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At least 1,513 records · Page 84Linked to original sources
PubMed1981

Interactions of adrenergic beta-receptor blockade (oxprenolol) and PCO2 in the anaesthetized dog: influence of intrinsic beta-sympathomimetic activity.

Effects of change in PaCO2 on systemic and coronary haemodynamics and on coronary sinus blood-gases have been studied in 10 open-chested dogs in which the lungs were ventilated with 0.8% halothane in oxygen, before and after administration of oxprenolol 0.3 mg kg-1 i.v. The hyperdynamic response of the circulation to hypercapnia was only marginally reduced after oxprenolol (cardiac output increased by 10% as opposed to 16% before oxprenolol). Before and after oxprenolol, hypocapnia caused large reductions of coronary blood flow (--24% and --20% respectively), while hypercapnia caused large increases of coronary blood flow (+ 59% and + 34% respectively). Oxprenolol does not appear to modify significantly the circulatory response to arterial carbon tension.

Anesthesia, General↗
PubMed1981

Oxprenolol and the circulation during anaesthesia in the dog: influence of intrinsic sympathomimetic activity.

Oxprenolol is a non-selective adrenergic beta-receptor antagonist displaying beta-mimetic activity. To test the hypothesis that beta-mimetic activity could minimize the response of the circulation to adrenergic beta-receptor blockade, cumulative dose-response curves to oxprenolol 0.1-1.6 mg kg-1 were obtained in seven anaesthetized dogs. Anaesthesia was maintained with 0.5% halothane supplementing nitrous oxide 66% in oxygen, under moderately hypocapnic IPPV. Oxprenolol, up to 0.4 mg kg-1 i.v., caused modest increases in heart rate, LV dP/dt max and cardiac output. With the largest dose (1.6 mg kg-1), significant increases in heart rate (+19%), LV dP/dt max (+13%) and cardiac output (+27%) were observed while arterial pressure remained unchanged and systemic vascular resistance decreased (-18%).

Anesthesia, Inhalation↗
PubMed1979

Defective cardiovascular reflexes and supersensitivity to sympathomimetic drugs in autonomic failure.

In 10 patients with chronic autonomic failure the clinical features and cardiovascular reflexes were correlated with the pressor responses to intravenous noradrenaline and tyramine. In all patients there was an exaggerated response to noradrenaline but a normal or only mildly exaggerated response to tyramine. Patients with lack of sinus arrhythmia and by implication baroreceptor reflex loss had greater responsiveness to pressor drugs than patients with preservation of this reflex. The responses to tyramine infusions imply that there must be sufficient noradrenaline released at defective sympathetic endings for a pressor response to occur. However, the lack of rise of plasma noradrenaline following tyramine, except in the patients with pure autonomic failure, clearly separates these responses from those of normal subjects. These results can be explained by the presence of lesions of both central and peripheral sympathetic pathways in patients with chronic autonomic failure and multiple system atrophy or Parkinsonism. The peripheral lesion, which is incomplete, may consist of replication of the receptors so causing supersensitivity with a duration of response that is little prolonged. The peripheral defect in the two patients with pure autonomic failure was found to be more complex and the prolonged response in one of these patients suggests the possibility of defective re-uptake or metabolism of noradrenaline. Clearly further study of the defects of sympathetic endings is required, including the use of other techniques such as catecholamine fluorescence. The extreme supersensitive responses underline the need for blood pressure monitoring during pressor drug studies prior to treatment, if the hazards of recumbent hypertension are to be avoided.

Adult↗
PubMed1984

Facilitation of calcium blocking and membrane effects by intrinsic sympathomimetic activity.

