Beta-sympathetic Blockade Research Articles

Power spectral analysis for autonomic influences in heart rate and blood pressure variability in fetal lambs.

Variability of R-R intervals and arterial blood pressure signals in chronically instrumented fetal lambs was analyzed by power spectral analysis based on an assumption of maximum entropy. There were four consistent components, very low (VL, 0.01-0.025 cycle/beat), low (L, 0.025-0.125 cycle/beat), middle (M, 0.125-0.2 cycle/beat), and high (H, 0.2-0.5 cycle/beat), in the normal heart rate variability and blood pressure spectra. Integrated peaks in the power spectrum were compared before and after the administration of sympathetic and parasympathetic blockades. beta-Sympathetic blockade reduced the spectral power in the VL and L frequency components. alpha-Sympathetic blockade reduced only the M frequency component in the spectrum of R-R interval variability. Parasympathetic blockade reduced the H and L frequency components in the R-R interval variability spectrum but increased these components in the systolic blood pressure variability spectrum. The results clearly demonstrate the association between fetal autonomic activity and change of power spectrum of heart rate and blood pressure variability.

The effect of change in sympatho-vagal balance on heart rate and blood pressure variability in the foetal lamb.

Cardiac and vascular function is mainly under autonomic nervous control within seconds to minutes, although the control is not mature at birth. We studied sympathovagal control of heart rate and blood pressure in chronically catheterized foetal lambs in the last trimester of gestation. Power spectral analysis was used to quantitate the frequency-specific heart rate variability (HRV) and blood pressure variability. We performed 15 experiments in seven foetal lambs. These preliminary studies showed that parasympathetic blockade by atropine (eight experiments) had no significant effect on the distribution of HRV to different frequencies. Beta-sympathetic blockade by propranolol (seven experiments) decreased the ratio of low and mid to high frequency (0.025-0.13 to 0.13-1.00 Hz) HRV (P = 0.02). The increased high frequency HRV in the absence of a similar increase in blood pressure variability and tracheal pressure variability suggests enhanced baroreflex responsiveness after propranolol administration. The frequency-specific sympathetic control of HRV in foetal lambs, the change in ratio of low and mid to high frequency HRV, might have clinical implications in estimating the level of foetal sympathetic activation in the follow-up of high-risk pregnancies.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns.

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Baroreflex control of myocardial contractility in conscious normotensive and renal hypertensive rabbits.

We have assessed resting myocardial contractility and its baroreflex control in normotensive and hypertensive conscious rabbits. Hypertension was induced by bilateral cellophane wrapping of the kidneys with experiments performed 6 weeks later during the established phase of hypertension. The peak rate of change of left ventricular pressure (peak LV dP/dt) was used as the index of myocardial contractility. Baroreflex control of contractility and heart period (HP) was assessed by constructing stimulus response curves relating change in mean arterial pressure (MAP), induced by balloon occluders around the abdominal aorta and inferior vena cava, to change in peak LV dP/dt and HP. These stimulus response curves were obtained in normotensive rabbits with and without cardiac pacing, and in both normotensive and hypertensive animals after cardiac beta sympathetic blockade with propranolol, vagal blockade with methylscopolamine, and combined cardiac autonomic blockade with propranolol and scopolamine, as well as in rabbits with intact autonomic effectors. Resting MAP was significantly higher in the hypertensive rabbits (119 +/- 2 mm Hg) compared to normotensive controls (76 +/- 1 mm Hg). Resting peak LV dP/dt was also greater by 51% in the hypertensive animals (7054 +/- 287 mm Hg sec-1) compared to controls (4690 +/- 223 mm Hg sec-1). There was no significant difference in the resting heart period or resting left ventricular end diastolic pressure. Transient changes in MAP induced by occlusion of the aortic or venous balloons produced significant alterations in peak LV dP/dt in normotensive animals with and without pacing and in hypertensive control animals. In animals with cardiac sympathetic block, the range and slope or sensitivity of the stimulus response curves were not significantly changed but in animals with vagal blockade the sensitivity was reduced by 90% and the range at 30 mm Hg by 88%. After propranolol and methylscopolamine were administered together, the stimulus no longer evoked a response. These experiments demonstrate that myocardial contractility is under baroreflex control and suggest that this is mediated principally via parasympathetic nerves to the heart. There was no significant difference between the sensitivity of baroreflex control of myocardial contractility in the normotensive (-84 +/- 14 mm Hg sec-1 per mm Hg) and the hypertensive (-110 +/- 14 mm Hg sec-1 per mm Hg) rabbits, unlike the baroreflex control of heart period where sensitivity was markedly impaired in the hypertensive (sensitivity 3.8 +/- 0.8 msec/mm Hg) compared to the normotensive (6.9 +/- 1.0 msec/mm Hg) animals.

