Why the study?
Does i.v. propranolol alter sympathetic nervous system activity and haemodynamic responses in patients with ischaemic heart disease?
Does i.v. propranolol alter sympathetic nervous system activity and haemodynamic responses in patients with ischaemic heart disease?
Acute beta-blockade with i.v. propranolol in ischaemic heart disease increases sympathetic nervous activity, likely due to reduced cardiac output and altered tissue metabolic state.
Answers are grounded in this paper and cite their sources.
Suggests sympathetic activation after acute i.v. propranolol in IHD; hypothesis-generating and should not yet change practice.
To study the mechanisms by which acute beta-adrenergic blockade may change the activity of the sympathetic nervous system we have measured haemodynamic responses including splanchnic blood flow in twenty-three patients with ischaemic heart disease at rest and during supine exercise before and after i.v. injection of 0.039 mmol (10 mg) dl-propranolol. After propranolol both at rest and on exercise blood pressure, cardiac output and heart rate decreased, while splanchnic vascular resistance increased; mixed venous oxygen saturation decreased whilst arterial oxygen saturation and oxygen uptake were unchanged. Plasma noradrenaline increased after propranolol, values correlating with mixed venous oxygen saturation and splanchnic vascular resistance, both at rest and during exercise before and after propranolol, only at rest was there any correlation with arterial blood pressure. The increase in sympathetic nervous activity after propranolol may be due to a reduction in cardiac output and thereby alteration of the metabolic state (oxygen or related factors) in tissues. Afferent neural signals from the tissues may play a significant role in the regulation of sympathetic nervous activity.
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Hansen et al. (1978) studied this question.
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