance. The compliance of the arterial tree has recently been reported to be increased in these patients, who are often treated with beta-blockers, but the effect of this treatment on arterial compliance has not been investigated. The aim of the present study was therefore to assess the effects of propranolol on the arterial compliance of patients with cirrhosis. Twenty patients with cirrhosis underwent a haemodynamic investigation with determination of splanchnic and systemic haemodynamics. Arterial compliance was determined as the ratio of the stroke volume to the pulse pressure and compared to normal values. All the patients had significant portal hypertension, with a mean hepatic venous pressure gradient (HVPG) of 17.8 mmHg, and responded to beta-blocker treatment with a significant reduction in the HVPG (-16%; P < 0.001). Arterial compliance was elevated (1.27 versus controls 1.01 ml/mmHg; P < 0.001), but remained almost unchanged during beta-adrenergic blockade (1.27 versus 1.29 ml/mmHg, +2%, ns), whereas systemic vascular resistance increased substantially (1083 versus 1378 dyn x s x cm-5, +27%; P < 0.001). The mean arterial blood pressure (-6%; P < 0.05), heart rate (-20%; P < 0.001), cardiac output (-25%; P < 0.001) and hepatic blood flow (-22%; P < 0.001) fell significantly. Treatment with beta-blockers increases small vessel (arteriolar) vascular tone towards the normal level, but does not affect the elevated compliance of the larger arteries in patients with cirrhosis.

Effect of beta-adrenergic blockade on elevated arterial and low systemic vascular resistance compliance in cirrhosis

Effect of beta-adrenergic blockade on elevated arterial and low systemic vascular resistance compliance in cirrhosis

Effect of beta-adrenergic blockade on elevated arterial and low systemic vascular resistance compliance in cirrhosis

Effect of beta-adrenergic blockade on elevated arterial and low systemic vascular resistance compliance in cirrhosis

Effect of Beta-adrenergic Blockade on Elevated Arterial Compliance and Low Systemic Vascular Resistance in Cirrhosis

Background: Patients with cirrhosis exhibit a characteristic hyperdynamic circulation with increased cardiac output and heart rate and reduced systemic vascular resistance. The compliance of the arterial tree has recently been reported to be increased in these patients, who are often treated with beta-blockers, but the effect of this treatment on arterial compliance has not been investigated. The aim of the present study was therefore to assess the effects of propranolol on the arterial compliance of patients with cirrhosis. Methods: Twenty patients with cirrhosis underwent a haemodynamic investigation with determination of splanchnic and systemic haemodynamics. Arterial compliance was determined as the ratio of the stroke volume to the pulse pressure and compared to normal values. Results: All the patients had significant portal hypertension, with a mean hepatic venous pressure gradient (HVPG) of 17.8 mmHg, and responded to beta-blocker treatment with a significant reduction in the HVPG (-16%; P < 0.001). Arterial compliance was elevated (1.27 versus controls 1.01 ml/mmHg; P

Heart rate and plasma cyclic AMP responses to isoproterenol infusion and effect of beta-adrenergic blockade in patients with postural orthostatic tachycardia syndrome.

To clarify the pathophysiological mechanism of postural orthostatic tachycardia syndrome (POTS). the responses of heart rate and the plasma cyclic AMP (cAMP) level to isoproterenol infusion in the supine position were evaluated in 10 POTS patients and 10 age-matched controls. Also, the effect of beta-adrenergic blockade on POTS was assessed using the headup tilt test. The POTS patients consisted of two men and eight women, with a mean age of 19.7 years (range. 15-28 years). An exaggerated increase of both heart rate and the plasma cAMP concentration after isoproterenol infusion at a low dose (1 microg/min) was observed in the POTS patients, but not in control subjects. Seven POTS patients received oral beta-blocker therapy. In five of these, symptoms were abolished and there was a smaller heart rate increase during the head-up tilt test. These data suggest that POTS may be more prevalent in young women and that beta-adrenergic hypersensitivity may play a role in the mechanisms of this syndrome. However, a larger series of patients need to be studied in the future.

Secretory immunoglobulin A and cardiovascular reactions to mental arithmetic, cold pressor, and exercise: Effects of beta-adrenergic blockade

Secretory immunoglobulin A and cardiovascular reactions to mental arithmetic, cold pressor, and exercise: Effects of beta-adrenergic blockade