Beta-sympathetic blockade with chronotropic compensation in the management of heart disease.

This presentation briefly describes the sympathetic and parasympathetic control of the heart, particularly in relation to coronary vascular effects. Autonomic disturbances following myocardial infarction and their significance are discussed. The influence of the autonomic system in chronic coronary heart disease is considered, particularly in relation to the beneficial effects which may be obtained by the combined use of beta-blocking drugs and cardiac pacing. Nine anginal patients with spontaneous or drug-induced bradycardia received temporary pacing and 27 others had pacemakers implanted. Pain was well controlled in the former group. Long term pacing produced worth-while benefit in 67% of the patients followed for periods up to 6 months, the figure falling to 50% among those followed for 24 months. Eight of the 27 relapsed. Thus, correction of bradycardia by pacing often produced a beneficial long term effect. A second group of 14 patients with ventricular arrhythmias was treated with beta-blocking agents combined with pacing. So far, 10 of these 14 have had their arrhythmias controlled either by the initial or by a modified drug regime. The results indicate that among patients with chronic coronary artery disease, beta-blockade to minimize cardiac sympathetic activity, coupled with pacing to prevent loss of chronotrophic control, often represents an effective combination for the management of refractory angina or arrhythmias.

Lack of effects of beta sympathetic blockade on the metabolic and respiratory responses to carbohydrate feeding

Increases in metabolic rate, heart rate and ventilation occur following carbohydrate feeding or during beta sympathetic stimulation. Furthermore, insulin secretion and hypokalemia are features common to both which raises the question as to whether these effects of carbohydrate depend upon an intact sympathetic nervous system. Accordingly, in the present study, we measured the effects of carbohydrate feeding (250 gram meal) before and after chronic beta sympathetic blockade in sex normal men. Before blockade metabolic rate (0 2 consumption) rose (P < 0.05) from a fasting mean of 248 ± 19.7 (SEM) ML 0 2/min to 292 ± 15.2 at 1 hr, 269 ± 13.7 at 2, and 262 ± 18.0 at 3 hr following the meal. During blockade (oral propranolol 80 mg p.o. Q 6 h for 3 days) the post-prandial increase in 0 2 consumption was also significant (P < 0.05) and almost identical to that found before blockade. A similar pattern was found for ventilation, heart rate, insulin secretion and hypokalemia, where the significant postprandial changes were not altered by blockade. A transient increase in serum triiodothyronine from a mean of 92 ± 8.4 μg/ML to 109 ± 9.4 occurred at 1 hr (P < 0.05) only during blockade. No other changes in thyroid hormonal concentrations occurred as a result of the meal. We conclude that although similarities exist between beta sympathetic stimulation and carbohydrate feeding, the post-prandial effects studied do not depend on intact beta sympathetic receptors.

Relative selective action of propranolol on cardiovascular and respiratory responses to isoproterenol.

Organ selectivity of beta sympathetic blockade with propranolol was studied in 6 normal men by comparing the cardiovascular and respiration responses during isoproterenol infusions before and after propranolol. Beta sympathetic blockade was achieved with propranolol and was considered present when there was no heart rate (HR) response to isoproterenol during an infusion tenfold greater than that which raised HR 25% during a control period. During blockade there was no change in HR or systolic or diastolic blood pressure during isoproterenol infusions. There was a consistent (p less than 0.05) rise in resting ventilation (+17%), oxygen consumption (+9%), and carbon dioxide production (+15%) with low-dose (raised HR 10% before blockade) isoproterenol infusion during blockade. These respiratory effects of low-dose isoproterenol during cardiovascular blockade were quantitatively similar to that before blockade. With infusion that raised HR 25%, there was a further increase in VE, VO2, and VCO2 before blockade but no further increase during beta blockade. Changes in acid-base status did not explain the increase in VE during blockade. We conclude that there are differences between effectiveness of propranolol blockade of the cardiovascular system and of the respiratory system.

Depressed myocardial function in the goat at high altitude.