The interactions between ICI 118, 587 (Corwin) a beta 1-selective partial adrenergic agonist, and atenolol (Tenormin), propranolol (Inderal) and verapamil were examined first in anaesthetised dogs pretreated with syrosingopine and vagotomised. ICI 118, 587 was administered iv in cumulative doses of 0.1 to 1000 micrograms X kg-1. In four animals, heart rate increased from 102 +/- 4 to 188 +/- 12 beats X min-1 with a KA of 2.5 +/- 0.9 micrograms X kg-1. ICI 118, 587 was then administered to five groups each of four animals pretreated with atenolol (250 micrograms X kg-1 and 500 micrograms X kg-1iv), propranolol (250 micrograms X kg-1 and 500 micrograms X kg-1) or verapamil (200 micrograms X kg-1 plus 5 micrograms X kg-1 X min-1 iv). Both atenolol and propranolol shifted the dose response curve to the right but verapamil did not. Atenolol did not lower the maximal heart rate response to ICI 118,587. Both propranolol and verapamil slowed heart rate significantly (P less than 0.05) after, but not before, ICI 118,587. Further studies were then carried out in vitro. Cat papillary muscles were superfused with physiological saline at pH 7.4 and with either atenolol or ICI 118,587 at 5 X 10(-5) mol X litre-1. Tension was recorded at Lmax over a [Ca2+] range of 0.5 to 8 X 10(-3)mol X litre-1. The pA2 for verapamil against Ca2+ in the presence of atenolol and ICI 118,587 was 5.25 +/- 0.10 and 6.57 +/- 0.22 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1986

Intrinsic sympathomimetic activity (ISA) of pindolol in patients with sinus node dysfunction.

The effects of pindolol treatment on mean heart rate (MHR) and the number of paced heart beats were investigated in a group of 12 patients, with frequency programmable pacemakers implanted to control symptomatic bradyarrhythmias resulting from sinus node dysfunction. In a randomized double blind cross over experiment the patients were treated with pindolol (5 mg t.i.d.) or with placebo. Before the study the pacemaker was programmed to its lowest frequency in the demand mode. In the pretreatment period and after 2 weeks treatment with either pindolol or placebo a 24-hour ambulatory ECG was recorded. MHR during the night (24.00-8.00) was slightly but significantly increased by pindolol treatment by 6.0% when compared to placebo (P less than 0.05). There was no difference in the daytime MHR during either treatment period. During pindolol treatment the number of paced beats was reduced in 8/12 patients and in 4 of these the reduction exceeded 98%. In 2 patients the number of paced beats increased. The results indicate that in some patients with sinus node dysfunction pindolol can effectively reduce the number of paced beats thereby preserving the atrial contribution to pump function.

Adult↗
PubMed1986

The effect of beta-adrenoreceptor antagonists on the inhibition of pendular movements of rabbit ileum produced by periarterial sympathetic nerve stimulation and some sympathomimetic amines.

The effects of propranolol and of the selective beta 1- and beta 2-adrenoreceptor blocking drugs atenolol and ICI 118,551 were determined on the inhibitory responses of isolated segments of rabbit ileum to noradrenaline, isoprenaline and salbutamol and to periarterial sympathetic nerve stimulation. Responses to isoprenaline (0.04-10.24 microM) and salbutamol (1.4-89.6 microM) were blocked by propranolol in concentrations up to 5.0 and 12.8 microM, respectively. Responses to sympathetic nerve stimulation were reduced but responses to noradrenaline (0.03-1.92 microM) were unaffected by propranolol in concentrations up to 10.0 and 5.0 microM, respectively. Atenolol in concentrations up to 30.0 microM blocked responses to isoprenaline (0.04-2.56 microM) but did not affect responses to noradrenaline, salbutamol or sympathetic nerve stimulation in concentrations up to 3.0, 3.0 and 1.0 microM, respectively. However, when responses to noradrenaline and sympathetic nerve stimulation were reduced by phentolamine (1.0 microM), atenolol then produced further reductions. Responses to isoprenaline (0.04-2.56 microM) and salbutamol (1.4-89.6 microM) were blocked by ICI 118,551 in concentrations up to 0.5 microM. Responses to sympathetic nerve stimulation were reduced but responses to noradrenaline were unaffected by ICI 118,551 in concentrations up to 0.01 and 0.3 microM, respectively. Salbutamol (0.1 microM) increased the inhibitory response to sympathetic nerve stimulation and this effect was blocked by ICI 118,551 (0.01 microM). It was concluded that blockade of beta 2-adrenoreceptors, presumably located on sympathetic nerve terminals, decreases the release of transmitter noradrenaline and that blockade of beta 1-adrenoreceptors, presumably located in longitudinal smooth muscle cells, reduces the response to transmitter noradrenaline when alpha-adrenoreceptors are also blocked.

Adrenergic beta-Antagonists↗