To determine if depressed myocardial function contributes to the reported decrease in cardiac performance at high altitude, six chronically instrumented, unsedated goats were studied before, during, and after 2-wk exposure to hypobaric hypoxia (PaO2 44 mmHg). Undistorted ventricular pressure wave form was obtained from a miniature transducer implanted in the left ventricular cavity. The relationship between (dP/dt)/28P and P was extrapolated to obtain Vmax as an index of myocardial function. With beta sympathetic blockade (practolol) and pacing to reproduce heart rates, Vmax was uniformly and significantly depressed (P less than 0.01) during chronic hypoxia, and returned to control values following descent to low altitude. Likewise, stroke volume following saline infusion was decreased at high altitude and returned to control values following descent. Acute relief of hypoxia at high altitude by administration of 100% oxygen by mask did not reverse the depressed Vmax. These findings indicate that chronic hypobaric hypoxia produces a depression of myocardial function which is reversible by chronic but not acute relief of hypoxia.

The Pattern and Mechanisms of Response to Oxygen by the Ductus Arteriosus and Umbilical Artery

Extract: Response of the ductus arteriosus and umbilical artery to changes in oxygen tension, to acetylcholine, and to sympathetic and parasympathetic blocking agents was studied in vitro in isolated rings obtained from 22 fetal lambs of 98− to 147-day gestation.After stabilization of tension at a baseline level (0.3—0.7 g) in a Po2, environment of 35–45 mm Hg, both increase of the Po2 to 550 mm Hg and decrease of the Po2 to 8 mm Hg of the bathing solution produced constriction. The mean maximal tension developed by the ductus arteriosus was 3.91 g at high P0, and 3.87 g at low Po2. The increase in maximal tension developed with advancing gestation was also similar at both high and low Po2.At Po2, levels of 8–550 mm Hg, acetylcholine produced a further increase in tension, whereas bradykinin only produced an increase in tension at high PO2. Alpha and beta sympathetic blockade had no effect on the constrictor response to oxygen. Atropine relaxed the ductus arteriosus and umbilical artery at both high and low Po2 levels; the degree of relaxation was related to drug concentration. Acetylcholin-esterase also relaxed the ductus arteriosus constricted by oxygen. The cholinesterase inhibitor, edrophonium, produced ductus constriction at P0, of 35–45 mm Hg with little further effect from high Po2. The constrictor effect of high or low Po2 on the ductus arteriosus and umbilical artery seems to be mediated through release of acetylcholine.

Endocrine disease and anaesthesia. A review of anaesthetic management in pituitary, adrenal and thyroid diseases.

Endocrine disease and anaesthesia. A review of anaesthetic management in pituitary, adrenal and thyroid diseases.

Combined alpha and beta sympathetic blockade in hyperthyroidism. Clinical and metabolic effects.

Clinical and metabolic effects of propranolol (4.6 to 10.3 mg/kg/day) and phenoxybenzamine hydrochloride (0.44 to 0.82 mg/kg/day) administered for an average of 71 days were studied in eight hyperthyroid patients. Body weight, oxygen consumption, kinemometric measurements of the Achilles reflex, and serum lipids (cholesterol, triglycerides, and phospholipids) were studied. Common thyroid function tests, including protein-bound iodine, 131I uptake, resin triiodothyronine uptake, and 131I scan of the thyroid gland, were made before and after treatment. Five normal male subjects (mean age, 22 years) given propranolol (3.2 to 5.0 mg/kg/day) and phenoxybenzamine hydrochloride (0.3 to 0.47 mg/kg/day) served as controls for oxygen consumption and Achilles reflex studies. The drugs altered the thyrotoxic findings toward normal in the following manner: mean oxygen consumption reduced -12% (P < 0.01); significant increase of Achilles reflex times (P < 0.01); mean weight gain of 9 lb or +7% (P < 0.03); and most of the common signs and symptoms of thyrotoxicosis eliminated or attenuated. No effects on serum lipids or thyroid function tests were observed. It is concluded that alpha and beta adrenergic receptor blocking agents attenuate the weight loss, increased oxygen consumption, reflex changes, and most signs and symptoms of thyrotoxicosis. Furthermore, these abnormalities of hyperthyroidism are mediated in part via the sympathetic nervous system. This form of therapy is effective as an adjunct in the interim management of thyrotoxicosis.

Combined Alpha- and Beta-Sympathetic Blockade in Hyperthyroidism: Clinical and Metabolic Effects.

Combined Alpha- and Beta-Sympathetic Blockade in Hyperthyroidism: Clinical and Metabolic Effects.

Influence of beta sympathetic blockade (propranolol) on the hemodynamics of hyperthyroidism

The circulatory effects of propranolol (0.15 to 0.38 mg. per kg. given intravenously) were studied in seven hyperthyroid patients during periods of rest and exercise before and after the administration of propranolol and the results compared with propranolol effects in euthyroid subjects. Indices of left ventricular work (LVWI); stroke work (SWI); left ventricular tension time (TTI); mean systolic ejection rate (MSER); and cardiac output (CI) were derived in the usual manner. The mean rate of left ventricular isovolumetric pressure development (MRIPD) was employed as an index of contractility. Propranolol altered the thyrotoxic hyperkinetic circulatory state toward euthyroid levels. The mean changes after administration of propranolol in exercising hyperthyroid patients were heart rate decreased 19 per cent (P < 0.01), TTI decreased 18 per cent (P < 0.01), MRIPD decreased 14 per cent (P < 0.01). Comparison of the data in hyperthyroid patients with those in normal subjects showed an exercise increment in CI (35 per cent) and TTI (38 per cent) and LVWI (95 per cent) (P < 0.05) in excess of that seen in euthyroid subjects. Since TTI is generally considered a major determinent of myocardial oxygen consumption, the ratio of LVWI:TTI was considered an estimate of myocardial efficiency. Following propranolol administration LVWI:TTI increased 14 per cent (P < 0.05), indicating enhanced efficiency. It is concluded that beta adrenergic blockade attenuates the positive inotropic and chronotropic effects of thyroid hormone and presumably reduces the exaggerated myocardial oxygen requirement of thyrotoxicosis. Myocardial efficiency is thereby improved. The study supports the concept that the cardiac effects of thyroid hormone are mediated at least in part via the sympathetic nervous system.

The pharmacology of beta sympathetic blockade

The pharmacology of beta sympathetic blockade

BETA-SYMPATHETIC BLOCKADE IN HYPERTHYROIDISM

BETA-SYMPATHETIC BLOCKADE IN HYPERTHYROIDISM

THE EFFECT OF BETA-SYMPATHETIC BLOCKADE ON ARTERIAL OXYGEN SATURATION IN FALLOT'S TETRALOGY.

In many patients with Fallot's tetralogy, the fall in arterial oxygen saturation that occurs during exercise can be reduced by prior administration of the beta-sympathetic blocking drug, pronethalol. In a few patients there is also a rise in arterial oxygen saturation at rest. During exercise, increased stimulation of beta-sympathetic receptors in the heart enhances myocardial contractility; this leads to more complete systolic emptying of the right ventricle, and increased systolic obstruction to ejection of blood into the pulmonary circulation by hypertrophied infundibular muscle. It is this dynamic component of the right ventricular outflow tract obstruction that is abolished or reduced by beta-sympathetic blockade. The phenomenon occurs most readily when valve or high infundibular stenosis is associated with infundibular muscle hypertrophy proximal to the organic obstruction, and can sometimes be demonstrated by angiocardiography. Beta-sympathetic blocking drugs may have a place in the treatment of cyanotic attacks in Fallot's tetralogy, and possibly in the long-term management of the patients in whom total correction has not yet been undertaken.

THE SPECIFIC DYNAMIC ACTION OF FOOD

ArticlesTHE SPECIFIC DYNAMIC ACTION OF FOODCharles M. WilhelmjCharles M. WilhelmjPublished Online:01 Apr 1935https://doi.org/10.1152/physrev.1935.15.2.202MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNutrition and Nutritional Support in Critically Ill Patients22 June 2016 | Journal of Intensive Care Medicine, Vol. 8, No. 1Lack of effects of beta sympathetic blockade on the metabolic and respiratory responses to carbohydrate feedingMetabolism, Vol. 30, No. 5l-serine dehydratase and l-serine-pyruvate aminotransferase activities in different animal speciesComparative Biochemistry and Physiology Part B: Comparative Biochemistry, Vol. 63, No. 4Familial life-long persistent fever of unknown origin responding to dexamethasone and uronic acidsThe American Journal of Medicine, Vol. 46, No. 1 More from this issue > Volume 15Issue 2April 1935Pages 202-220 https://doi.org/10.1152/physrev.1935.15.2.202History Published online 1 April 1935 Published in print 1 April 1935 Metrics